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Daniel A. Arber - One of the best experts on this subject based on the ideXlab platform.
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Mixed Phenotype Acute Leukemia A Study of 61 Cases Using World Health Organization and European Group for the Immunological Classification of Leukaemias Criteria
2016Co-Authors: Am Clin J Pathol, Olga K. Weinberg, Daniel A. Arber, Am Clin Pathol J DecemberAbstract:Objectives: The 2008 World Health Organization (WHO) classification system grouped bilineal and biphenotypic acute Leukemias together under a new heading of mixed phenotype acute leukemia (MPAL). The lineage-specific marker criteria have also changed for a diagnosis of MPAL. The goal of this study was to characterize clinical significance of this new group. Methods: Sixty-one patients diagnosed with MPAL using either European Group for the Immunological Classification of Leukaemias (EGIL) criteria or 2008 WHO criteria were included in this study. Results: Sixteen patients (26%) diagnosed with acute biphenotypic leukemia using EGIL criteria did not fulfill 2008 WHO criteria for MPAL. Cytogenetic data wer
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mixed phenotype acute leukemia a study of 61 cases using world health organization and european group for the immunological classification of leukaemias criteria
American Journal of Clinical Pathology, 2014Co-Authors: Olga K. Weinberg, Mahesh Seetharam, Li Ren, Ash A Alizadeh, Daniel A. ArberAbstract:Objectives The 2008 World Health Organization (WHO) classification system grouped bilineal and biphenotypic acute Leukemias together under a new heading of mixed phenotype acute leukemia (MPAL). The lineage-specific marker criteria have also changed for a diagnosis of MPAL. The goal of this study was to characterize clinical significance of this new group. Methods Sixty-one patients diagnosed with MPAL using either European Group for the Immunological Classification of Leukaemias (EGIL) criteria or 2008 WHO criteria were included in this study. Results Sixteen patients (26%) diagnosed with acute biphenotypic leukemia using EGIL criteria did not fulfill 2008 WHO criteria for MPAL. Cytogenetic data were available for 32 patients, and the most common abnormality was t(9;22) (five of 32 cases). Clinical outcome data suggested that younger patients with MPAL (≤21 years) had better overall survival (OS) in both the EGIL and WHO groups (EGIL, P = .0403; WHO, P = .0601). Compared with 177 patients with acute myeloid leukemia (AML), MPAL patients had better OS (P = .0003) and progression-free survival (P = .0001). However, no difference in OS between MPAL and 387 patients with acute lymphoblastic leukemia was present (P = .599). Conclusions As defined by the 2008 WHO classification, fewer patients are now classified as having MPAL than with the EGIL criteria. In this study, patients with MPAL have a better clinical outcome compared with patients with AML.
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cd79 alpha expression in acute myeloid leukemia high frequency of expression in acute promyelocytic leukemia
American Journal of Pathology, 1996Co-Authors: Daniel A. Arber, K A Jenkins, Marilyn L SlovakAbstract:Abstract CD79 alpha is a subunit of an intracytoplasmic protein reported to be specific for B lymphocytes, including immature B lineage cells. To evaluate expression of the CD79 alpha antigen in acute myeloid leukemia (AML), we studied forty-eight cases of AML by paraffin section immunohistochemistry. The cases included four MO, nine M1, nine M2, ten M3, ten M4, and six M5 AMLs using criteria of the French-American-British cooperative group. Eleven cases demonstrated cytoplasmic staining for the CD79 alpha antigen, including one M1, nine M3, and one M5 AML. These CD79 alpha-positive cases represented 5% of all non-promyelocytic AMLs and 90% of all acute promyelocytic Leukemias studied. All acute promyelocytic Leukemias had the characteristic t(15;17)(q24;q21), including two cases of the microgranular variant (M3v). No other B-lineage-associated antigens were found in the CD79 alpha-positive cases, with the exception of a subpopulation of CD19-positive leukemic cells in one patient. The two non-promyelocytic Leukemias that expressed CD79 alpha had no evidence of t(15;17) and did not express any additional B-lineage-associated antigens that might suggest a mixed lineage proliferation. This study demonstrates that CD79 alpha expression in acute leukemia is not restricted to B-lineage acute lymphoblastic Leukemias and that CD79 alpha expression is frequently associated with t(15;17) acute myeloid leukemia.
Miguel A Sanz - One of the best experts on this subject based on the ideXlab platform.
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obesity is a risk factor for acute promyelocytic leukemia evidence from population and cross sectional studies studies and correlation with flt3 mutations and polyunsaturated fatty acid metabolism
Haematologica, 2019Co-Authors: Luca Mazzarella, Edoardo Botteri, Anthony Matthews, Elena Gatti, Davide Di Salvatore, Vincenzo Bagnardi, Massimo Breccia, Pau Montesinos, Teresa Bernal, Miguel A SanzAbstract:: Obesity correlates with hematological malignances including Leukemias, but risk of specific leukemia subtypes like Acute Promyelocytic Leukemia and underlying molecular mechanisms are poorly understood. We explored multiple datasets for correlation between leukemia, Body Mass Index and molecular features. In a population-based study (n=5.2 million), we correlated Body Mass Index with promyelocytic, other acute myeloid, lymphoid or other Leukemias. In cross-sectional studies, we tested body mass index deviation in promyelocytic leukemia trial cohorts from what expected based on national surveys. We interrogated The Cancer Genome Atlas for transcriptional signatures and mutations enriched in promyelocytic leukemia and/or obesity and confirmed correlation between body mass and FLT3 mutations in promyelocytic leukemia cohorts by logistic regression. In the population-based study, Hazard Ratio per 5 kg/m2 increase was: promyelocytic leukemia 1.44 (95% CI 1.0-2.08); non-promyelocytic acute myeloid Leukemias 1.17 (1.10-1.26); lymphoid Leukemias 1.04 (1.0-1.09); other 1.10 (1.04-1.15). In cross-sectional studies, body mass deviated significantly from expected (Italy p<0.001, Spain p=0.011, USA p<0.001). Promyelocytic leukemia showed upregulation of polyunsaturated fatty acid metabolism genes. Oddds of FLT3 mutations were higher in obese acute myeloid Leukemias (Odds Ratio=2.4, p=0.007), whether promyelocytic or not, a correlation confirmed in the pooled promyelocytic leukemia cohorts (OR 1.22, 1.05-1.43 per 5 kg/m2). These results strengthen the evidence for obesity as a bona fide risk factor for myeloid Leukemias and in particular APL. FLT3 mutations and polyunsaturated fatty acid metabolism may play a previously underappreciated role in obesity-associated leukemogenesis.
Nathalie Droin - One of the best experts on this subject based on the ideXlab platform.
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setbp1 mutations in 658 patients with myelodysplastic syndromes chronic myelomonocytic leukemia and secondary acute myeloid Leukemias
Leukemia, 2013Co-Authors: Olivier Kosmider, Raphael Itzykson, Nathalie Droin, Frederik DammAbstract:SETBP1 mutations in 658 patients with myelodysplastic syndromes, chronic myelomonocytic leukemia and secondary acute myeloid Leukemias
Luca Mazzarella - One of the best experts on this subject based on the ideXlab platform.
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obesity is a risk factor for acute promyelocytic leukemia evidence from population and cross sectional studies studies and correlation with flt3 mutations and polyunsaturated fatty acid metabolism
Haematologica, 2019Co-Authors: Luca Mazzarella, Edoardo Botteri, Anthony Matthews, Elena Gatti, Davide Di Salvatore, Vincenzo Bagnardi, Massimo Breccia, Pau Montesinos, Teresa Bernal, Miguel A SanzAbstract:: Obesity correlates with hematological malignances including Leukemias, but risk of specific leukemia subtypes like Acute Promyelocytic Leukemia and underlying molecular mechanisms are poorly understood. We explored multiple datasets for correlation between leukemia, Body Mass Index and molecular features. In a population-based study (n=5.2 million), we correlated Body Mass Index with promyelocytic, other acute myeloid, lymphoid or other Leukemias. In cross-sectional studies, we tested body mass index deviation in promyelocytic leukemia trial cohorts from what expected based on national surveys. We interrogated The Cancer Genome Atlas for transcriptional signatures and mutations enriched in promyelocytic leukemia and/or obesity and confirmed correlation between body mass and FLT3 mutations in promyelocytic leukemia cohorts by logistic regression. In the population-based study, Hazard Ratio per 5 kg/m2 increase was: promyelocytic leukemia 1.44 (95% CI 1.0-2.08); non-promyelocytic acute myeloid Leukemias 1.17 (1.10-1.26); lymphoid Leukemias 1.04 (1.0-1.09); other 1.10 (1.04-1.15). In cross-sectional studies, body mass deviated significantly from expected (Italy p<0.001, Spain p=0.011, USA p<0.001). Promyelocytic leukemia showed upregulation of polyunsaturated fatty acid metabolism genes. Oddds of FLT3 mutations were higher in obese acute myeloid Leukemias (Odds Ratio=2.4, p=0.007), whether promyelocytic or not, a correlation confirmed in the pooled promyelocytic leukemia cohorts (OR 1.22, 1.05-1.43 per 5 kg/m2). These results strengthen the evidence for obesity as a bona fide risk factor for myeloid Leukemias and in particular APL. FLT3 mutations and polyunsaturated fatty acid metabolism may play a previously underappreciated role in obesity-associated leukemogenesis.
Dennis P Omalley - One of the best experts on this subject based on the ideXlab platform.
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t cell large granular leukemia and related proliferations
American Journal of Clinical Pathology, 2007Co-Authors: Dennis P OmalleyAbstract:Session 9 of the 2005 Society for Hematopathology/European Association for Haematopathology Workshop focused on large granular lymphocyte (LGL) Leukemias and related disorders. T-cell LGL (T-LGL) Leukemias, discussed herein, account for 2% to 3% of cases of small lymphocytic leukemia. T-LGL diseases cover a heterogeneous spectrum of disorders that include reactive conditions, typically associated with autoimmune disease, to outright leukemia. These disorders are found in older people, with an average age at initial examination of approximately 60 years and a median survival of more than 10 years in T-LGL leukemia. Systemic symptoms and neutropenia are common at initial examination. Lymphocytosis, composed of small mature lymphocytes with increased cytoplasm, is common. The spleen and bone marrow are involved in T-LGL leukemia, although morphologic findings may be subtle. The immunophenotype is typically that of CD3+/CD8+ cytotoxic T cells. Some cases may be due to chronic immune stimulation, with subsequent clonal escape and proliferation of a neoplastic population of lymphocytes.
