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<title>Permanent Hematology-Oncology Job in Amarillo, TX Seeks 2 Hem/Onc providers Texas with Enterprise Medical Service</title>
<link>http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_texas/page_7.html</link>
<description><![CDATA[Established private cancer center is seeking two additional medical oncologists for their practice.  They currently have 3 full time and 1 part time on staff.  They also have 2 nurse practitioners.   ]]></description>
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<item rdf:about="http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_new_york/page_4.html">
<title>Permanent Hematology-Oncology Job in Upstate New York New York with Enterprise Medical Service</title>
<link>http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_new_york/page_4.html</link>
<description><![CDATA[Hospital in upstate New York is seeking an additional Hem/Onc.  They are building a brand new state of the art cancer center.  Can expect to see an average of 15-20 patients per day.  Call will be 1:2 ]]></description>
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<title>Permanent Hematology-Oncology Job in Southern Illinois Illinois with Enterprise Medical Service</title>
<link>http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_illinois/page_9.html</link>
<description><![CDATA[Hospital system in southern Illinois is seeking an additional Hem/Onc for their area.  The new physician can choose to join 1 other Hem/Onc who is in a solo practice, or can become an employee of the ]]></description>
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<item rdf:about="http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_texas/page_6.html">
<title>Permanent Hematology-Oncology Job in Corpus Christi, TX Area Texas with Enterprise Medical Service</title>
<link>http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_texas/page_6.html</link>
<description><![CDATA[Comprehensive Cancer Center with solid support staff is seeking an additional Hem/Onc for their center.  The center has a State-of-the-art Infusion Center, on site Radiation Oncology.  You would be teaming ]]></description>
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<title>Permanent Hematology-Oncology Job in St. Cloud, MN Minnesota with Enterprise Medical Service</title>
<link>http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_minnesota/page_2.html</link>
<description><![CDATA[We are assisting the Veterans Affairs medical clinics in the upper Midwest with the recruitment of an additional Hematology Oncology physician.   They currently have 1 Hem/Onc on staff who works part ]]></description>
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<title>Permanent Hematology-Oncology Job in Abilene, TX opportunity Texas with Enterprise Medical Service</title>
<link>http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_texas/page_4.html</link>
<description><![CDATA[Excellent employed opportunity for a BC/BE Hematology/Oncologist in affiliation with a modern, well-equipped cancer center. They currently have 3 other Hem/Oncs on staff.  The group is very busy, currently ]]></description>
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<item rdf:about="http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_florida/page_12.html">
<title>Permanent Hematology-Oncology Job in Panhandle of Florida Florida with Enterprise Medical Service</title>
<link>http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_florida/page_12.html</link>
<description><![CDATA[Join an established hospital based Cancer Center in coastal FL. Call will be 1:7   Center has 3 Offices in the FL panhandle and south AL. Will work out of 1 office.   The center has 14 chemo chairs and ]]></description>
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<item rdf:about="http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_pennsylvania/page_13.html">
<title>Permanent Hematology-Oncology Job in Closed proximity to Philly &#x26; Baltimore Pennsylvania with Enterprise Medical Service</title>
<link>http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_pennsylvania/page_13.html</link>
<description><![CDATA[Group in eastern PA is seeking a BC/BE hematologist/oncologist for their practice. They currently have 6 physicians in the group. The group is supported by the hospitals Cancer Center which is developing ]]></description>
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<item rdf:about="http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_kansas/page_3.html">
<title>Permanent Hematology-Oncology Job in Kansas City, KS Academic opportunity Kansas with Enterprise Medical Service</title>
<link>http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_kansas/page_3.html</link>
<description><![CDATA[University Medical Center is looking for a physician who is Board Certified in either or both IM and Hematology, or if an Oncologist must be will to do Mostly Hematology. This is an academic position ]]></description>
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<item rdf:about="http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_arizona/page_8.html">
<title>Permanent Hematology-Oncology Job in Academic Opportunity in Arizona Arizona with Enterprise Medical Service</title>
<link>http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_arizona/page_8.html</link>
<description><![CDATA[Academic institution in Arizona is seeking an additional faculty member.  This is an established Medical Oncology program.  They are looking for a physician to teach GU.  This is an excellent opportunity ]]></description>
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<item rdf:about="http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_arizona/page_7.html">
<title>Permanent Hematology-Oncology Job in Southwest Arizona Arizona with Enterprise Medical Service</title>
<link>http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_arizona/page_7.html</link>
<description><![CDATA[Academic program in the Southwest is seeking TWO fellowship trained Bone Marrow Transplant Specialist.  The academic center has an established Medical/Hematology Oncology program and they will be adding ]]></description>
</item>

<item rdf:about="http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_pennsylvania/page_9.html">
<title>Permanent Hematology-Oncology Job in EXCELLENT OPPORTUNITY in a prestigious college tow Pennsylvania with Enterprise Medical Service</title>
<link>http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_pennsylvania/page_9.html</link>
<description><![CDATA[Excellent opportunity in central PA to join an established MSG.  This group currently has 52 providers and 1 Hem/Onc.  They are looking to add 3 more Oncologists to the group.  They are building a state ]]></description>
</item>

<item rdf:about="http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_north_carolina/page_15.html">
<title>Permanent Hematology-Oncology Job in Practice is less than 2 hours from Raleigh, NC North Carolina with Enterprise Medical Service</title>
<link>http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_north_carolina/page_15.html</link>
<description><![CDATA[Large MSG in North Carolina is looking for an Oncologist who is moving out of state due to family reasons.  The new physician would be walking into a readymade practice with 1 other full time and 1 part ]]></description>
</item>

<item rdf:about="http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_oregon/page_8.html">
<title>Permanent Hematology-Oncology Job in Great Location  1  hours from Portland Oregon with Enterprise Medical Service</title>
<link>http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_oregon/page_8.html</link>
<description><![CDATA[Join a hospital based oncology group.  The group currently has a part time Medical Oncologist. This physician is very busy and they really need a full time Medical/Hematology Oncology provider.  The hospital ]]></description>
</item>

<item rdf:about="http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_north_carolina/page_13.html">
<title>Permanent Hematology-Oncology Job in Northwest North Carolina North Carolina with Enterprise Medical Service</title>
<link>http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_north_carolina/page_13.html</link>
<description><![CDATA[Join one other Medical Oncologist in a hospital based cancer center.  The center also employs a Radiation Oncologist.  Chemo Nurses, register dietician, radiation therapist as well as a full support and ]]></description>
</item>

<item rdf:about="http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_georgia/page_11.html">
<title>Permanent Hematology-Oncology Job in East Central Georgia Georgia with Enterprise Medical Service</title>
<link>http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_georgia/page_11.html</link>
<description><![CDATA[Join an established/busy Medical/Hematology Oncology group in Georgia.  The need is due to growth and demand in the area.  There are currently 3 physicians in the group. Partnership track is 2 years. ]]></description>
</item>

<item rdf:about="http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_wyoming/page_2.html">
<title>Permanent Hematology-Oncology Job in Northwestern Wyoming Position Wyoming with Enterprise Medical Service</title>
<link>http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_wyoming/page_2.html</link>
<description><![CDATA[Single specialty group of Hematologists/Oncologists seeking an additional partner.  Walk into a ready made practice of a retiring physician. Work a 4 day week, no call,  in the office in the cancer center ]]></description>
</item>

<item rdf:about="http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_washington/page_12.html">
<title>Permanent Hematology-Oncology Job in Opportunity in Central Washington Washington with Enterprise Medical Service</title>
<link>http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_washington/page_12.html</link>
<description><![CDATA[  Join 4 medical oncologists and 2 radiation oncologists treating a culturally diverse population throughout Central Washington. Will work out of a state of the art 42,000 sq. ft. cancer center.  Work ]]></description>
</item>

<item rdf:about="http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_florida/page_11.html">
<title>Permanent Hematology-Oncology Job in Beautiful, Sunny, Fort Lauderdale Florida with Enterprise Medical Service</title>
<link>http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_florida/page_11.html</link>
<description><![CDATA[Join an established Hem/Onc in private practice in Ft. Lauderdale, FL.  This is a busy practice seeing an average of 100 patients per week.  Strong support staff with five RN's and two MA's.  Chemo done ]]></description>
</item>

<item rdf:about="http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_oregon/page_7.html">
<title>Permanent Hematology-Oncology Job in Southwest Oregon Oregon with Enterprise Medical Service</title>
<link>http://www.physemp.com/physician_jobs/all_hematology_oncology_jobs_in_oregon/page_7.html</link>
<description><![CDATA[Join a large successful Single Specialty Oncology Group in Oregon.  This group currently has 8 Hem/Oncs and 2 PA's.  They have 3 offices and work out of 2 hospitals.  State of the art equipment including ]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fhon.898">
<title>New antimicrobial agents for the treatment of bacterial infections in cancer patients</title>
<link>http://dx.doi.org/10.1002%2Fhon.898</link>
<description><![CDATA[Patients with cancer develop serious bacterial infections often, especially during periods of severe and prolonged neutropenia. Antibiotic usage for the prevention and treatment of bacterial infections in these high-risk patients leads to selection pressures resulting in the emergence and spread of resistant organisms. Many organisms acquire several resistance mechanisms, making them multi-drug-resistant (MDR) (defined as resistance to three or more different classes of antibiotics). These infections are associated with increased morbidity, mortality and costs. The development of novel antimicrobial agents with activity against pathogens that have become resistant to currently available agents is one strategy for combating resistant organisms. Several novel agents have either recently been approved, or are in various stages of development and are discussed in detail. It is unlikely that these agents will have a major impact on reducing the development and spread of MDR organisms. Consequently, the judicious use of currently available agents referred to as Antimicrobial Stewardship, and the development of and adherence to appropriate Infection Control policies and procedures are vital components in the management of these high-risk patients. Copyright © 2009 John Wiley & Sons, Ltd.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fhon.900">
<title>How would I manage a sample submitted for flow cytometry analysis for suspicious chronic lymphocytic leukaemia</title>
<link>http://dx.doi.org/10.1002%2Fhon.900</link>
<description><![CDATA[Samples submitted for a suspect of chronic lymphocytic leukemia are the most frequently observed in flow cytometry laboratories. These cases require not only a precise and prompt diagnosis but also an evaluation on the possibility of performing additional prognostic tests. We will propose two sequential flow cytometry panels and a personal opinion on how to manage these samples for both diagnostic and prognostic assessment, taking into account the published guidelines and recommendations. Copyright © 2009 John Wiley & Sons, Ltd.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fhon.901">
<title>Telomeres and telomerase in chronic myeloid leukaemia: impact for pathogenesis, disease progression and targeted therapy</title>
<link>http://dx.doi.org/10.1002%2Fhon.901</link>
<description><![CDATA[Telomeres are specialized structures localized at the end of human chromosomes. Due to the end replication problem, each cell division results in a loss of telomeric repeats in normal somatic cells. In germ line and stem cells, the multicomponent enzyme telomerase maintains the length of telomere repeats. However, elevated telomerase activity has also been reported in the majority of solid tumours as well as in acute and chronic leukaemia. Chronic myeloid leukaemia (CML) serves as a model disease to study telomere biology in clonal myeloproliferative disorders. In CML, telomere shortening correlates with disease stage, duration of chronic phase (CP), prognosis measured by the Hasford risk score and the response to disease-modifying therapeutics such as the tyrosine kinase inhibitor Imatinib. In addition, telomerase activity (TA) is already increased in CP CML and further upregulated with disease progression to accelerated phase and blast crisis (BC). Furthermore, a correlation of TA with increased genetic instability as well as a shorter survival of the patients has been reported. Here, we review the current state of knowledge of the role of telomere and telomerase biology in CML and discuss the possible impact of novel treatment approaches. Copyright © 2009 John Wiley & Sons, Ltd.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fhon.904">
<title>Nucleophosmin (NPM1) mutations in adult and childhood acute myeloid leukaemia: towards definition of a new leukaemia entity</title>
<link>http://dx.doi.org/10.1002%2Fhon.904</link>
<description><![CDATA[Nucleophosmin (NPM) is a ubiquitously expressed chaperone protein that shuttles rapidly between the nucleus and cytoplasm, but predominantly resides in the nucleolus. It plays key roles in ribosome biogenesis, centrosome duplication, genomic stability, cell cycle progression and apoptosis. Somatic mutations in exon 12 of the NPM gene (NPM1) are the most frequent genetic abnormality in adult acute myeloid leukaemia (AML), found in approximately 35% of all cases and up to 60% of patients with normal karyotype (NK) AML. In children, NPM1 mutations are far less frequent, occurring in 8-10% of all AML cases, and in approximately 25% of those with a NK. NPM1 mutations lead to aberrant localization of the NPM protein into the cytoplasm, thus the designation, NPMc+ AML. NPMc+ AML is seen predominantly in patients with a NK and is essentially mutually exclusive of recurrent chromosomal translocations. Patients with NPM1 mutations are twice as likely as those who lack an NPM1 mutation to also have a FMS-like tyrosine kinase (FLT3) internal tandem duplication (ITD) mutation. NPMc+ AML is also characterized by a unique gene expression signature and microRNA signature. NPMc+ AML has important prognostic significance, as NPMc+ AML, in the absence of a coexisting FLT3-ITD mutation, is associated with a favourable outcome. NPM1 mutations have also shown great stability during disease evolution, and therefore represent a possible marker for minimal residual disease detection. Given its distinctive biologic and clinical features and its clear clinical relevance, NPMc+ AML is included as a provisional entity in the 2008 WHO classifications. There is still much to be learned about this genetic alteration, including its exact role in leukaemogenesis, how it interacts with other mutations and why it confers a more favourable prognosis. Further, it represents a potential therapeutic target warranting research aimed at identifying novel small molecules with activity in NPMc+ AML. Copyright © 2009 John Wiley & Sons, Ltd.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fhon.902">
<title>Improved survival in red blood cell transfusion dependent patients with primary myelofibrosis (PMF) receiving iron chelation therapy</title>
<link>http://dx.doi.org/10.1002%2Fhon.902</link>
<description><![CDATA[Many patients with primary myelofibrosis (PMF) become red blood cell (RBC) transfusion dependent (TD), risking iron overload (IOL). Iron chelation therapy (ICT) may decrease the risk of haemosiderosis associated organ dysfunction, though its benefit in PMF is undefined. To assess the effect of TD and ICT on survival in PMF, we retrospectively reviewed 41 patients. Clinical data were collected from the database and by chart review. The median age at PMF diagnosis was 64 (range 43-86) years. Median white blood cell (WBC) count at diagnosis was 7.6 (range 1.2-70.9) × 109/L; haemoglobin 104 (62-145) G/L; platelets 300 (38-2088) × 109/L. Lille, Strasser, Mayo and International Prognostic System (IPS) scores were: low risk, n = 15, 8, 11, 3; intermediate, n = 15, 19, 9, 16; high, n = 5, 11, 5, 7; respectively. Primary PMF treatment was: supportive care, n = 23; hydroxyurea, n = 10; immunomodulatory, n = 4; splenectomy, n = 2. Sixteen patients were RBC transfusion independent (TI) and 25 TD; of these 10 received ICT for a median of 18.3 (0.1-117) months. Pre-ICT ferritin levels were a median of 2318 (range 263-8400) and at follow up 1571 (1005-3211 µg/L (p = 0.01). In an analysis of TD patients, factors significant for overall survival (OS) were: WBC count at diagnosis (p = 0.002); monocyte count (p = 0.0001); Mayo score (p = 0.05); IPS (p = 0.02); number of RBC units (NRBCU) transfused (p = 0.02) and ICT (p = 0.003). In a multivariate analysis, significant factors were: NRBCU (p = 0.001) and ICT (p = 0.0001). Five year OS for TI, TD-ICT and TD-NO ICT were: 100, 89 and 34%, respectively (p = 0.003). The hazard ratio (HR) for receiving >20 RBCU was 7.6 (95% Confidence Intervals [CI] 1.2-49.3) and for ICT was 0.15 (0.03-0.77). In conclusion, 61% of PMF patients developed RBC-TD which portended inferior OS; however patients receiving ICT had comparatively improved OS, suggesting a clinical benefit. Prospective studies of IOL and the impact of ICT in PMF are warranted. Copyright © 2009 John Wiley & Sons, Ltd.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fhon.903">
<title>Continuous infusion idarubicin and intravenous busulphan as conditioning regimen to autologous stem cell transplantation for patients with acute myeloid leukaemia</title>
<link>http://dx.doi.org/10.1002%2Fhon.903</link>
<description><![CDATA[The current study aimed to evaluate the efficacy and toxicity of a combination of intravenous (iv) busulfan (Bu) and continuous infusion Idarubicin (IDA) as a conditioning regimen to autologous haematopoietic stem cell transplantation (ASCT) in patients with acute myeloid leukaemia (AML). The protocol included IDA at 20 mg/sqm daily as 3 days continuous infusion (from day -13 to -11) and intravenous BU at 3.2 mg/kg daily from day -5 to -2. Patients aged over 60 years received a reduced schedule (2 days IDA and 3 days BU at the same dose). Twenty-five patients with a median age of 51 years (28-72) were enrolled. All patients received peripheral blood stem cells (PBSC). The median interval between diagnosis and ASCT was 4 months. The median number of CD34+ cells infused was 5.9 × 10E6/kg. The median number of days to PMN >500/cmm and platelets >20000/cmm was 10 and 13, respectively. In order to perform a comparison in terms of haematological and non haematological toxicity, a group of 30 patients, who were previously autografted after conditioning with IDA and oral Bu was considered. Selection of factors for a matched pair analysis included median age, percentage of subjects aged over 60 years, median CD34+ cell received, cytogenetic and molecular findings and per cent of secondary AML. As compared to previous series, the occurrence of severe mucositis was dramatically reduced (80% vs. 12%, p < 0.0001). In addition, need and duration of total parenteral nutrition (TPN), iv antibiotic therapy and hospitalization were also significantly reduced. We conclude that replacement of oral with intravenous BU results in a more favourable toxicity profile. A longer follow-up is required to assess a potential advantage in terms of disease free survival (DFS). Copyright © 2009 John Wiley & Sons, Ltd.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fhon.896">
<title>The therapeutic effect of rituximab on CD5-positive and CD5-negative diffuse large B-cell lymphoma</title>
<link>http://dx.doi.org/10.1002%2Fhon.896</link>
<description><![CDATA[The prognosis of diffuse large B-cell lymphoma (DLBCL) has improved markedly in recent years of rituximab era. The prognosis of de novo CD5-positive DLBCL is reported to be poor, but the effect of rituximab on this type of lymphoma remains unclear. To investigate the effect of rituximab on CD5-positive DLBCL, we collected DLBCL patients and analysed prognostic factors. A total of 157 patients with DLBCL who were immunophenotyped with flow-cytometry (FCM) and treated with chemotherapy were subjected to analysis. Those treated with radiotherapy alone or with supportive therapy only were not included. Patients diagnosed in 2003 or later were treated with rituximab combined chemotherapy. There were 95 males and 62 females. Their age ranged from 20 to 91 years old, and the median was 65 years. Nineteen patients were diagnosed as having de novo CD5-positive DLBCL. Rituximab was given alongside chemotherapy in 85 patients. Of these, 11 were positive for CD5 and 74 were negative. The addition of rituximab improved the overall survival (OS) of DLBCL patients (2-year OS: 82% vs. 70%, p = 0.01). For CD5-negative DLBCL, patients treated with rituximab showed 2-year OS of 84%, which was significantly better than those treated without rituximab (70%, p = 0.008). However, for CD5-positive DLBCL, the prognosis was not statistically different between the patients treated with and without rituximab (59% vs. 50%, p = 0.72). Although rituximab improved the prognosis of DLBCL, such improvement was restricted to the CD5-negative group. Further investigation is required to improve the prognosis of patients with CD5-positive DLBCL. Copyright © 2009 John Wiley & Sons, Ltd.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fhon.897">
<title>Anaplastic large cell lymphoma: one or more entities among T-cell lymphoma?</title>
<link>http://dx.doi.org/10.1002%2Fhon.897</link>
<description><![CDATA[Anaplastic large cell lymphoma (ALCL) is a subtype of peripheral T-cell lymphoma (PTCL) first described in 1985 as a lymphoid malignancy characterized by marked cellular pleomorphism, propensity to grow cohesively, tendency to invade lymph node sinuses and diffuse expression of CD30 . The discovery of the t(2;5), involving the anaplastic lymphoma kinase (ALK) gene on chromosome 2 and the nucleophosmin (NPM) gene on chromosome 5 in the majority of systemic ALCL, has soon pointed out that ALCL is a clinically and biologically heterogeneous disease. While ALK-positive (ALK+) ALCL is usually characterized by onset in children and young adults and better prognosis, epidemiology, poor outcome and possibly genetic defects of ALK-negative (ALK-) ALCL suggest that this neoplasms should be considered an independent pathological entity. The aim of this review is to illustrate clinical features, histology, immunophenotype, genetics and biology of ALCL and discuss possible relationship(s) among different T-non-Hodgkin lymphoma (T-NHL). Copyright © 2009 John Wiley & Sons, Ltd.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fhon.892">
<title>KHSV- EBV- post-transplant effusion lymphoma with plasmablastic features: variant of primary effusion lymphoma?</title>
<link>http://dx.doi.org/10.1002%2Fhon.892</link>
<description><![CDATA[Primary effusion lymphoma (PEL) is a rare type of B-cell non-Hodgkin lymphoma (NHL), which predominantly occurs in HIV-infected individuals, and is pathogenetically linked with Kaposi sarcoma (KS)-associated herpes virus/human herpes virus-8 (KSHV/HHV-8) infection with or without evidence of Epstein-Barr virus (EBV) co-infection. Although uncommon, PELs have been reported in immunocompetent patients and recipients of solid organ allografts. Rare cases of KSHV- EBV+ post-transplant effusion lymphomas resembling PEL have also been described, as have KSHV- EBV- effusion lymphomas, the latter including those arising in individuals with chronic liver disease. We report a unique KSHV- EBV- post-transplant effusion lymphoma associated with serum paraproteins, occurring in an HIV- individual, which had cytologic features and phenotype similar to PEL, and displayed a complex karyotype including isochromosome 12p and translocation t(8;22), resulting in rearrangement of c-MYC. Copyright © 2009 John Wiley & Sons, Ltd.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fhon.886">
<title>Immunotherapy with cytokine induced killer cells in solid and hematopoietic tumours: a pilot clinical trial</title>
<link>http://dx.doi.org/10.1002%2Fhon.886</link>
<description><![CDATA[Background and Objectives: CIK cells are a novel population of efficient immune effector cells with high antitumour activity mainly due to the high proliferation of CD3+CD56+ cells, so may play a role in the development of new forms of adoptive cellular immunotherapy. We started a pilot clinical trial with autologous CIK cells in patients with refractory lymphoma and metastatic solid tumours. This study was aimed at determining the feasibility of generating a sufficient number of CIK cells in heavily pretreated patients and at assessing treatment toxicity. Design and Methods: CIK cells were generated from peripheral blood mononuclear cells (MNC) and incubated in the presence of IFN-[gamma] followed by OKT3 and IL-2. Treatment schedule consisted of three cycles of CIK cells infusions at an interval of 3 weeks. Results: At present 12 patients were enrolled: 6 advanced lymphomas, 5 metastatic kidney carcinoma and 1 hepatocellular carcinoma (HCC). The median number of transferred cells per patient was 28 × 109 (range, 6-61). Protocol adherence was excellent and the toxicity profile was favourable. After CIK cells infusion, the absolute median count of lymphocytes, CD3+, CD8+ and CD3+CD56+ cells significantly increased in patient's peripheral blood. Clinical outcome appeared promising: three patients had complete response (CR) and two patients had stabilization of disease with a median follow-up of 33 months (range, 9-44). Interpretations and Conclusions: These preliminary data showed that adoptive immunotherapy with CIK cells is a safe therapy with some suggestion of efficacy that significantly enhances immune functions increasing absolute numbers of effector cells without side effects. If confirmed in larger scale studies, these promising results may have a favourable impact on conventional treatment strategy of malignancies. Copyright © 2009 John Wiley & Sons, Ltd.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fhon.889">
<title>Comorbidities and FLT3-ITD abnormalities as independent prognostic indicators of survival in Elderly acute myeloid leukaemia patients</title>
<link>http://dx.doi.org/10.1002%2Fhon.889</link>
<description><![CDATA[Elderly acute myeloid leukaemia (AML) patients have a dismal prognosis due to biological features of disease in itself and to presence of comorbidities. Aim of this study was to evaluate the prognostic impact of comorbidity prognostic score systems applied in our population of patients. as well as other clinical-biological features. We retrospectively considered the outcome of 120 patients aged >65 years diagnosed as having AML between January 2001 and December 2005. Comorbidities were evaluated by using Charlson comorbidity index (CCI), Hematopoietic cell transplantation comorbidity index (HCTCI) and a score proposed by Dombret et al. in 2007. Median patient age was 67 years. Forty-six patients were treated with intensive chemotherapy and 23 reached a complete remission. Seventy-four patients received only supportive therapies or low-dose chemotherapy. Multivariate analysis showed the effects of leukocytosis (p = 0.0013), antecedent Myelodysplastic syndrome (MDS) (p = 0.011), FLT3 abnormalities (p = 0.032), CCI (p = 0.0037) and Dombret et al. score (p = 0.045) as independent prognostic parameters for survival. Based on these variables we were able to stratify patients in low and high risk, with different median overall survival: patients were considered as low risk if they had none or only one of the above mentioned adverse factors for survival, with a median overall survival of 447 days. Patients with two or more adverse factors were categorized as high risk: this subgroup had a median overall survival of 227 days (p = 0.001). Comorbidities are independent factors that influence survival. Application of CCI and Dombret score may help to better identify patients at diagnosis who can benefit from intensive chemotherapy. Copyright © 2009 John Wiley & Sons, Ltd.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fhon.890">
<title>Involved field radiotherapy for limited stage Hodgkin lymphoma: balancing treatment efficacy against long-term toxicities</title>
<link>http://dx.doi.org/10.1002%2Fhon.890</link>
<description><![CDATA[Limited stage Hodgkin lymphoma (HL) refers to patients with stage IA or IIA disease in the absence of any bulky mass or unfavourable prognostic factors. In this group, the long-term disease control with treatment can be expected in more than 90%, and management has now been directed to make strategies to reduce late morbidities related to therapy. With the advent of very effective chemotherapy, the role of radiation therapy has evolved from a first line single modality treatment, to an adjuvant therapy following brief cycles of chemotherapy. Optimal radiation volume and dose parameters have been refined in the combined modality setting. Furthermore, with the progress in diagnostic functional imaging and advances in radiotherapy, it is possible to accurately deliver low to moderate doses of radiation to defined regions resulting in durable control of disease. This review will evaluate the literature that shapes the current standard of care in limited stage Hodgkin lymphoma with special emphasis on the use of limited field radiotherapy. Copyright © 2009 John Wiley & Sons, Ltd.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fhon.891">
<title>A multicentre phase II trial of gemcitabine for the treatment of patients with newly diagnosed, relapsed or chemotherapy resistant mantle cell lymphoma: SAKK 36/03</title>
<link>http://dx.doi.org/10.1002%2Fhon.891</link>
<description><![CDATA[Mantle cell lymphoma (MCL) has a poor prognosis with often short and incomplete remissions. We aimed to test the efficacy and tolerability of gemcitabine in treating MCL. Gemcitabine was given in doses of 1000 mg/m2 as a 30 min infusion on days 1 and 8 of each 3 week cycle for a maximum of nine cycles. Eighteen patients with a median age of 70 years were recruited. MCL was newly diagnosed in half of patients and relapsed in the remainder. Fifteen patients had Ann Arbor stage IV. The best-recorded responses were 1 CR (complete remission), 4 PRs (partial responses), 8 SDs (stable diseases) and 4 PDs (diseases progression). The response rate (RR) (CR + PR) was 5 (28%; 95% confidence interval: 7.1, 48.5). The patient achieving a CR had stage IV disease. Most haematological adverse events occurred during the first chemotherapy cycle. Three patients developed non-haematological serious adverse events: dyspnea, glomerular microangiopathy with haemolytic uremic syndrome (HUS) and hyperglycaemia. The median time-to-progression and treatment response duration (TRD) was 8.0 (95% confidence interval: 5.5, 9.3) and 10.6 (95% confidence interval: 5.5, 10.9) months, respectively. We conclude that Gemcitabine is well tolerated, moderately active and can induce disease stabilization in patients with MCL. Copyright © 2009 John Wiley & Sons, Ltd.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fhon.894">
<title>Analysis of Bcr-Abl kinase domain mutations in Korean chronic myeloid leukaemia patients: poor clinical outcome of P-loop and T315I mutation is disease phase dependent</title>
<link>http://dx.doi.org/10.1002%2Fhon.894</link>
<description><![CDATA[Despite durable responses to imatinib in chronic myeloid leukaemia (CML), mutations in Bcr-Abl kinase domain (KD) are known to induce imatinib resistance and cause poor clinical outcome. We characterized Bcr-Abl KD mutations in 137 Korean CML patients with imatinib resistance (n = 111) or intolerance (n = 26) using allele specific oligonucleotide polymerase chain reaction (PCR) and direct sequencing. Seventy (51%) patients harboured 81 mutations of 20 different types with increasing prevalence in advanced phase. Nine (13%) patients had multiple mutations. No mutation was found in intolerant patients. T315I was the most common mutation and P-loop was the hottest spot in Bcr-Abl KD. Patients harbouring P-loop mutation, T315I, or multiple mutations showed poor overall survival and progression free survival compared with patients harbouring other mutations. Survival analysis according to disease phase of mutation being detected and type of mutations provided correlation between P-loop or T315I mutation and poor overall survival in blast crisis, but not in accelerated phase (AP) or chronic phase (CP), indicating poor clinical outcome of particular mutations depends on disease phase. CML patients with imatinib resistance showed high rate (63%) of mutations in Bcr-Abl KD and therefore CML patients who do not respond to imatinib should be the candidates for mutation screening as molecular monitoring. Copyright © 2009 John Wiley & Sons, Ltd.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fhon.899">
<title>MPL W515L/K mutations in 343 Chinese adults with JAK2V617F mutation-negative chronic myeloproliferative disorders detected by a newly developed RQ-PCR based on TaqMan MGB probes</title>
<link>http://dx.doi.org/10.1002%2Fhon.899</link>
<description><![CDATA[Acquired mutations in the juxtamembrane region of MPL (W515L or W515K), the receptor for thrombopoietin, have been reported in patients with primary essential thrombocythemia (ET) or primary myelofibrosis (PMF). The mutations were detected by the newly developed real-time quantitative PCR (RQ-PCR) with TaqMan MGB probes and followed by the sequencing analysis. DNA samples were from 343 Chinese adults with JAK2V617F mutation-negative chronic myeloproliferative disorders (cMPDs). Reference curves were obtained using cloned fragments of MPL containing either the wild-type or MPL W515L or MPL W515K mutated sequence; the predicted sensitivity level was at least 0.5%(0.1-0.5%) for MPL W515L and 0.5%(0.2-0.5%) for MPL W515K mutant allele in a wild-type background. The detection rates of MPL W515 mutations were 3.5% in 199 ET patients (7/199), 12.5% in 24 PMF patients (3/24) and 5.6% in 36 cMPD-unclassed patients (2/36), respectively. No MPL W515 mutations were detected in 32 polycythemia vera (PV) patients, 40 chronic myeloid leukaemia (CML) patients, 12 hypereosinophilic syndrome (HES) patients and 29 normal volunteers. The mean calculated burden of MPL mutant alleles using RQ-PCR for MPL W515L/K was 24.88 ± 14.80% (range, 1.10-56.32%). MPL W515L/K patients presented lower haemoglobin levels, compared with the patients with JAK2V617F mutation-positive cMPDs (p < 0.01). The results demonstrated that RQ-PCR was a reliable and sensitive method for large-scale screening of the MPL W515L/K mutation in patients suspected to have a cMPD. It can also provide a quantitative estimate of mutant allele burden that might be useful for both patient prognosis and monitoring response to therapy. Copyright © 2009 John Wiley & Sons, Ltd.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fhon.888">
<title>CD26 expression in mature B-cell neoplasia: its possible role as a new prognostic marker in B-CLL</title>
<link>http://dx.doi.org/10.1002%2Fhon.888</link>
<description><![CDATA[CD26 (dipeptidyl peptidase IV, DPP IV) is widely expressed by T and natural killer (NK) cells, epithelial and endothelial cells of different tissues, and it is strongly upregulated in activated B-cells; moreover it plays a regulatory role in the neoplastic transformation and progression of various types of tumours. CD26 expression was evaluated by means of flow cytometry in various peripheral B-cell lymphoid tumours: 12 follicular and 12 mantle cell lymphomas, 20 multiple myelomas (MMs), 12 hairy cell leukaemias (HCLs), 112 chronic lymphocytic leukaemias (CLLs), 20 CD5negative B-cell chronic lymphoproliferative diseases (CD5neg B-CLPDs) and 12 diffuse large cell lymphomas (DLCLs). CD26 expression was absent or barely detectable in follicular and mantle cell lymphomas, high in MMs and HCLs, and variable in CLLs, in CD5neg B-CLPDs and in DLCLs. CD26 significantly correlated with CD49d and CD38 expressions (p < 0.0001) in B-CLLs, and there was a significant correlation between CD26 and ZAP-70 expressions or IgVH mutational status (p < 0.0001). After a median follow-up of 36 months, 65 B-CLL patients were treated; taking 10% as the best CD26 cut-off value, Kaplan-Meier curves revealed a significantly shorter time to treatment in the CD26-positive cases (p < 0.0001). Overall, our data indicate that CD26 expression may identify subsets of B-CLL patients with an unfavourable clinical outcome in terms of therapeutic need, thus suggesting its potential role as a marker (together with CD38 and CD49d) in a future routine cytofluorimetric panel to be validated for the prognostic stratification of B-CLLs. Copyright © 2009 John Wiley & Sons, Ltd.]]></description>
</item>

<item rdf:about="http://www.springerlink.de/content/r3q00x268gn26412/">
<title>Thrombocytopenia as first manifestation of splenic angiosarcoma</title>
<link>http://www.springerlink.de/content/r3q00x268gn26412/</link>
<description><![CDATA[Thrombocytopenia as first manifestation of splenic angiosarcoma
	Content Type Journal ArticleCategory Letter to the EditorDOI 10.1007/s00277-009-0778-7Authors
		Simon Raffel, Charité Campus Virchow Klinikum Department of Hematology and Oncology Augustenburger Platz 1 13353 Berlin GermanyBert Hildebrandt, Charité Campus Virchow Klinikum Department of Hematology and Oncology Augustenburger Platz 1 13353 Berlin GermanyChristian Grieser, Charité Campus Virchow Klinikum Department of Radiology Augustenburger Platz 1 13353 Berlin GermanyStefan Pahl, Charité Campus Mitte Institute of Pathology Charitéplatz 1 10117 Berlin GermanyIsrid Sturm, Charité Campus Virchow Klinikum Department of Hematology and Oncology Augustenburger Platz 1 13353 Berlin Germany
	

	
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]]></description>
</item>

<item rdf:about="http://www.springerlink.de/content/y727411813210568/">
<title>Predictors of hematological abnormalities in patients with chronic hepatitis C treated with interferon and ribavirin</title>
<link>http://www.springerlink.de/content/y727411813210568/</link>
<description><![CDATA[Abstract&nbsp;&nbsp;Hematological abnormalities including neutropenia, anemia, and thrombocytopenia are commonly seen in patients with chronic
 hepatitis C treated with pegylated interferon and ribavirin. The aim of this study was to identify factors which would help
 to predict the development of hematological abnormalities in patients with chronic hepatitis C treated with pegylated interferon
 and ribavirin. During a 4-year period, all patients with chronic hepatitis C started on treatment with pegylated interferon
 and ribavirin were identified. Patients were defined as having hematological abnormalities if they had the presence of either
 anemia, neutropenia, thrombocytopenia, or a combination of the above during treatment with pegylated interferon and ribavirin.
 A total of 136 patients with chronic hepatitis C were included in this study. Fifty-two (38.2%) of the patients developed
 significant hematological abnormalities during treatment with pegylated interferon and ribavirin with 28 (20.6%), 30 (22.1%),
 and 11 (8.1%) developed neutropenia, anemia, and thrombocytopenia, respectively. Genotype 1, history of hypertension, low
 baseline platelet count, low baseline hemoglobin, as well as a raised creatinine were significant factors associated with
 the development of hematological abnormalities. Significant hematological abnormalities are commonly present in patients with
 chronic hepatitis C treated with pegylated interferon and ribavirin. This study identifies pretreatment parameters that may
 help identify high-risk patients who are more likely to develop hematological abnormalities during treatment for chronic hepatitis
 C.
 
	Content Type Journal ArticleCategory Original ArticleDOI 10.1007/s00277-009-0774-yAuthors
		Jagdish S. Nachnani, University of Missouri Kansas City School of Medicine Division of Gastroenterology 2301 Holmes Street Kansas City MO 64108 USAGowtham A. Rao, VA Medical Center Kansas City Division of Gastroenterology Kansas City MO 64108 USADeepti Bulchandani, VA Medical Center Kansas City Division of Gastroenterology Kansas City MO 64108 USAPrashant K. Pandya, VA Medical Center Kansas City Division of Gastroenterology Kansas City MO 64108 USALaura M. Alba, University of Missouri Kansas City School of Medicine Division of Gastroenterology 2301 Holmes Street Kansas City MO 64108 USA
	

	
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]]></description>
</item>

<item rdf:about="http://www.springerlink.de/content/t7700283t0w040g7/">
<title>Lenalidomide in 5q minus myelodysplastic syndrome: how long is enough?</title>
<link>http://www.springerlink.de/content/t7700283t0w040g7/</link>
<description><![CDATA[Lenalidomide in 5q minus myelodysplastic syndrome: how long is enough?
	Content Type Journal ArticleCategory Letter to the EditorDOI 10.1007/s00277-009-0775-xAuthors
		Donat Dürr, Stadtspital Triemli Medical Oncology Birmensdorferstrasse 497 CH-8063 Zurich SwitzerlandRaffaele Daniele Siciliano, Stadtspital Triemli Medical Oncology Birmensdorferstrasse 497 CH-8063 Zurich SwitzerlandYvonne Hummel, Stadtspital Triemli Medical Oncology Birmensdorferstrasse 497 CH-8063 Zurich SwitzerlandAlix O’Meara, Stadtspital Triemli Medical Oncology Birmensdorferstrasse 497 CH-8063 Zurich SwitzerlandAnita Hirschi, Stadtspital Triemli Medical Oncology Birmensdorferstrasse 497 CH-8063 Zurich SwitzerlandRoger Burkhard, Stadtspital Triemli Medical Oncology Birmensdorferstrasse 497 CH-8063 Zurich SwitzerlandHanspeter Honegger, Stadtspital Triemli Medical Oncology Birmensdorferstrasse 497 CH-8063 Zurich Switzerland
	

	
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]]></description>
</item>

<item rdf:about="http://www.springerlink.de/content/w20pt451t5836172/">
<title>Comparison of various criteria in predicting treatment response and prognosis of patients with myelodysplastic syndrome treated with azacitidine</title>
<link>http://www.springerlink.de/content/w20pt451t5836172/</link>
<description><![CDATA[Abstract&nbsp;&nbsp;This study was performed to identify whether cytogenetics, International Prognostic Scoring System (IPSS), or World Health
 Organization Classification-Based Prognostic Scoring System are predictive of the efficacy of azacitidine in patients with
 myelodysplastic syndrome (MDS). We retrospectively reviewed the clinical records of 113 patients with MDS treated with azacitidine.
 The “response alternating disease natural history,” “cytogenetic response,” and “hematologic improvement” were assessed by
 serial bone marrow biopsy, cytogenetic study, and hemogram analyses. The complete and partial remission rates were 17.6% and
 3.9% in 51 evaluable patients. There were no significant differences in response rate in the different cytogenetic/IPSS/WPSS
 groups. The overall hematologic response (HR) rate was 49.6%, and the HR rate was significantly greater in patients classed
 as “very high” risk according to the WPSS compared with other patient groups. The 1-year overall survival (OS) rate was higher
 among patients with HR compared with those without HR (80.9% vs 63.3%, p = 0.046), and the 1-year OS rate among patients classed as being at high risk by each criteria was similar to that of patients
 classed as being at low risk. The hazard ratio of death among patients with HR compared with those without HR was 0.17 (95%
 CI 0.04–0.69) for high + very high risk group based on WPSS. Patients in the WPSS high-risk group had an increased HR rate
 compared with other patient groups, and the achievement of HR was associated with a significant increase in OS. Azacitidine
 showed similar efficacy in all patient groups, even in patients with poor cytogenetics and in high-risk groups.
 
	Content Type Journal ArticleCategory Original ArticleDOI 10.1007/s00277-009-0771-1Authors
		Dae-Young Kim, University of Ulsan College of Medicine Department of Hematology, Asan Medical Center 86, Asanbyeongwon-gil Songpa-gu Seoul 138-736 South KoreaJe-Hwan Lee, University of Ulsan College of Medicine Department of Hematology, Asan Medical Center 86, Asanbyeongwon-gil Songpa-gu Seoul 138-736 South KoreaJung-Hee Lee, University of Ulsan College of Medicine Department of Hematology, Asan Medical Center 86, Asanbyeongwon-gil Songpa-gu Seoul 138-736 South KoreaKyoo-Hyung Lee, University of Ulsan College of Medicine Department of Hematology, Asan Medical Center 86, Asanbyeongwon-gil Songpa-gu Seoul 138-736 South KoreaYoe-Kyeoung Kim, Chonnam National University College of Medicine Department of Internal Medicine, Chonnam National University Hwasun Hospital Gwangju KoreaJae Sook Ahn, Chonnam National University College of Medicine Department of Internal Medicine, Chonnam National University Hwasun Hospital Gwangju KoreaHyeoung-Joon Kim, Chonnam National University College of Medicine Department of Internal Medicine, Chonnam National University Hwasun Hospital Gwangju KoreaInho Kim, Seoul National University College of Medicine Department of Internal Medicine, Seoul National University Hospital Seoul South KoreaSung-Soo Yoon, Seoul National University College of Medicine Department of Internal Medicine, Seoul National University Hospital Seoul South KoreaSeonyang Park, Seoul National University College of Medicine Department of Internal Medicine, Seoul National University Hospital Seoul South KoreaSung Hwa Bae, Daegu Catholic University College of Medicine Department of Internal Medicine, Daegu Catholic University Medical Center Gyeongsan South KoreaSoo-Mee Bang, Seoul National University College of Medicine Department of Internal Medicine, Seoul National University Bundang Hospital 300 Gumi-dong, Bundang-gu Seongnam-si Gyeongi-do 463-707 South KoreaHong Ghi Lee, Konkuk University College of Medicine Department of Internal Medicine, Konkuk University Medical Center Seoul South KoreaHo-Jin Shin, Pusan National University College of Medicine Department of Internal Medicine, Pusan National University Hospital Pusan South KoreaJae Hoon Lee, Gachon University of Medicine and Science Department of Internal Medicine, Gachon University Gil Medical Center Incheon South KoreaYoo Hong Min, Yonsei University College of Medicine Department of Internal Medicine, Severance Hospital Seoul South KoreaJong-Ho Won, Soon Chun Hyang University College of Medicine Department of Internal Medicine, Soon Chun Hyang University Hospital Seoul South KoreaYeung-Chul Mun, Ewha Womans University School of Medicine Department of Internal Medicine, Ewha Womans University Medical Center Seoul South KoreaDoyeun Oh, Pochon CHA University College of Medicine Department of Internal Medicine, Bundang CHA Hospital Seongnam South KoreaKorean Society of Hematology AML/MDS Working Party
	

	
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]]></description>
</item>

<item rdf:about="http://www.springerlink.de/content/y76k77m735826284/">
<title>Clostridium difficile-associated diarrhoea, a frequent complication in patients with acute myeloid leukaemia</title>
<link>http://www.springerlink.de/content/y76k77m735826284/</link>
<description><![CDATA[Abstract&nbsp;&nbsp;Diarrhoea occurs frequently in neutropenic patients with acute leukaemia receiving chemotherapy and may be caused by either
 infection- or drug-induced cytotoxicity. Since Clostridium difficile is the most common cause of nosocomial infectious diarrhoea in non-haematologic patients, we were interested in its incidence
 in patients with acute myeloid leukaemia (AML). In this retrospective study, we analysed 134 patients with AML receiving a
 total of 301 chemotherapy courses. Diarrhoea occurred during 33% of all courses in 58 patients. C. difficile-associated diarrhoea (CDAD) occurred in 18% of all patients and 9% of all treatment courses. Almost one third of diarrhoea
 episodes were caused by C. difficile. CDAD was associated with older age (58 vs. 50&nbsp;years), number of antibiotics administered (2 vs. 1), duration of antibiotic
 therapy (7 vs. 4&nbsp;days), ceftazidime as the antibiotic of choice (75% vs. 54%) and duration of neutropenia (12 vs. 7&nbsp;days)
 prior to onset of diarrhoea. An increased risk for CDAD was seen for prolonged neutropenia. CDAD responded well to oral metronidazole
 and/or vancomycin and no patient died of this complication. In conclusion, CDAD is common in patients with AML receiving chemotherapy.
 C. difficile enterotoxin testing of stool specimens should be included in all symptomatic patients.
 
	Content Type Journal ArticleCategory Original ArticleDOI 10.1007/s00277-009-0772-0Authors
		Enrico Schalk, Magdeburg University Hospital Department of Haematology/Oncology Leipziger Str. 44 39120 Magdeburg GermanyUlrich R. M. Bohr, Magdeburg University Hospital Department of Gastroenterology, Hepatology and Infectious Diseases Magdeburg GermanyBrigitte König, Magdeburg University Hospital Department of Medical Microbiology Magdeburg GermanyKatrin Scheinpflug, Magdeburg University Hospital Department of Haematology/Oncology Leipziger Str. 44 39120 Magdeburg GermanyMartin Mohren, Magdeburg University Hospital Department of Haematology/Oncology Leipziger Str. 44 39120 Magdeburg Germany
	

	
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]]></description>
</item>

<item rdf:about="http://www.springerlink.de/content/067257417555w82q/">
<title>Improvement of the thermal amplitude after rituximab treatment for cold agglutinin disease with Waldenstr&#xF6;m&#x2019;s macroglobulinemia</title>
<link>http://www.springerlink.de/content/067257417555w82q/</link>
<description><![CDATA[Improvement of the thermal amplitude after rituximab treatment for cold agglutinin disease with Waldenström’s macroglobulinemia
	Content Type Journal ArticleCategory Letter to the EditorDOI 10.1007/s00277-009-0773-zAuthors
		Norimichi Hattori, Showa University School of Medicine Division of Hematology, Department of medicine 1-5-8 Hatanodai, Shinagawa-Ku Tokyo 142-8666 JapanNoriko Ishii, Showa University School of Medicine Department of Blood Transfusion Shinagawa-Ku Tokyo JapanHirotsugu Ariizumi, Showa University School of Medicine Division of Hematology, Department of medicine 1-5-8 Hatanodai, Shinagawa-Ku Tokyo 142-8666 JapanDaisuke Adachi, Showa University School of Medicine Division of Hematology, Department of medicine 1-5-8 Hatanodai, Shinagawa-Ku Tokyo 142-8666 JapanIsao Matsuda, Showa University School of Medicine Division of Hematology, Department of medicine 1-5-8 Hatanodai, Shinagawa-Ku Tokyo 142-8666 JapanTsuyoshi Nakamaki, Showa University School of Medicine Division of Hematology, Department of medicine 1-5-8 Hatanodai, Shinagawa-Ku Tokyo 142-8666 JapanShigeru Tomoyasu, Showa University School of Medicine Division of Hematology, Department of medicine 1-5-8 Hatanodai, Shinagawa-Ku Tokyo 142-8666 Japan
	

	
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]]></description>
</item>

<item rdf:about="http://www.springerlink.de/content/b824247102681818/">
<title>Thrombocytopenia with rituximab treatment&#x2014;splenomegaly as the risk factor</title>
<link>http://www.springerlink.de/content/b824247102681818/</link>
<description><![CDATA[Thrombocytopenia with rituximab treatment—splenomegaly as the risk factor
	Content Type Journal ArticleCategory Letter to the EditorDOI 10.1007/s00277-009-0768-9Authors
		Jagdish Adiyodi, University Hospital Aintree Department of Haematology Lower Lane Liverpool L9 7AL UKJecko Thachil, University of Liverpool Liverpool UKStephen Hawkins, University of Liverpool Liverpool UKIan Hincks, University Hospital Aintree Department of Haematology Lower Lane Liverpool L9 7AL UKBarrie E. Woodcock, University Hospital Aintree Department of Haematology Lower Lane Liverpool L9 7AL UKRahuman Salim, University Hospital Aintree Department of Haematology Lower Lane Liverpool L9 7AL UK
	

	
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]]></description>
</item>

<item rdf:about="http://www.springerlink.de/content/t0w663172728h7u6/">
<title>Post-rituximab Burkitt transformation of PTLD: loss of CD20 expression accompanied by a switch in light-chain expression</title>
<link>http://www.springerlink.de/content/t0w663172728h7u6/</link>
<description><![CDATA[Post-rituximab Burkitt transformation of PTLD: loss of CD20 expression accompanied by a switch in light-chain expression
	Content Type Journal ArticleCategory Letter to the EditorDOI 10.1007/s00277-009-0769-8Authors
		Yu-Yan Hwang, Queen Mary Hospital Department of Medicine UMU, 4/F, Professorial Block, Pokfulam Road Hong Kong ChinaKai Y. Wong, Queen Mary Hospital Department of Pathology Hong Kong ChinaRock Y. Y. Leung, Queen Mary Hospital Department of Pathology Hong Kong ChinaSimon H. M. Wong, Queen Mary Hospital Department of Radiology Hong Kong ChinaSee-Ching Chan, Queen Mary Hospital Department of Surgery Hong Kong ChinaGopesh Srivastava, Queen Mary Hospital Department of Pathology Hong Kong ChinaWing Y. Au, Queen Mary Hospital Department of Medicine UMU, 4/F, Professorial Block, Pokfulam Road Hong Kong China
	

	
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]]></description>
</item>

<item rdf:about="http://www.springerlink.de/content/80134k89k48h2546/">
<title>Total therapy-based treatment for multiple myeloma&#x2014;a single center experience</title>
<link>http://www.springerlink.de/content/80134k89k48h2546/</link>
<description><![CDATA[Abstract&nbsp;&nbsp;Incorporation of novel biological agents has become the cornerstone of treatment in multiple myeloma. For the last 4&nbsp;years
 we have adopted the more intensified approach, previously published as total therapy 3 by the Arkansas group and used it with
 local modifications. This study aims to evaluate the efficacy and safety of the Arkansas protocol-based treatment outside
 clinical trial in a tertiary medical center in Israel. We retrospectively analyzed 23 patients. Seventy-three percent of the
 patients achieved very good partial remission (VGPR) before autologous stem cell transplantation (ASCT). Eighty-six percent
 of the patients achieved at least VGPR after tandem ASCT. Two-year overall survival was estimated as 70%. Four patients died
 during treatment, one as a result of disease progression. We conclude that this protocol is effective and rather safe. Further
 clinical trials should assess which subgroups of patients would benefit most from this approach.
 
	Content Type Journal ArticleCategory Original ArticleDOI 10.1007/s00277-009-0767-xAuthors
		Hila Magen-Nativ, Beilinson Hospital Institute of Hematology, Davidoff Cancer Center, Rabin Medical Center Petah-Tiqva Israel 49100Ron Ram, Beilinson Hospital Institute of Hematology, Davidoff Cancer Center, Rabin Medical Center Petah-Tiqva Israel 49100Moshe Yeshurun, Beilinson Hospital Institute of Hematology, Davidoff Cancer Center, Rabin Medical Center Petah-Tiqva Israel 49100Anat Gafter-Gvili, Beilinson Hospital Institute of Hematology, Davidoff Cancer Center, Rabin Medical Center Petah-Tiqva Israel 49100Pia Raanani, Beilinson Hospital Institute of Hematology, Davidoff Cancer Center, Rabin Medical Center Petah-Tiqva Israel 49100Ofer Shpilberg, Beilinson Hospital Institute of Hematology, Davidoff Cancer Center, Rabin Medical Center Petah-Tiqva Israel 49100
	

	
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]]></description>
</item>

<item rdf:about="http://www.springerlink.de/content/m488168421528352/">
<title>Peri-operative thrombosis prophylaxis in the Chinese versus Caucasian population</title>
<link>http://www.springerlink.de/content/m488168421528352/</link>
<description><![CDATA[Peri-operative thrombosis prophylaxis in the Chinese versus Caucasian population
	Content Type Journal ArticleCategory Letter to the EditorDOI 10.1007/s00277-009-0765-zAuthors
		Samir Mardini, Mayo Clinic Plastic Surgery 200 First Street, SW Rochester MN 55905 USAChristopher J. Salgado, University Hospitals Cleveland / Case Western University Plastic Surgery 11100 Euclid Avenue Cleveland OH 44106 USALun-Jou Lo, Chang-Gung Memorial Hospital Plastic Surgery No. 199 Tunghwa Road Taipei Taiwan Republic of ChinaHung-Chi Chen, E-Da Hospital/I-Shou University Plastic Surgery 1 E-Da Road, Jiau-shu Tsuen, Yan-Chau Shiang Kaohsiung County Taiwan Republic of China
	

	
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]]></description>
</item>

<item rdf:about="http://www.springerlink.de/content/231788t374452x26/">
<title>A prognostic score for AIDS-related diffuse large B-cell lymphoma in Brazil</title>
<link>http://www.springerlink.de/content/231788t374452x26/</link>
<description><![CDATA[Abstract&nbsp;&nbsp;The aim of this study was to evaluate a prognostic score for aids-related lymphoma (ARL). A retrospective study of 104 patients
 with ARL treated between January 1999 and December 2007 was conducted. Diffuse large B-cell lymphoma (DLBC) was the most observed
 histological type (79.8%). The median CD4 lymphocyte count at lymphoma diagnosis was 125 cells per microliter. Treatment response
 could be evaluated in 83 (79.8%) patients, and 38 (45.8%) reached complete remission (CR); overall response rate was 51.8%
 (95 CI = 38.5–65.1%). After a median follow-up of 48&nbsp;months, the 4-year overall survival (OS) rate among all patients was
 35.8%, with a median survival time of 9.7&nbsp;months (95% CI = 5.5–13.9&nbsp;months). The survival risk factors observed in multivariate
 analysis (previous AIDS and high-intermediate/high international prognostic index (IPI)) were combined to construct a risk
 score, which divided the whole patient population in three distinct groups as low, intermediate, and high risk. When this
 score was applied to DLBC patients, a clear distinction in response rates and in OS could be demonstrated. Median disease-free
 survival (DFS) for patients that achieved CR was not reached, and DFS in 4&nbsp;years was 83.0%. Our results show that the reduced
 OS observed could be explained by poor immune status with advanced stage of disease seen in our population of HIV-positive
 patients. Further studies will be needed to clarify the role of different treatment approaches for ARL in the setting of marked
 immunosuppression and to identify a group of patients to whom intensive therapy could be performed with a curative intent.
 
	Content Type Journal ArticleCategory Original ArticleDOI 10.1007/s00277-009-0761-3Authors
		Paula Yurie Tanaka, Instituto de Infectologia Emílio Ribas Hematology Section Av. Dr. Arnaldo, 165-2.andar São Paulo 01246-900 BrazilLuis Fernando Pracchia, São Paulo University Hematology Department, Hospital das Clínicas São Paulo BrazilMarcelo Bellesso, São Paulo University Hematology Department, Hospital das Clínicas São Paulo BrazilDalton Alencar Fischer Chamone, São Paulo University Hematology Department, Hospital das Clínicas São Paulo BrazilEdenilson Eduardo Calore, Instituto de Infectologia Emílio Ribas Pathology Section São Paulo BrazilJuliana Pereira, São Paulo University Hematology Department, Hospital das Clínicas São Paulo Brazil
	

	
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]]></description>
</item>

<item rdf:about="http://www.springerlink.de/content/935320832q847917/">
<title>Non-Hodgkin lymphoma involving stomach and ovary: extending the Krukenberg tumor concept</title>
<link>http://www.springerlink.de/content/935320832q847917/</link>
<description><![CDATA[Non-Hodgkin lymphoma involving stomach and ovary: extending the Krukenberg tumor concept
	Content Type Journal ArticleCategory Letter to the EditorDOI 10.1007/s00277-009-0770-2Authors
		Constantinos Christopoulos, “Amalia Fleming” General Hospital First Department of Internal Medicine Melissia Athens 15127 GreeceMarina Skopeliti, “Amalia Fleming” General Hospital First Department of Internal Medicine Melissia Athens 15127 GreeceEvagelos Rotas, “Amalia Fleming” General Hospital First Department of Internal Medicine Melissia Athens 15127 GreeceAnastasios Mavridis, “Amalia Fleming” General Hospital First Department of Internal Medicine Melissia Athens 15127 GreeceSotiria Savva, “Amalia Fleming” General Hospital Department of Pathology Athens GreeceEfstathios Papavassiliou, “Amalia Fleming” General Hospital Department of Gastroenterology Athens Greece
	

	
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]]></description>
</item>

<item rdf:about="http://www.springerlink.de/content/p3156p6044m37487/">
<title>Increased bone resorption is implicated in the pathogenesis of bone loss in hemophiliacs: correlations with hemophilic arthropathy and HIV infection</title>
<link>http://www.springerlink.de/content/p3156p6044m37487/</link>
<description><![CDATA[Abstract&nbsp;&nbsp;Osteoporosis has been recently recognized as a severe comorbidity factor in hemophilia. However, its pathogenesis is still
 obscure. We evaluated the incidence of osteoporosis in 90 hemophilia patients and investigated possible correlations with
 clinical and laboratory data. Out of the 90 patients, 80 (89%) had severe hemophilia, and 35 (38.9%) were human immunodeficiency
 virus (HIV)-positive. Hemophilic arthropahty was assessed using World Federation of Hemophilia clinical score and Petterson
 radiological score. Bone mineral density of the lumbar spine (LS) and femoral neck (FN) were measured using dual-energy X-ray
 absortiometry. Bone turnover was evaluated by the measurement of: (1) bone resorption markers [N-terminal cross-linking telopeptide
 of collagen type I (NTX), C-terminal cross-linking telopeptide of collagen type I (CTX), and tartrate-resistant acid phosphatase
 isoform-5b (TRACP-5b)], (2) bone formation markers [bone-alkaline phosphatase (bALP) and osteocalcin], and (3) osteoclast
 stimulators (receptor activator of nuclear factor-κB ligand, osteoprotegerin, and tumor necrosis factor-alpha). Osteopenia
 or osteoporosis was observed in 86% and 65% of the patients in FN and LS, respectively. Osteoporosis was more common among
 HIV-positive patients in both FN (65.3% vs 41.6%; p&nbsp;=&nbsp;0.007) and LS (17.86% vs 5.41%, p&nbsp;=&nbsp;0.004). The severity of osteoporosis in FN correlated with the patients' total clinical and radiological score (p&nbsp;=&nbsp;0.001). Hemophilia patients showed increased osteoclastic activity (significant increase of TRACP-5b, NTX, and CTX), which
 was not accompanied by a comparable increased bone formation (reduced osteocalcin and borderline increase of bALP). In multivariate
 analysis, HIV infection (p = 0.05) and total clinical score (p = 0.001) were independent risk factors for osteoporosis development. We conclude that there is a high prevalence of osteoporosis
 among hemophiliacs, which is related to the severity of arthropathy and is enhanced by HIV infection. We report for the first
 time a high bone resorption that seems not to be balanced by a comparable bone formation.
 
	Content Type Journal ArticleCategory Original ArticleDOI 10.1007/s00277-009-0759-xAuthors
		Olga Katsarou, “Laiko” General Hospital 2nd Blood Transfusion Center and Hemophilia Center Agiou Thoma 17 11527 Athens GreeceEvangelos Terpos, 251 General Air Force Hospital Department of Medical Research Athens GreecePantelis Chatzismalis, “Laiko” General Hospital 2nd Blood Transfusion Center and Hemophilia Center Agiou Thoma 17 11527 Athens GreeceStefanos Provelengios, “Laiko” General Hospital 2nd Blood Transfusion Center and Hemophilia Center Agiou Thoma 17 11527 Athens GreeceTheophanis Adraktas, “Laiko” General Hospital 2nd Blood Transfusion Center and Hemophilia Center Agiou Thoma 17 11527 Athens GreeceDimitrios Hadjidakis, Athens University, Attikon and Evgenidion Hospitals 2nd Department of Internal Medicine-Propaedeutic, Research Institute and Diabetes Center Athens GreeceAnna Kouramba, “Laiko” General Hospital 2nd Blood Transfusion Center and Hemophilia Center Agiou Thoma 17 11527 Athens GreeceAnastasia Karafoulidou, “Laiko” General Hospital 2nd Blood Transfusion Center and Hemophilia Center Agiou Thoma 17 11527 Athens Greece
	

	
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]]></description>
</item>

<item rdf:about="http://www.springerlink.de/content/fpm3413p67692rp5/">
<title>Echocardiographic findings in patients with sickle cell disease</title>
<link>http://www.springerlink.de/content/fpm3413p67692rp5/</link>
<description><![CDATA[Abstract&nbsp;&nbsp;Pulmonary hypertension is a complication of sickle cell disease that is associated with increased mortality. Whether this
 complication is associated with hemolysis has been questioned. Systolic pulmonary artery blood pressure can be estimated from
 echocardiography-determined tricuspid regurgitation velocity (TRV). A velocity of 2.5&nbsp;m/s or higher suggests possible pulmonary
 hypertension. A retrospective review of hospital records from adult patients with sickle cell disease undergoing echocardiography
 in 2006 and 2007 was performed at a tertiary level hospital. Echocardiographic, demographic, and clinical laboratory data
 were collected. Echocardiographic results were available for 105 adult sickle cell patients. Of these, 62 (59%) had a TRV
 ≥2.5&nbsp;m/s and 24 (22.8%) had a TRV ≥3.0&nbsp;m/s. Mitral valve regurgitation was observed in 44% and left ventricular abnormalities
 (defined by either hypertrophy or dilation) in 28% of cases. Elevated TRV had independent and significant associations with
 greater age, higher serum lactate dehydrogenase (LDH) concentration, and lower hemoglobin concentration. We confirmed that
 elevated TRV is common among hospital-based adults with sickle cell disease. Significant, independent associations were found
 with both elevated LDH concentration and degree of anemia, suggesting that hemolytic and other mechanisms contribute to pulmonary
 hypertension in patients with sickle cell disease.
 
	Content Type Journal ArticleCategory Original ArticleDOI 10.1007/s00277-009-0764-0Authors
		Shahla G. Naoman, Howard University Center for Sickle Cell Disease and Department of Medicine 1840 7th Street, NW, Room # 201 Washington DC 20001 USAMehdi Nouraie, Howard University Center for Sickle Cell Disease and Department of Medicine 1840 7th Street, NW, Room # 201 Washington DC 20001 USAOswaldo L. Castro, Howard University Center for Sickle Cell Disease and Department of Medicine 1840 7th Street, NW, Room # 201 Washington DC 20001 USACatherine Nwokolo, Howard University Center for Sickle Cell Disease and Department of Medicine 1840 7th Street, NW, Room # 201 Washington DC 20001 USAMargaret Fadojutimi-Akinsiku, Howard University Center for Sickle Cell Disease and Department of Medicine 1840 7th Street, NW, Room # 201 Washington DC 20001 USASharmin Diaz, Howard University Center for Sickle Cell Disease and Department of Medicine 1840 7th Street, NW, Room # 201 Washington DC 20001 USAGeorgia Willie-Carnegie, Howard University Division of Cardiology 2041 Georgia Avenue, NW, Suite 6C03 Washington DC 20060 USANewton Andrews, Howard University Division of Cardiology 2041 Georgia Avenue, NW, Suite 6C03 Washington DC 20060 USAVictor R. Gordeuk, Howard University Center for Sickle Cell Disease and Department of Medicine 1840 7th Street, NW, Room # 201 Washington DC 20001 USA
	

	
		Journal Annals of HematologyOnline ISSN 1432-0584Print ISSN 0939-5555
	
]]></description>
</item>

<item rdf:about="http://www.springerlink.de/content/77520193tp620619/">
<title>Prevalence and analysis of t(14;18) and t(11;14) chromosomal translocations in healthy Indian population</title>
<link>http://www.springerlink.de/content/77520193tp620619/</link>
<description><![CDATA[Abstract&nbsp;&nbsp;Hematopoietic malignancies like leukemia and lymphoma are characteristically associated with various chromosomal translocations.
 Follicular lymphoma (FL) and mantle cell lymphoma (MCL) are two subtypes of non-Hodgkin’s lymphoma which possess t(14;18)
 and t(11;14) translocations, respectively. The incidence of FL and MCL is higher in the western countries as compared to India.
 Interestingly, the associated translocations are also found in healthy individuals in western population, which is 50–80%
 for t(14;18), whereas t(11;14) occurs at a very low frequency. However, there are no studies to explore these translocations
 in healthy Indian population, which could explain the lower incidence of FL and MCL. We employed Southern hybridization following
 nested PCR to detect above translocations in healthy individuals from India. Our results suggest that this assay can detect
 one t(14;18) translocation event in up to 107 normal cells where as one t(11;14) in 108 normal cells. According to our results, 87 out of 253 individuals carry t(14;18) indicating 34% prevalence in the population.
 The presence of this translocation was also detectable at the transcript level. Although, no gender-based difference was observed,
 an age-dependent increase in the prevalence of translocation was found in adults. However, even after studying 210 people,
 we could not detect any t(11;14) translocation, indicating that it is uncommon in Indian population. These results suggest
 that lower incidence of FL and MCL in India could be attributed to lower prevalence of these translocations in healthy individuals.
 
	Content Type Journal ArticleCategory Original ArticleDOI 10.1007/s00277-009-0755-1Authors
		Mridula Nambiar, Indian Institute of Science Department of Biochemistry Bangalore 560 012 IndiaSathees C. Raghavan, Indian Institute of Science Department of Biochemistry Bangalore 560 012 India
	

	
		Journal Annals of HematologyOnline ISSN 1432-0584Print ISSN 0939-5555
	
]]></description>
</item>

<item rdf:about="http://www.springerlink.de/content/n7114k47g2315036/">
<title>A novel beta-globin mutation (HBB:c.107A&#x3E;G; or codon 35&#xA0;&#x3B2; (A&#x2192;G)) at alpha&#x2013;beta chain interfaces</title>
<link>http://www.springerlink.de/content/n7114k47g2315036/</link>
<description><![CDATA[A novel beta-globin mutation (HBB:c.107A>G; or codon 35 β (A→G)) at alpha–beta chain interfaces
	Content Type Journal ArticleCategory Letter to the EditorDOI 10.1007/s00277-009-0760-4Authors
		Ravindra Kumar, Sanjay Gandhi Postgraduate Institute of Medical Sciences Department of Genetics Lucknow UP India 226014Parag M. Tamhankar, Sanjay Gandhi Postgraduate Institute of Medical Sciences Department of Genetics Lucknow UP India 226014Inusha Panigrahi, Postgraduate Institute of Medical Education and Research Department of Pediatrics Chandigarh IndiaAshwin Dalal, Center for DNA Fingerprinting and Diagnostics Diagnostic Division Hyderabad IndiaSarita Agarwal, Sanjay Gandhi Postgraduate Institute of Medical Sciences Department of Genetics Lucknow UP India 226014
	

	
		Journal Annals of HematologyOnline ISSN 1432-0584Print ISSN 0939-5555
	
]]></description>
</item>

<item rdf:about="http://www.springerlink.de/content/325m474740226u02/">
<title>Screening of platelet concentrates for bacterial contamination: spectrum of bacteria detected, proportionof transfused units, and clinical follow-up</title>
<link>http://www.springerlink.de/content/325m474740226u02/</link>
<description><![CDATA[Abstract&nbsp;&nbsp;Screening of platelet concentrates (PCs) for bacterial contamination with cultivation methods is carried out as a routine
 procedure in some countries. The aim is to prevent the transfusion of contaminated PCs. The German Evaluation of Regular Monitoring
 Study Group conducted a prospective multicenter study on 52,243 PCs to investigate the prevalence of bacteria (BacT/ALERT,
 bioMerieux). This study describes the detected bacterial spectrum, the proportion of PCs with a positive test result that
 had been transfused, and the results of the clinical follow-up. One hundred thirteen (67%) of 169 potentially or confirmed
 positive units had already been transfused at the time of the first positive signal. The transfusion of units contaminated
 by Staphylococcus aureus, Serratia marcescens, and 73% of the units contaminated with Staphylococcus epidermidis, Staphylococcus capitis, or Staphylococcus saccharolyticus was prevented. In contrast, 85% of units with Propionibacterium acnes were transfused. A clonal relationship of the isolates from the pooled PCs and from the associated red blood cell concentrates
 was found in all investigated cases. The follow-up revealed six febrile reactions to culture-positive PCs not classified as
 transfusion reaction (TRs) by treating physicians. This demonstrates the importance of hemovigilance. Serious septic reactions
 due to Klebsiella pneumoniae in two units of one apheresis PC that had tested false-negative were reported; one had a fatal outcome. Culture systems reduce
 the risk of transfusion of contaminated PCs but cannot guarantee sterility. Physicians must be aware of bacterial contamination
 of PCs as a potential cause of TRs and must report all adverse events.
 
	Content Type Journal ArticleCategory Original ArticleDOI 10.1007/s00277-009-0762-2Authors
		Gabriele Walther-Wenke, German Red Cross Blood Service West Muenster GermanyHubert Schrezenmeier, German Red Cross Blood Service Baden-Wuerttemberg – Hessia and Ost Ulm GermanyRobert Deitenbeck, German Red Cross Blood Service West Hagen GermanyGabriele Geis, Ruhr-Universität Bochum Department of Medical Microbiology Bochum GermanyJürgen Burkhart, Bavarian Red Cross Blood Service Munich GermanyBritta Höchsmann, German Red Cross Blood Service Baden-Wuerttemberg – Hessia and Ost Ulm GermanyWalid Sireis, German Red Cross Blood Service Baden-Wuerttemberg – Hessia and Ost Frankfurt GermanyMichael Schmidt, German Red Cross Blood Service Baden-Wuerttemberg – Hessia and Ost Frankfurt GermanyErhard Seifried, German Red Cross Blood Service Baden-Wuerttemberg – Hessia and Ost Frankfurt GermanyWolfgang Gebauer, German Red Cross Blood Service NSTOB Oldenburg GermanyUte-Maja Liebscher, German Red Cross Blood Service Baden-Wuerttemberg – Hessia and Ost Dresden GermanyFranz Weinauer, Bavarian Red Cross Blood Service Munich GermanyThomas H. Müller, German Red Cross Blood Service NSTOB Springe Germany
	

	
		Journal Annals of HematologyOnline ISSN 1432-0584Print ISSN 0939-5555
	
]]></description>
</item>

<item rdf:about="http://www.springerlink.de/content/tv8514v621080wm2/">
<title>The same genetic defect in three Tunisian families with Bernard Soulier syndrome: a probable founder Stop mutation in GPIbbeta</title>
<link>http://www.springerlink.de/content/tv8514v621080wm2/</link>
<description><![CDATA[Abstract&nbsp;&nbsp;GPIbα, GPIbβ, and GPIX are three candidate genes for a rare genetic bleeding disorder named Bernard Soulier syndrome (BSS).
 These genes are unique in the genome and encode for glycoprotein subunits of the GPIb-IX complex. Quantitative or qualitative
 deficiency in this complex is often associated with BSS. Here, we report the novel variant of BSS in which Ser23 of GPIbβ
 is substituted by a Stop codon causing a premature termination of translation, recently described in one family. This genetic
 defect is revealed in three unrelated BSS patients. The pedigree was determined for two families (F1 and F2) and revealed
 the homozygosity of the mutation in the two patients and its heterozygosity in parents. In the third family, the patient DNA
 was heterozygote with the same Ser23 Stop mutation in addition to two missense heterozygote mutations (Asp 51 Gly) and (Ala
 55 to Pro). We studied the effect of the Ser23 Stop mutation on the expression of the complex. Our findings confirm that the
 identified GPIbβ mutation is responsible for the BSS phenotype and hampers the GPIb-IX complex to form on the platelets’ surface.
 Regarding the scarcity of the BSS syndrome, the occurrence of the same mutation in three unrelated families would suggest
 a BSS founder mutation in Tunisia.
 
	Content Type Journal ArticleCategory Original ArticleDOI 10.1007/s00277-009-0763-1Authors
		Basma HadjKacem, Centre de Biotechnologie de Sfax Laboratoire de Génétique Moléculaire des Eucaryotes BP“1177”3018 Sfax TunisiaHenda Elleuch, Centre Régional de Transfusion Sanguine de Sfax Sfax TunisiaRamzi Trigui, Centre de Biotechnologie de Sfax Laboratoire de Génétique Moléculaire des Eucaryotes BP“1177”3018 Sfax TunisiaJalel Gargouri, Centre Régional de Transfusion Sanguine de Sfax Sfax TunisiaAli Faouzi Gargouri, Centre de Biotechnologie de Sfax Laboratoire de Génétique Moléculaire des Eucaryotes BP“1177”3018 Sfax Tunisia
	

	
		Journal Annals of HematologyOnline ISSN 1432-0584Print ISSN 0939-5555
	
]]></description>
</item>

<item rdf:about="http://www.springerlink.de/content/r7806148m515778g/">
<title>Treatment of K562 cells with 1,25-dihydroxyvitamin D3 induces distinct alterations in the expression of apoptosis-related genes BCL2, BAX, BCLXL, and p21</title>
<link>http://www.springerlink.de/content/r7806148m515778g/</link>
<description><![CDATA[Abstract&nbsp;&nbsp;Apoptosis, or programmed cell death, is a very important phenomenon in cytotoxicity induced by anticancer treatment. 1α,25-Dihydroxyvitamin
 D3 (1,25-(OH)2D3), the active metabolite of vitamin D, inhibits the growth of multiple types of cancer cells including breast, colon, and
 prostate cancer cell lines. We studied alterations in the mRNA expression levels of BCL2, BAX, CYC, BCL-XL, and VDR genes
 in the K562 chronic myeloid leukemia cell line in response to treatment with 1,25-(OH)2D3. Morphological observation of K562 cells was evaluated by the staining with Wright's solution. Cell percentage at different
 phases of the cell cycle was measured, and apoptosis was measured by flow cytometry. The expression levels of the apoptosis-related
 genes were analyzed by real-time reverse transcription polymerase chain reaction. We found that treatment with 1,25-(OH)2D3 down-regulates BCL2 and BCL-XL mRNA expressions, as well as up-regulates expressions of BAX and p21 mRNA. The expression
 pattern of CYC and VDR genes were not influenced. However, K562 cells treated with 1,25-(OH)2D3 caused an arrest of cell cycle progression in G1 phase resulting in a decreased number of cells in the S phase, complemented
 by an accumulation of cells in the G0–G1 phases. Our data show the modulatory effects of 1,25-(OH)2D3 treatment in apoptosis-related genes in K562 cells.
 
	Content Type Journal ArticleCategory Original ArticleDOI 10.1007/s00277-009-0766-yAuthors
		Sefa Kizildag, Dokuz Eylul University Department of Medical Biology and Medical Genetics, Faculty of Medicine 35340 İnciralti İzmir TurkeyHalil Ates, Dokuz Eylul University Department of Hematology/Oncology, Faculty of Medicine İzmir TurkeyServet Kizildag, Dokuz Eylul University Department of Biochemistry, Faculty of Medicine İzmir Turkey
	

	
		Journal Annals of HematologyOnline ISSN 1432-0584Print ISSN 0939-5555
	
]]></description>
</item>

<item rdf:about="http://www.springerlink.de/content/0217n3262l080865/">
<title>Role of 18FDG-PET/CT in detecting relapse during follow-up of patients with Hodgkin&#x2019;s lymphoma</title>
<link>http://www.springerlink.de/content/0217n3262l080865/</link>
<description><![CDATA[Abstract&nbsp;&nbsp;The role of 18FDG-PET/CT during follow-up of patients affected by Hodgkin’s lymphoma (HL) in complete remission after treatment is not fully
 elucidated, since a wide use of 18F fluorodeoxyglucose positron emission tomography/computed tomography (18FDG-PET/CT) in this setting could be limited by a relative high rate of false-positive results. Herein, we summarize a retrospective
 analysis of 27 patients with Hodgkin’s lymphoma in complete remission after the first-line (n = 20) or salvage (n = 7) therapy receiving serial 18FDG-PET/CT scans during follow-up. Out of 165 scans, 13 were suspected for relapse, which was confirmed in seven patients.
 All relapses were correctly identified by 18FDG-PET/CT positivity, with a 100% sensitivity; false-positive rate was 46% and negative predictive value was 100%. True-positive
 findings were mostly associated with multiple sites, subdiaphragmatic involvement, and/or previous sites of disease. According
 to our results, we conclude that performing routine PET/CT scan during follow-up of those patients who are at high risk of
 relapse would be advisable, although caution must be adopted when interpreting PET/CT results due to the relatively high rate
 of false-positive findings. If FDG abnormal uptake is present at multiple nodal sites, subdiaphragmatic lymph nodes, or previous
 sites of disease, histological verification of PET abnormal findings is warranted.
 
	Content Type Journal ArticleCategory Original ArticleDOI 10.1007/s00277-009-0752-4Authors
		R. Crocchiolo, San Raffaele Scientific Institute Hematology and BMT Unit Milan ItalyF. Fallanca, San Raffaele Scientific Institute Division of Nuclear Medicine Milan ItalyG. Giovacchini, San Raffaele Scientific Institute Division of Nuclear Medicine Milan ItalyA. J. M. Ferreri, San Raffaele Scientific Institute Unit of Lymphoid Malignancies Milan ItalyA. Assanelli, San Raffaele Scientific Institute Hematology and BMT Unit Milan ItalyC. Verona, San Raffaele Scientific Institute Unit of Lymphoid Malignancies Milan ItalyA. Pescarollo, San Raffaele Scientific Institute Hematology and BMT Unit Milan ItalyM. Bregni, Ospedale San Giuseppe Oncology Unit Milan ItalyM. Ponzoni, San Raffaele Scientific Institute Unit of Lymphoid Malignancies Milan ItalyL. Gianolli, San Raffaele Scientific Institute Division of Nuclear Medicine Milan ItalyF. Fazio, San Raffaele Scientific Institute Division of Nuclear Medicine Milan ItalyF. Ciceri, San Raffaele Scientific Institute Hematology and BMT Unit Milan Italy
	

	
		Journal Annals of HematologyOnline ISSN 1432-0584Print ISSN 0939-5555
	
]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21467">
<title>Iron overload and chronically transfused patients: Numbers, scales, and clinical research</title>
<link>http://dx.doi.org/10.1002%2Fajh.21467</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21468">
<title>Synergistic antitumor effects of lenalidomide and rituximab on mantle cell lymphoma in vitro and in vivo</title>
<link>http://dx.doi.org/10.1002%2Fajh.21468</link>
<description><![CDATA[Rituximab (RTX), a chimeric anti-CD20 antibody, is associated with direct induction of apoptosis and antibody-dependent cell-mediated cytotoxicity (ADCC) with clinical efficacy in mantle cell lymphoma (MCL). Lenalidomide (LEN), a novel immunomodulatory agent, sensitizes tumor cells and enhances ADCC. Our study attempted to elucidate the mechanism of LEN-enhanced RTX-mediated cytotoxicity of MCL cells. We found that LEN and RTX induced growth inhibition of both cultured and fresh primary MCL cells. LEN enhanced RTX-induced apoptosis via upregulating phosphorylation of c-Jun N-terminal protein kinases (JNK), Bcl-2, Bad; increasing release of cytochrome-c; enhancing activation of caspase-3, -8, -9 and cleavage of PARP. Meanwhile, LEN activated NK cells and increased CD16 expression on CD56lowCD16+ NK cells. Whole PBMCs but not NK cell-depleted PBMCs treated with LEN augmented 30% of RTX-dependent cytotoxicity. Daily treatment with LEN increased NK cells by 10-folds in SCID mice, and combination of LEN and RTX decreased tumor burden and prolonged survival of MCL-bearing SCID mice. Taken together, our study demonstrates that LEN plus RTX provides a synergistically therapeutic effect on MCL cells by enhancing apoptosis and RTX-dependent NK cell-mediated cytotoxicity and may be an optimal combination in the clinical trial of relapsed or refractory MCL. Am. J. Hematol. 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21466">
<title>The role of antiphospholipid antibodies toward the protein C/protein S system in venous thromboembolic disease</title>
<link>http://dx.doi.org/10.1002%2Fajh.21466</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21459">
<title>Acute weight gain and diastolic dysfunction as a potent risk complex for post stem cell transplant atrial fibrillation</title>
<link>http://dx.doi.org/10.1002%2Fajh.21459</link>
<description><![CDATA[The management of atrial fibrillation (AF) following stem cell transplant (SCTX) is often challenging because of the universal presence of profound bone marrow suppression. The incidence of and risk factors for AF/flutter following SCTX are not well known. A total of 395 multiple myeloma (MM) patients consecutively underwent SCTX between 2002 and 2005 at the Mayo Clinic, and 383 of whom, mean age 57 ± 9 years, had no history of evidence of AF/flutter constituted the study population. During 1,002 person-years of follow up, 39 (10%) patients developed first AF/flutter (incidence of 39 per 1,000 person years), and 28 of these (72%) occurred within 21 days of SCTX. In multivariable-adjusted analyses, weight gain of [ge]7% in the 1st week post-SCTX (HR 3.68; P = 0.0120) and presence of diastolic dysfunction at MM diagnosis (HR 2.294; P = 0.0082) were independent predictors of AF/flutter. The risk of AF/flutter post-SCTX increased by about ninefold when both factors were present. Compared to age and sex-matched MM patients without SCTX, the risk of AF/flutter differed significantly only over the 1st year after MM diagnosis, during which SCTX was performed for the majority. Beyond the 1st year, there was no significant difference in risk of AF/flutter between the two groups. The data suggested that SCTX was associated with significantly increased risk of first AF/flutter, which typically occurred within the first 21 days of the transplant. Weight gain of [ge]7% was strongly predictive of first AF/flutter, and the risk was augmented by the presence of diastolic dysfunction at baseline. Am. J. Hematol. 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21458">
<title>FLT3 mutations have no prognostic impact in elderly patients with acute myeloid leukemia and normal karyotype</title>
<link>http://dx.doi.org/10.1002%2Fajh.21458</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21463">
<title>Quantifying the reduction in immunoglobulin use over time in patients with chronic immune thrombocytopenic purpura receiving romiplostim (AMG 531)</title>
<link>http://dx.doi.org/10.1002%2Fajh.21463</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21461">
<title>Overexpression of nucleolin in engrafted acute myelogenous leukemia cells</title>
<link>http://dx.doi.org/10.1002%2Fajh.21461</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21455">
<title>An age-adapted approach for the use of D-dimers in the exclusion of deep venous thrombosis</title>
<link>http://dx.doi.org/10.1002%2Fajh.21455</link>
<description><![CDATA[A normal D-dimer (DD) concentration for the exclusion of deep venous thrombosis (DVT) has a low specificity in older patients and compression ultrasonography is often required. Three D-dimer assays, STA Liatest, Tina-quant, and Innovance, are evaluated in symptomatic outpatients suspected for DVT with emphasis on its performance in older patients by using different cut-off levels. This study includes 466 outpatients suspected for having DVT. The diagnostic accuracy, measured as sensitivity and area under the curve of the receiver operation characteristic curve is good for all DD assays. The specificity of the DD assays combined with a low pretest probability varies from 42.6 to 51.5%. The specificity of the three DD assays in patients [ge]60 years varies, however, between 24.6 and 40.9%. Several cut-off values in different age-subgroups are studied. For patients <60 years, the most accurate cut-off value is 500 [mu]g/L for all DD assays. For patients [ge]60 years, a threshold of 750 [mu]g/L has the best results with NPV of 100% for all assays and specificity of 48.5% (STA Liatest), 60.6% (Tina-quant), and 49.2% (Innovance), respectively. For the three assays, the number needed to test (NNT) decreases in both subgroups of patients compared to the standard algorithm. A cut-off level of 750 [mu]g/L for patients [ge]60 years improves the clinical performance of DD assays in combination with the PTP score without the loss of NPV. The NNT improves substantially with an age-adapted algorithm. Am. J. Hematol., 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21462">
<title>Paraneoplastic pemphigus associated with systemic mastocytosis</title>
<link>http://dx.doi.org/10.1002%2Fajh.21462</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21457">
<title>Technical aspects and clinical applications of measuring BCR-ABL1 transcripts number in chronic myeloid leukemia</title>
<link>http://dx.doi.org/10.1002%2Fajh.21457</link>
<description><![CDATA[Chronic myeloid leukemia (CML) is a myeloproliferative disorder characterized by a triphasic clinical course, the morphologic expansion of a terminally differentiated myeloid cell and the presence of the BCR-ABL1 fusion gene, the hallmark of CML. The fusion gene is usually, but not always, associated with a Philadelphia chromosome, the result of a reciprocal exchange of genetic material between chromosome 22 and chromosome 9, which leads to the production of the activated BCR-ABL1 gene and oncoprotein. The breakpoint in the BCR gene occurs commonly downstream of exons e13 or e14 (M-BCR) and less frequently downstream of exons e1 and e2 (m-BCR). Less than 1% of cases carry a breakpoint downstream of exon 6 or 8 ("variant fusion genes") or exon 19 ([mu]-BCR). Breakpoints in the ABL1 gene cluster upstream of exon a2 (or of exon a3 in less than 5% of patients with CML). Conventional cytogenetic, fluorescence in situ hybridization, and molecular testing for the BCR-ABL1 fusion gene are key investigations for the diagnosis and monitoring of CML. Treatment using tyrosine kinase inhibitors has revolutionized the management of CML with hematologic and cytogenetic response within 12-18 months observed in >85% of patients. Nevertheless, between 15 and 20% of patients may evolve to blastic phase. Measurement of low level or "minimal" residual disease using molecular tests is becoming the gold-standard approach to measure response to therapy due to its higher sensitivity compared to other routine techniques. The technical aspects and clinical applications of molecular monitoring will be the main focus of this article. Am. J. Hematol., 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21453">
<title>Changes in red cell ion transport, reduced intratumoral neovascularization, and some mild motor function abnormalities accompany targeted disruption of the Mouse Kell gene (Kel)</title>
<link>http://dx.doi.org/10.1002%2Fajh.21453</link>
<description><![CDATA[Kell (ECE-3), a highly polymorphic blood group glycoprotein, displays more than 30 antigens that produce allo-antibodies and, on red blood cells (RBCs), is complexed through a single disulfide bond with the integral membrane protein, XK. XK is a putative membrane transporter whose absence results in a late onset form of neuromuscular abnormalities known as the McLeod syndrome. Although Kell glycoprotein is known to be an endothelin-3-converting enzyme, the full extent of its physiological function is unknown. To study the functions of Kell glycoprotein, we undertook targeted disruption of the murine Kel gene by homologous recombination. RBCs from Kel(-/-) mice lacked Kell glycoprotein, Kell/XK complex, and endothelin-3-converting enzyme activity and had reduced levels of XK. XK mRNA levels in spleen, brain, and testis were unchanged. In Kel(-/-) mice RBC Gardos channel activity was increased and the normal enhancement by endothelin-3 was blunted. Analysis of the microvessels of tumors produced from LL2 cells indicated that the central portion of tumors from wild-type mice were populated with many mature blood vessels, but that vessels in tumors from Kel(-/-) mice were fewer and smaller. The absence of Kell glycoprotein mildly affected some motor activities identified by foot splay on the drop tests. The targeted disruption of Kel in mouse enabled us to identify phenotypes that would not be easily detected in humans lacking Kell glycoprotein. In this regard, the Kell knockout mouse provides a good animal model for the study of normal and/or pathophysiological functions of Kell glycoprotein. Am. J. Hematol., 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21456">
<title>Patterns of hepatic iron distribution in patients with chronically transfused thalassemia and sickle cell disease</title>
<link>http://dx.doi.org/10.1002%2Fajh.21456</link>
<description><![CDATA[Patients with sickle cell disease (SCD) appear to be at lower risk of endocrinopathies and cardiac dysfunction than those with thalassemia major (TM). Circulating redox active iron is lower in these patients, possibly due to increased systemic inflammation and circulating cytokines. Hepcidin synthesis is upregulated during chronic inflammation, reducing intestinal iron absorption and promoting retention of iron in the reticuloendothelial cells. Hence, we hypothesized that livers of patients with SCD would exhibit greater iron deposition in sinusoidal spaces relative to hepatocytes and less in portal tracts when compared to patients with TM. To test this hypothesis, iron scoring analysis was performed on 70 clinically indicated liver biopsy specimens from children and young adults with the two syndromes. Sinusoidal scores were lower in around 1 of 4 patients with TM but the relative iron loading in hepatocytes, and portal tracts was identical in both diseases. Sinusoidal iron burdens saturated at low hepatic iron concentration (HIC) while hepatocyte and portal iron depots increased proportionally to HIC. Liver fibrosis was increased in patients with TM regardless of their chronic hepatitis status. Overall, liver iron distribution was relatively insensitive to differences in disease type and to the presence or absence of hepatitis. Am. J. Hematol., 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21452">
<title>Hemoglobin lansing: A novel hemoglobin variant causing falsely decreased oxygen saturation by pulse oximetry</title>
<link>http://dx.doi.org/10.1002%2Fajh.21452</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21451">
<title>DHFR 19-bp insertion/deletion polymorphism and MTHFR C677T in adult acute lymphoblastic leukaemia: Is the risk reduction due to intracellular folate unbalancing?</title>
<link>http://dx.doi.org/10.1002%2Fajh.21451</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21449">
<title>Phase II study of bryostatin 1 and vincristine for aggressive non-Hodgkin lymphoma relapsing after an autologous stem cell transplant</title>
<link>http://dx.doi.org/10.1002%2Fajh.21449</link>
<description><![CDATA[Bryostatin 1, isolated from a marine bryozoan, enhances the efficacy of cytotoxic agents through modulation of the protein kinase C pathway and is active in combination with vincristine for diffuse large B-cell lymphoma. Further, the apoptotic frequency of peripheral blood T lymphocytes as determined by flow cytometry may predict which patients will respond to this combination. We tested the efficacy and safety of bryostatin 1 50 [mu]g/m2 given over 24 hr and vincristine 1.4 mg/m2 on days 1 and 15 every 28 days in aggressive B-cell non-Hodgkin lymphoma (NHL) relapsing after autologous stem cell transplantation. End points included tumor response, toxicity, and survival. Responses were correlated with an increase in apoptotic frequency of CD5+ cells by flow cytometry using annexin V staining. Fourteen patients were enrolled with 13 being evaluable for a response. The overall response rate was 31% with two patients achieving a complete response. The most common toxicities were Grade 3 lymphopenia (seven patients), Grade 3 to 4 neutropenia (two patients), and Grade 3 hypophosphatemia (two patients). Median progression-free and overall survivals for all patients were 5.7 and 21.4 months, respectively. One patient demonstrated an increase in T-cell apoptotic frequency, also achieving a complete response. Bryostatin 1 and vincristine have efficacy in select patients with aggressive NHL. Future investigations of agents targeting the protein kinase C pathway may benefit from early response assessment using flow cytometry to evaluate T-cell apoptosis. Am. J. Hematol., 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21448">
<title>Sequential evaluation of serum hepcidin in anemic myeloma patients: Study of correlations with myeloma treatment, disease variables, and anemia response</title>
<link>http://dx.doi.org/10.1002%2Fajh.21448</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21446">
<title>Improvement in hemolysis and pulmonary arterial systolic pressure in adult patients with sickle cell disease during treatment with hydroxyurea</title>
<link>http://dx.doi.org/10.1002%2Fajh.21446</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21445">
<title>3rd Annual Sickle Disease Research and Educational Symposium and Annual National Sickle Cell Disease Scientific Meeting</title>
<link>http://dx.doi.org/10.1002%2Fajh.21445</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21454">
<title>Osteopetrosis - More than only a disease of the bone</title>
<link>http://dx.doi.org/10.1002%2Fajh.21454</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21464">
<title>2009 BioIron Program Book</title>
<link>http://dx.doi.org/10.1002%2Fajh.21464</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21447">
<title>A single-center experience in 20 patients with infantile malignant osteopetrosis</title>
<link>http://dx.doi.org/10.1002%2Fajh.21447</link>
<description><![CDATA[Infantile malignant osteopetrosis (IMO) includes various genetic disorders that affect osteoclast development and/or function. Genotype-phenotype correlation studies in IMO have been hampered by the rarity and heterogeneity of the disease and by the severity of the clinical course, which often leads to death early in life. We report on the clinical and molecular findings and treatment in 20 consecutive patients (11 males, nine females) with IMO, diagnosed at a single center in the period 1991-2008. Mean age at diagnosis was 3.9 months, and mean follow-up was 66.75 months. Mutations in TCIRG1, OSTM1, ClCN7, and TNFRSF11A genes were detected in nine, three, one, and one patients, respectively. Six patients remain genetically undefined. OSTM1 and ClCN7 mutations were associated with poor neurologic outcome. Among nine patients with TCIRG1 defects, six presented with hypogammaglobulinemia, and one showed primary pulmonary hypertension. Fourteen patients received hematopoietic cell transplantation; of these, nine are alive and eight of them have evidence of osteoclast function. These data may provide a basis for informed decisions regarding the care of patients with IMO. Am. J. Hematol. 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21438">
<title>Splenic hyalohyphomycosis, molecularly and immunologically consistent with invasive aspergillosis, in a patient with acute lymphoblastic leukemia</title>
<link>http://dx.doi.org/10.1002%2Fajh.21438</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21440">
<title>Genome-wide association studies and the genetic dissection of complex traits</title>
<link>http://dx.doi.org/10.1002%2Fajh.21440</link>
<description><![CDATA[The availability of affordable high throughput technology for parallel genotyping has opened the field of genetics to genome-wide association studies (GWAS), and in the last few years hundreds of articles reporting results of GWAS for a variety of heritable traits have been published. What do these results tell us? Although GWAS have discovered a few hundred reproducible associations, this number is underwhelming in relation to the huge amount of data produced, and challenges the conjecture that common variants may be the genetic causes of common diseases. We argue that the massive amount of genetic data that result from these studies remains largely unexplored and unexploited because of the challenge of mining and modeling enormous data sets, the difficulty of using nontraditional computational techniques and the focus of accepted statistical analyses on controlling the false positive rate rather than limiting the false negative rate. In this article, we will review the common approach to analysis of GWAS data and then discuss options to learn more from these data. We will use examples from our ongoing studies of sickle cell anemia and also GWAS in multigenic traits. Am. J. Hematol., 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21421">
<title>Hydroxycarbamide-induced dermopathy</title>
<link>http://dx.doi.org/10.1002%2Fajh.21421</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21410">
<title>Near total effacement of bone marrow by medulloblastoma</title>
<link>http://dx.doi.org/10.1002%2Fajh.21410</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21399">
<title>Dutcher bodies</title>
<link>http://dx.doi.org/10.1002%2Fajh.21399</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21397">
<title>Russell bodies and Mott cells</title>
<link>http://dx.doi.org/10.1002%2Fajh.21397</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21394">
<title>MRI findings in aplastic anemia</title>
<link>http://dx.doi.org/10.1002%2Fajh.21394</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21403">
<title>A T-lineage neoplasm - Which one?</title>
<link>http://dx.doi.org/10.1002%2Fajh.21403</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21329">
<title>Symptomatic intracardiac diffuse large B-cell lymphoma</title>
<link>http://dx.doi.org/10.1002%2Fajh.21329</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21326">
<title>Monoblastic sarcoma cutis preceding acute monoblastic leukemia</title>
<link>http://dx.doi.org/10.1002%2Fajh.21326</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fajh.21321">
<title>Petechial bleeding after sunburn in a patient with mild thrombocytopenia</title>
<link>http://dx.doi.org/10.1002%2Fajh.21321</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a912889221~db=all~jumptype=rss">
<title>CLINICAL PROFILE AND HOME MANAGEMENT OF SICKLE CELL-RELATED PAIN: The Enugu (Nigeria) Experience</title>
<link>http://www.informaworld.com/smpp/content~content=a912889221~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a912890325~db=all~jumptype=rss">
<title>THE BENEFIT OF ATG IN IMMUNOSUPPRESSIVE THERAPY OF CHILDREN WITH MODERATE APLASTIC ANEMIA</title>
<link>http://www.informaworld.com/smpp/content~content=a912890325~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a912887479~db=all~jumptype=rss">
<title>RHABDOMYOSARCOMA OF THE EXTREMITIES: A Focus on Tumors Arising in the Hand and Foot</title>
<link>http://www.informaworld.com/smpp/content~content=a912887479~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a912887591~db=all~jumptype=rss">
<title>INCIDENCE OF PRIMARY CENTRAL NERVOUS SYSTEM TUMORS AMONG CHILDREN IN BELGRADE (SERBIA), 1991-2004</title>
<link>http://www.informaworld.com/smpp/content~content=a912887591~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a912889983~db=all~jumptype=rss">
<title>PANEL REACTIVE ANTIBODY IN THALASSEMIC SERUM INHIBITS PROLIFERATION AND DIFFERENTIATION OF CORD BLOOD CD34 + CELLS IN VITRO</title>
<link>http://www.informaworld.com/smpp/content~content=a912889983~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a912888004~db=all~jumptype=rss">
<title>ALLOGENEIC STEM CELL TRANSPLANTATION FOR MYELODYSPLASTIC SYNDROMES IN CHILDREN: A Report from the Spanish Working Party for Blood and Marrow Transplantation in Children (GETMON)</title>
<link>http://www.informaworld.com/smpp/content~content=a912888004~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a912888061~db=all~jumptype=rss">
<title>SEVERE HYPOCHROMIC MICROCYTIC ANEMIA IN A PATIENT WITH CONGENITAL ATRANSFERRINEMIA</title>
<link>http://www.informaworld.com/smpp/content~content=a912888061~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a912889236~db=all~jumptype=rss">
<title>EFFECT OF SOMATOSTATIN ANALOGUE OCTREOTIDE IN MEDULLOBLASTOMA IN XENOGRAFT AND CELL CULTURE STUDY</title>
<link>http://www.informaworld.com/smpp/content~content=a912889236~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a912889492~db=all~jumptype=rss">
<title>SUCCESSFUL TREATMENT OF KASABACH-MERRITT SYNDROME WITH VINCRISTINE AND DIAGNOSIS OF THE HEMANGIOMA USING THREE-DIMENSIONAL IMAGING</title>
<link>http://www.informaworld.com/smpp/content~content=a912889492~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a912887513~db=all~jumptype=rss">
<title>A NOVEL L218P MUTATION IN NADH-CYTOCHROME B5 REDUCTASE ASSOCIATED WITH TYPE I RECESSIVE CONGENITAL METHEMOGLOBINEMIA</title>
<link>http://www.informaworld.com/smpp/content~content=a912887513~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a911106651~db=all~jumptype=rss">
<title>PLASMA HEPARANASE AS A SIGNIFICANT MARKER OF TREATMENT RESPONSE IN CHILDREN WITH HODGKIN LYMPHOMA: Pilot Study</title>
<link>http://www.informaworld.com/smpp/content~content=a911106651~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a911109013~db=all~jumptype=rss">
<title>ALLOGENEIC CORD BLOOD TRANSPLANTATION IN CHILDREN WITH HEMATOLOGICAL MALIGNANCIES: A Long-Term Follow-Up Single-Center Study</title>
<link>http://www.informaworld.com/smpp/content~content=a911109013~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a911096517~db=all~jumptype=rss">
<title>EXTRA-OSSEOUS EWING SARCOMA</title>
<link>http://www.informaworld.com/smpp/content~content=a911096517~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a911100515~db=all~jumptype=rss">
<title>BONE MARROW TRANSPLANTATION OR HYDROXYUREA FOR SICKLE CELL ANEMIA: Long-Term Effects on Semen Variables and Hormone Profiles</title>
<link>http://www.informaworld.com/smpp/content~content=a911100515~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a911115025~db=all~jumptype=rss">
<title>ANTIBODY TITRATION AND IMMUNE RESPONSE OF IRANIAN &#x3B2;-THALASSEMIC PATIENTS TO HEPATITIS B VIRUSE VACCINE (BOOSTER EFFECT)</title>
<link>http://www.informaworld.com/smpp/content~content=a911115025~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a911099888~db=all~jumptype=rss">
<title>GROWTH STATUS IN CHILDREN AND ADOLESCENTS WITH SICKLE CELL DISEASE</title>
<link>http://www.informaworld.com/smpp/content~content=a911099888~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a911108151~db=all~jumptype=rss">
<title>CD10 AND CD34 EXPRESSION IN CHILDHOOD ACUTE LYMPHOBLASTIC LEUKEMIA IN MOROCCO: Clinical Relevance and Outcome</title>
<link>http://www.informaworld.com/smpp/content~content=a911108151~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a911124244~db=all~jumptype=rss">
<title>HEPATITIS G VIRUS INFECTION IN MULTITRANSFUSED EGYPTIAN CHILDREN</title>
<link>http://www.informaworld.com/smpp/content~content=a911124244~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a911129516~db=all~jumptype=rss">
<title>TRENDS IN SURVIVAL AFTER CHILDHOOD CANCER IN SLOVENIA BETWEEN 1957 AND 2007</title>
<link>http://www.informaworld.com/smpp/content~content=a911129516~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a911114143~db=all~jumptype=rss">
<title>SPERM CRYOPRESERVATION PRACTICES AMONG ADOLESCENT CANCER PATIENTS AT RISK FOR INFERTILITY</title>
<link>http://www.informaworld.com/smpp/content~content=a911114143~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a911121214~db=all~jumptype=rss">
<title>SPONTANEOUS THROMBOSIS OF HEPATIC ANEURYSMS IN AN INFANT WITH WISKOTT-ALDRICH SYNDROME</title>
<link>http://www.informaworld.com/smpp/content~content=a911121214~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a911102319~db=all~jumptype=rss">
<title>MULTIPLE CHROMOSOME ABNORMALITIES IN THE PLEURAL FLUID OF A PATIENT WITH RECURRENT EWING SARCOMA</title>
<link>http://www.informaworld.com/smpp/content~content=a911102319~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a910575591~db=all~jumptype=rss">
<title>THROMBOLYTICS FOR HYPERACUTE STROKE IN CHILDREN</title>
<link>http://www.informaworld.com/smpp/content~content=a910575591~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a910575883~db=all~jumptype=rss">
<title>HEMORHEOLOGICAL PARAMETERS IN CHILDREN WITH IRON-DEFICIENCY ANEMIA AND THE ALTERATIONS IN THESE PARAMETERS IN RESPONSE TO IRON REPLACEMENT</title>
<link>http://www.informaworld.com/smpp/content~content=a910575883~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a910575627~db=all~jumptype=rss">
<title>HAPLOIDENTICAL HEMATOPOIETIC STEM CELL TRANSPLANTATION IN CHILD HEMATOLOGIC MALIGNANCIES WITH G-CSF-MOBILIZED MARROW GRAFTS WITHOUT T-CELL DEPLETION: A Single-Center Report of 45 Cases</title>
<link>http://www.informaworld.com/smpp/content~content=a910575627~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a910577213~db=all~jumptype=rss">
<title>HYPEREOSINOPHILIC SYNDROME IN CHILDHOOD: Clinical and Molecular Features of Two Cases</title>
<link>http://www.informaworld.com/smpp/content~content=a910577213~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a910576427~db=all~jumptype=rss">
<title>THE CASE OF A 1-YEAR-OLD GIRL WITH HEREDITARY HYPERFERRITINEMIA CATARACT SYNDROME</title>
<link>http://www.informaworld.com/smpp/content~content=a910576427~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a910575547~db=all~jumptype=rss">
<title>ANAPLASTIC LARGE CELL LYMPHOMA WITH PRIMARY INVOLVEMENT OF SKELETAL MUSCLE: A Rare Case Report and Review of the Literature</title>
<link>http://www.informaworld.com/smpp/content~content=a910575547~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a910575680~db=all~jumptype=rss">
<title>POLAND SYNDROME WITH INTRACRANIAL GERM CELL TUMOR IN A CHILD</title>
<link>http://www.informaworld.com/smpp/content~content=a910575680~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a909912007~db=all~jumptype=rss">
<title>RHABDOMYOLYSIS DUE TO Escherichia coli SEPSIS IN THREE PEDIATRIC PATIENTS WITH ACUTE LYMPHOBLASTIC LEUKEMIA</title>
<link>http://www.informaworld.com/smpp/content~content=a909912007~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a909912913~db=all~jumptype=rss">
<title>PARVOVIRUS B19-INDUCED PERSISTENT PURE RED CELL APLASIA IN A CHILD WITH T-CELL IMMUNODEFICIENCY</title>
<link>http://www.informaworld.com/smpp/content~content=a909912913~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a909912723~db=all~jumptype=rss">
<title>ALTERED IRON METABOLISM IN CHILDREN WITH HUMAN IMMUNODEFICIENCY VIRUS DISEASE</title>
<link>http://www.informaworld.com/smpp/content~content=a909912723~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a909911835~db=all~jumptype=rss">
<title>ACUTE LYMPHOBLASTIC LEUKEMIA SECONDARY TO CHEMORADIOTHERAPY FOR PERIVASCULAR EPITHELIOID CELL TUMOR OF UTERUS</title>
<link>http://www.informaworld.com/smpp/content~content=a909911835~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a909911945~db=all~jumptype=rss">
<title>CHOOSING THERAPY FOR ADOLESCENT FEMALES WITH CANCER: Fertility Should Matter</title>
<link>http://www.informaworld.com/smpp/content~content=a909911945~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a909911931~db=all~jumptype=rss">
<title>RELAPSE OF PRIMITIVE MEDIASTINAL LYMPHOMA AS A MYELOID MASS FOLLOWING BEAM AUTOLOGOUS TRANSPLANT AND SUBSEQUENT REFRACTORINESS TO MATCHED UNRELATED UMBILICAL CORD BLOOD ALLOGRAFT</title>
<link>http://www.informaworld.com/smpp/content~content=a909911931~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a909911891~db=all~jumptype=rss">
<title>TRANSFORMATION OF MYELODYSPLASTIC SYNDROME TO T-CELL ACUTE LYMPHOBLASTIC LEUKEMIA IN A YOUNG ADULT</title>
<link>http://www.informaworld.com/smpp/content~content=a909911891~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a908622265~db=all~jumptype=rss">
<title>DIFFERENTIAL microRNA EXPRESSION IN CHILDHOOD B-CELL PRECURSOR ACUTE LYMPHOBLASTIC LEUKEMIA</title>
<link>http://www.informaworld.com/smpp/content~content=a908622265~db=all~jumptype=rss</link>
<description><![CDATA[
]]></description>
</item>

<item rdf:about="http://www.informaworld.com/smpp/content~content=a908623719~db=all~jumptype=rss">
<title>INCIDENCE OF AND RISK FACTORS FOR CHILDHOOD THROMBOSIS: A Single-Center Experience in Ankara, Turkey</title>
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<title>EXPRESSION OF PTEN AND SHP1, INVESTIGATED FROM TISSUE MICROARRAYS IN PEDIATRIC ACUTE LYMPHOBLASTIC, LEUKEMIA</title>
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<title>BONE FRACTURE: An Unusual Presentation of Acute Megakaryoblastic Leukemia</title>
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<title>SUCCESSFUL USE OF TERBUTALINE IN PERSISTENT PRIAPISM IN A 12-YEAR-OLD BOY WITH CHRONIC MYELOID LEUKEMIA</title>
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<item rdf:about="http://www.informaworld.com/smpp/content~content=a906492123~db=all~jumptype=rss">
<title>REVIEWER ACKNOWLEDGMENT</title>
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