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Join a strong group in scenic Montana. Beautiful cancer center with state of the art equipment. :: Montana :: CompHealth Inc
Job 917814 Medical Director opportunity for a physician with leadership skills to join a progressive cancer care team. Highly competitive compensation Bonus plan with extra incentives Tumor Board Clinical
Hematology/Medical Oncology in Washington. High income potential and $300K plus the first year! :: Washington :: CompHealth Inc
Job 916966 Beautiful location in the North West. Family community with excellent public and private schools. New state of the art cancer center with top equipment. Strong support staff in a team environment.
Partnership Opportunity for an Oncologist who is looking for a long term practice in Iowa. :: Iowa :: CompHealth Inc
Job 917544 Strong well established practice is seeking a partner to join their growing practice Competitive Compensation in line with MGMA Bonus/ Production Incentives Flexible Schedule Light Call which

Hematological Oncology

Silibinin can induce differentiation as well as enhance vitamin D3-induced differentiation of human AML cells ex vivo and regulates the levels of differentiation-related transcription factors
Jing Zhang, Jonathan S Harrison, Milan Uskokovic, Michael Danilenko, George P Studzinski Wed, 28 Oct 2009 04:28:00 -0000
Induction of terminal differentiation is a conceptually attractive approach for the therapy of neoplastic diseases. Although vitamin D derivatives (deltanoids) can induce differentiation of AML cells in vitro, so far deltanoids have not been successfully brought to the clinic, due to the likelihood of life-threatening hypercalcemia. Here, we incubated freshly obtained blood cells from patients with AML with a plant antioxidant (PAOx), silibinin (SIL), alone or together with a deltanoid. Twenty patients with AML (all subtypes except M3) were available for this study, and in 14 (70%), SIL (60 µM) either induced differentiation ex vivo, or enhanced differentiation induced by deltanoids, or both. Interestingly, SIL acting alone induced differentiation only in cases in which chromosome aberrations could not be detected. In eleven samples sufficient material was available for a limited analysis of the underlying events. Quantitative RT-PCR showed that differentiation markers were upregulated at the mRNA level by both SIL and deltanoids, suggesting that intracellular signaling pathways upstream of transcription factors (TFs) were activated by these agents. Western analysis for proteins which function as TFs in deltanoid-induced monocytic differentiation, such as members of Jun and C/EBP families, surprisingly demonstrated that SIL upregulated all these TFs in the cases tested. This suggests that although the presence of SIL may not always be sufficient to induce differentiation, it can serve as a differentiation enabling factor for blasts obtained from a large proportion of patients with AML. Thus, SIL/deltanoid combinations warrant further consideration as preventive/therapeutic regimens in human leukaemia. Copyright © 2009 John Wiley & Sons, Ltd.
Burkitt lymphoma versus diffuse large B-cell lymphoma: a practical approach
Cristiana Bellan, Lazzi Stefano, De Falco Giulia, Emily A Rogena, Leoncini Lorenzo Tue, 20 Oct 2009 22:14:00 -0000
Burkitt Lymphoma (BL) is listed in the World Health Organization (WHO) classification of lymphoid tumours as an 'aggressive B-cell non-Hodgkin's lymphoma', characterized by a high degree of proliferation of the malignant cells and deregulation of the c-MYC gene. The main diagnostic challenge in BL is to distinguish it from diffuse large B-cell lymphoma (DLBCL). While in children BL and DLBCL types probably do not differ clinically, and the differential diagnosis between BL and DLBCL may theoretically appear clear-cut, in adults daily practice shows the existence of cases that have morphological features, immunophenotypic and cytogenetics intermediate between DLBCL and BL, and cannot be classified with certainty in these categories. Distinguishing between BL and DLBCL is critical, as the two diseases require different management. This review summarizes the current practical approach, including the use of a large panel of antibodies, and cytogenetic and molecular diagnostic techniques, to distinguish between BL, DLBCL and the provisional category of 'B-cell lymphoma, unclassifiable, with features intermediate between diffuse large B-cell lymphoma and Burkitt lymphoma', now listed in the updated WHO classification. Copyright © 2009 John Wiley & Sons, Ltd.
Outcomes for lymphoid malignancies in the Nurses' Health Study (NHS) as compared to the Surveillance, Epidemiology and End Results (SEER) Program
Gregory A Abel, Kimberly A Bertrand, Craig C Earle, Francine Laden Wed, 28 Oct 2009 04:30:00 -0000
Vital statistics for the lymphoid malignancies obtained from the Surveillance, Epidemiology and End Results (SEER) Program have seldom been directly compared to data from alternative national databases. While SEER is recognized as the standard, some lymphoid malignancies - especially the chronic ones - may be underreported. We compared the incidence, all-cause and cause-specific mortality for Hodgkin's lymphoma (HL), non-Hodgkin's lymphoma (NHL), multiple myeloma (MM) and chronic lymphocytic leukaemia (CLL) in SEER to that in the Nurses' Health Study (NHS), a national cohort study of 121 700 female registered nurses, matching for age and race. In over 2.5 million person-years, the incidence of HL was the same as in SEER (SIR = 1.01 [0.75, 1.26]), while the incidence of NHL, CLL and MM were slightly higher. All-cause mortality was lower for the lymphoid malignancies except for MM, which was the same; there were no differences in cause-specific mortality, except for MM (HR = 1.26 [1.07, 1.48]). Our analysis suggests that, at least among white women, SEER is a reliable data source with respect to lymphoid malignancies. Copyright © 2009 John Wiley & Sons, Ltd.

Annals of Hematology

Salvage treatment with upfront melphalan 100 mg/m2 and consolidation with novel drugs for fulminant progression of multiple myeloma
Wed, 18 Nov 2009 19:15:05 -0000
Abstract  Patients (pts) with fulminant progression (FPG) of multiple myeloma (MM) after autologous stem cell transplantation (ASCT) have poor prognosis. Pancytopenia, extramedullary disease, and/or renal impairment are often present, and treatment options are limited. We have retrospectively evaluated 31 pts with FPG of MM after ASCT who were treated upfront salvage therapy with melphalan 100 mg/m2 (MEL 100) followed by PBSC support and consolidation therapy using regimens containing thalidomide (n = 16) or bortezomib (n = 15). The overall response rate (ORR) was 58% (18/31). After MEL 100, one patient achieved complete remission (3%), 26% of pts very good partial remission, 29% of pts partial remission, and 42% of pts stable disease. Progression within 3 months after MEL 100 occurred in 35% of pts. The median follow-up from MEL 100 was 8 months. The median TTP was 5 months (range, 2–15 months), and the median OS was 8 months (range, 3–23 months). There were no treatment-related deaths. In fulminant progression of MM, upfront MEL 100 is a safe salvage regimen with good response rate (ORR, 58%). Treatment with upfront MEL 100 followed by a thalidomide- or bortezomib-based regimen can prolong overall survival to more than 12 months in 33% of pts with fulminant progression of MM. Content Type Journal ArticleCategory Original ArticleDOI 10.1007/s00277-009-0862-zAuthors Marta Krejci, Masaryk University Hospital Department of Internal Medicine–Hematooncology Jihlavska 20 Brno 625 00 Czech RepublicZdenek Adam, Masaryk University Hospital Department of Internal Medicine–Hematooncology Jihlavska 20 Brno 625 00 Czech RepublicTomas Buchler, Thomayer University Hospital 1st Faculty of Medicine, Department of Oncology Prague Czech RepublicAndrea Krivanova, Masaryk University Hospital Department of Internal Medicine–Hematooncology Jihlavska 20 Brno 625 00 Czech RepublicLudek Pour, Masaryk University Hospital Department of Internal Medicine–Hematooncology Jihlavska 20 Brno 625 00 Czech RepublicLenka Zahradova, Masaryk University Hospital Department of Internal Medicine–Hematooncology Jihlavska 20 Brno 625 00 Czech RepublicMichal Holanek, Masaryk University Hospital Department of Internal Medicine–Hematooncology Jihlavska 20 Brno 625 00 Czech RepublicViera Sandecka, Masaryk University Hospital Department of Internal Medicine–Hematooncology Jihlavska 20 Brno 625 00 Czech RepublicJiri Mayer, Masaryk University Hospital Department of Internal Medicine–Hematooncology Jihlavska 20 Brno 625 00 Czech RepublicJiri Vorlicek, Masaryk University Hospital Department of Internal Medicine–Hematooncology Jihlavska 20 Brno 625 00 Czech RepublicRoman Hajek, Masaryk University Hospital Department of Internal Medicine–Hematooncology Jihlavska 20 Brno 625 00 Czech Republic Journal Annals of HematologyOnline ISSN 1432-0584Print ISSN 0939-5555
Clinical efficacy of a bortezomib, cyclophosphamide, thalidomide, and dexamethasone (Vel-CTD) regimen in patients with relapsed or refractory multiple myeloma: a phase II study
Wed, 18 Nov 2009 00:06:17 -0000
Abstract  The clinical efficacy and safety of a four-drug combination of bortezomib, cyclophosphamide, thalidomide, and dexamethasone was assessed for patients with relapsed or refractory multiple myeloma. Seventy patients received at least two cycles of treatment with bortezomib 1.3 mg/m2 intravenously on days 1, 4, 8, and 11; cyclophosphamide 150 mg/m2 orally on days 1–4; thalidomide 50 mg/day orally every day; and dexamethasone 20 mg/m2 intravenously on days 1, 4, 8, and 11. The overall best response rate was 88%, with 46% complete response, 9% very good partial response, and 33% partial response. After a median follow-up of 12.6 months, the median progression-free survival (PFS) was 14.6 months with a 3-year PFS of 14% and the median overall survival (OS) was 31.6 months with a 3-year OS of 47%. Grade 3 or 4 adverse events included thrombocytopenia (12%), neutropenia (4%), peripheral sensory neuropathy (3%), with thrombosis being very rare (<1%). Bortezomib combined with cyclophosphamide, thalidomide, and dexamethasone is a highly effective salvage therapy with manageable toxicity for patients with relapsed or refractory multiple myeloma. Content Type Journal ArticleCategory Original ArticleDOI 10.1007/s00277-009-0856-xAuthors Yeo-Kyeoung Kim, Chonnam National University Medical School Gwangju Republic of KoreaSang-Kyun Sohn, Kyungpook National University Medical School Daegu Republic of KoreaJae-Hoon Lee, Gachon University Incheon Republic of KoreaDeok-Hwan Yang, Chonnam National University Medical School Gwangju Republic of KoreaJoon-Ho Moon, Kyungpook National University Medical School Daegu Republic of KoreaJae-Sook Ahn, Chonnam National University Medical School Gwangju Republic of KoreaHyeoung-Joon Kim, Chonnam National University Medical School Gwangju Republic of KoreaJe-Jung Lee, Chonnam National University Medical School Gwangju Republic of KoreaThe Korean Multiple Myeloma Working Party (KMMWP), Center for Biomedical Human Resources at Chonnam National University The Brain Korea 21 Project Gwangju Republic of Korea Journal Annals of HematologyOnline ISSN 1432-0584Print ISSN 0939-5555
Erratum to: Results of FLT3 mutation screening and correlations with immunophenotyping in 169 Brazilian patients with acute myeloid leukemia
Wed, 18 Nov 2009 00:06:16 -0000
Erratum to: Results of FLT3 mutation screening and correlations with immunophenotyping in 169 Brazilian patients with acute myeloid leukemia Content Type Journal ArticleCategory ErratumDOI 10.1007/s00277-009-0860-1Authors Antonio R. Lucena-Araujo, University of São Paulo Hematology Division, Department of Internal Medicine, National Institute of Science and Technology on Cell Based Therapy, Medical School of Ribeirão Preto Ribeirão Preto BrazilDanielle L. Souza, University of São Paulo Hematology Division, Department of Internal Medicine, National Institute of Science and Technology on Cell Based Therapy, Medical School of Ribeirão Preto Ribeirão Preto BrazilFabio Morato de Oliveira, University of São Paulo Hematology Division, Department of Internal Medicine, National Institute of Science and Technology on Cell Based Therapy, Medical School of Ribeirão Preto Ribeirão Preto BrazilMariana Tereza Lira Benicio, University of São Paulo Hematology Division, Department of Internal Medicine, National Institute of Science and Technology on Cell Based Therapy, Medical School of Ribeirão Preto Ribeirão Preto BrazilLorena L. Figueiredo-Pontes, University of São Paulo Hematology Division, Department of Internal Medicine, National Institute of Science and Technology on Cell Based Therapy, Medical School of Ribeirão Preto Ribeirão Preto BrazilBarbara A. Santana-Lemos, University of São Paulo Hematology Division, Department of Internal Medicine, National Institute of Science and Technology on Cell Based Therapy, Medical School of Ribeirão Preto Ribeirão Preto BrazilGuilherme A. dos Santos, University of São Paulo Hematology Division, Department of Internal Medicine, National Institute of Science and Technology on Cell Based Therapy, Medical School of Ribeirão Preto Ribeirão Preto BrazilRafael H. Jacomo, University of São Paulo Hematology Division, Department of Internal Medicine, National Institute of Science and Technology on Cell Based Therapy, Medical School of Ribeirão Preto Ribeirão Preto BrazilAnemari R. Dinarte-Santos, University of São Paulo Department of Genetics, National Institute of Science and Technology on Cell Based Therapy, Medical School of Ribeirão Preto Av. Bandeirantes, 3900 14048-900 Ribeirão Preto São Paulo BrazilMihoko Yamamoto, Federal University of São Paulo Department of Hematology and Hemotherapy São Paulo BrazilWilson A. Silva-Jr, University of São Paulo Department of Genetics, National Institute of Science and Technology on Cell Based Therapy, Medical School of Ribeirão Preto Av. Bandeirantes, 3900 14048-900 Ribeirão Preto São Paulo BrazilMaria de Lourdes Chauffaille, Federal University of São Paulo Department of Hematology and Hemotherapy São Paulo BrazilEduardo M. Rego, University of São Paulo Hematology Division, Department of Internal Medicine, National Institute of Science and Technology on Cell Based Therapy, Medical School of Ribeirão Preto Ribeirão Preto Brazil Journal Annals of HematologyOnline ISSN 1432-0584Print ISSN 0939-5555

American Journal of Hematology

Definitions of the phenotypic manifestations of sickle cell disease
Samir K. Ballas, Susan Lieff, Lennette J. Benjamin, Carlton D. Dampier, Matthew M. Heeney, Carolyn Hoppe, Cage S. Johnson, Zora R. Rogers, Kim Smith-Whitley, Winfred C. Wang, Marilyn J. Telen, on Behalf of the Investigators at the Comprehensive Sickle Cell Centers Thu, 24 Sep 2009 11:38:00 -0000
Sickle cell disease (SCD) is a pleiotropic genetic disorder of hemoglobin that has profound multiorgan effects. The low prevalence of SCD ([sim]100,000/US) has limited progress in clinical, basic, and translational research. Lack of a large, readily accessible population for clinical studies has contributed to the absence of standard definitions and diagnostic criteria for the numerous complications of SCD and inadequate understanding of SCD pathophysiology. In 2005, the Comprehensive Sickle Cell Centers initiated a project to establish consensus definitions of the most frequently occurring complications. A group of clinicians and scientists with extensive expertise in research and treatment of SCD gathered to identify and categorize the most common complications. From this group, a formal writing team was formed that further reviewed the literature, sought specialist input, and produced definitions in a standard format. This article provides an overview of the process and describes 12 body system categories and the most prevalent or severe complications within these categories. A detailed Appendix provides standardized definitions for all complications identified within each system. This report proposes use of these definitions for studies of SCD complications, so future studies can be comparably robust and treatment efficacy measured. Use of these definitions will support greater accuracy in genotype-phenotype studies, thereby achieving a better understanding of SCD pathophysiology. This should nevertheless be viewed as a dynamic rather than final document; phenotype descriptions should be reevaluated and revised periodically to provide the most current standard definitions as etiologic factors are better understood, and new diagnostic options are developed. Am. J. Hematol. 2009. © 2009 Wiley-Liss, Inc.
On being metachromatic: Mystique and misunderstanding in mastocytosis
Jason Gotlib Fri, 23 Oct 2009 14:51:00 -0000
No abstract.
Idiotype-pulsed antigen presenting cells following autologous transplantation for multiple myeloma may be associated with prolonged survival
Martha Q. Lacy, Sumithra Mandrekar, Angela Dispenzieri, Suzanne Hayman, Shaji Kumar, Francis Buadi, David Dingli, Mark Litzow, Peter Wettstein, Douglas Padley, Brian Kabat, Dennis Gastineau, S. Vincent Rajkumar, Morie A. Gertz Fri, 09 Oct 2009 14:05:00 -0000
Vaccines are attractive as consolidation therapy after autologous stem cell transplantation (ASCT) for multiple myeloma (MM). We report the results of a phase II trial of the immunotherapeutic, APC8020 (MylovengeTM), given after ASCT for MM. We compared the results with that of other patients with MM who underwent ASCT at Mayo Clinic during the same time period. Twenty-seven patients were enrolled on the trial between July, 1998 and June, 2001, and the outcomes were compared to that of 124 consecutive patients transplanted during the same period, but not enrolled on the trial. The median (range) follow-up for patients still alive from the vaccine trial is 6.5 (2.9-8 years), and 7.1 (6-8 years) in the control group. The median age was 57.4 range (36.1-71.3) in the DB group and 56.4 (range, 30-69) in the trial group. Known prognostic factors including PCLI, B2M, and CRP were comparable between the groups. The median overall survival for the trial patients was 5.3 years (95% CI: 4.0 years - N/A) compared to 3.4 years (95% CI: 2.7-4.6 years) for the DB group (P = 0.02). The median time to progression and progression-free survival for the trial group was similar to the DB group. Although not a controlled trial, the vaccines given after ASCT appear to be associated with improved overall survival compared to historical controls. This approach warrants further investigation to confirm this and define the role of vaccine therapy in myeloma. Am. J. Hematol. 2009. © 2009 Wiley-Liss, Inc.

Pediatric Hematology and Oncology: Articles recently published in

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Zhang, JinhuaZhang, JihongYang, YanminLu, ChunweiTong, Haixia
HYDROXYUREA-INDUCED HEMATOLOGICAL RESPONSE IN TRANSFUSION-INDEPENDENT BETA-THALASSEMIA INTERMEDIA: Case Series and Review of Literature
Rashidi, ArminZeinali, SyrusBagheri, AlirezaHedayati-Asl, Amir AbbasEhsani, Mohammad Ali

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