Progression of myelodysplasia to acute lymphoblastic leukaemia: Implications for disease biology

Disperati, Patricia; Ichim, Christine V.; Tkachuk, Denis; Chun, Kathy; Schuh, Andre C.; Wells, Richard A.

doi:10.1016/j.leukres.2005.06.011

Cited by 68 publications

(40 citation statements)

References 52 publications

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“…Although it is generally thought that MDS arises in a pluripotent stem progenitor cell, there is some debate as to whether the T-cell population is involved in this disorder. 27 As shown in Figure 2D, the amplification at band 17q12 was absent in the CD3 ϩ cells of 2 patients (patients 3 and 14) and clearly detectable in another (patient 33). Known high-frequency CNVs present in the CD34 ϩ fractions at chromosome 5q (patients 14 and 33) and chromosome 19p (patient 3) were clearly detectable in the CD3 ϩ cell populations and served as internal controls for the CD3 ϩ aCGH analysis in each case ( Figure 2D).…”

Section: Amplification Of the Hominoid Oncoprotein Tbc1d3 Is A Novel mentioning

confidence: 79%

High-resolution whole genome tiling path array CGH analysis of CD34+ cells from patients with low-risk myelodysplastic syndromes reveals cryptic copy number alterations and predicts overall and leukemia-free survival

Starczynowski

Vercauteren

Telenius

et al. 2008

Blood

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Section: Amplification Of the Hominoid Oncoprotein Tbc1d3 Is A Novel mentioning

confidence: 79%

High-resolution whole genome tiling path array CGH analysis of CD34+ cells from patients with low-risk myelodysplastic syndromes reveals cryptic copy number alterations and predicts overall and leukemia-free survival

Starczynowski

Vercauteren

Telenius

et al. 2008

Blood

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“…8 In total, 30-50% of MDS cases progress to acute myeloid leukaemia (AML). [9][10][11] Chronic myelomonocytic leukaemia (CMML), initially classified morphologically as a MDS by the French-American-British cooperative group, 12 was later classified by the World Health Organization (WHO) (2008) as a mixed MDS/ myeloproliferative neoplasm; 4 MDS with 20-30% bone marrow (BM) blast cells was classified as AML by the WHO. 4 Similarly to MDS, CMML and AML are also commonly diagnosed later in life.…”

Section: Introductionmentioning

confidence: 99%

Safety and efficacy of azacitidine in Belgian patients with high-risk myelodysplastic syndromes, acute myeloid leukaemia, or chronic myelomonocytic leukaemia: results of a real-life, non-interventional post-marketing survey

Béguin

Selleslag

Meers

et al. 2014

Acta Clinica Belgica

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Objectives: We evaluated azacitidine (Vidaza H ) safety and efficacy in patients with myelodysplastic syndrome (MDS), acute myeloid leukaemia (AML), and chronic myelomonocytic leukaemia (CMML), in a real-life setting. Treatment response, dose, and schedule were assessed. Methods: This non-interventional, post-marketing survey included 49/50 patients receiving azacitidine at 14 Belgian haematology centres from 2010-2012. Treatment-emergent adverse events (TEAEs), including treatment-related TEAEs, and serious TEAEs (TESAEs) were recorded throughout the study. Treatment response [complete response (CR), partial response (PR), haematological improvement (HI), stable disease (SD), treatment failure (TF)) and transfusion-independence (TI) were evaluated at completion of a 1-year observation period (1YOP) or at treatment discontinuation, and overall survival (OS), at study conclusion. Results: The median age of patients was 74.7 (range: 43.9-87.8) years; 69.4% had MDS, 26.5% had primary or secondary AML, and 4.1% had CMML. Treatment-related TEAEs, grade 3-4 TEAEs, and TESAEs were reported in 67.3%, 28.6%, and 18.4% of patients, respectively. During 1YOP, patients received a median of 7 (1-12) treatment cycles. Treatment response was assessed for 38/49 patients. Among MDS and CMML patients (n529), 41.4% had CR, PR, or HI, 41.4% had SD, and 17.2% had TF. Among AML patients (n59), 44.4% had CR or PR, 33.3% had SD, and 22.2% had TF. TI was observed in 14/32 (43.8%) patients who were transfusion-dependent at baseline. Median (95% confidence interval) OS was 490 (326-555) days; 1-year OS estimate was 0.571 (0.422-0.696). Conclusions: Our data support previous findings that azacitidine has a clinically acceptable safety profile and shows efficacy.

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“…11,13 Quanto à sua etiologia, a SMD pode ser classificada como SMD primária ou de novo e secundária. A doença primária não possui uma etiologia totalmente elucidada, sabese que ela pode advir de infecções virais, exposição ao benzeno, radiações ionizantes 6,8,14 e, mais raramente, de anormalidades congênitas.…”

Section: 35unclassified

“…52,53,54 As anomalias cromossômicas em SMD são clonais, não ocorrem ao acaso e constituem-se, em geral, na perda de material genético, o que sugere a inativação de genes supressores tumorais necessários para o desenvolvimento de células mieloides normais. As alterações cromossômicas mais frequentes na SMD envolvem os cromossomos 5,7,8,11,13,17,20, 21 e X. 52,53 Com base na citogenética, as alterações cromossômicas da SMD podem ser divididas em cariótipo normal, perdas isoladas, translocações balanceadas e cariótipos complexos (três ou mais anomalias).…”

Section: Aspectos Laboratoriais No Diagnóstico De Smdunclassified

Síndromes mielodisplásicas: aspectos moleculares, laboratoriais e a classificação OMS 2008

Moraes¹,

Licínio²,

Pagnussat³

et al. 2009

Rev. Bras. Hematol. Hemoter.

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As síndromes mielodisplásicas (SMDs) IntroduçãoAs síndromes mielodisplásicas (SMDs) constituem um grupo heterogêneo de doenças hematopoéticas que acometem indivíduos de todas as idades, sobretudo adultos. [1][2][3][4] As SMDs são originadas no microambiente medular, a partir de uma mutação somática das células progenitoras hematopoéticas (stem cell), 3,5 o que leva a uma desordem nas vias de sinalização intracelular, resultando em um aumento da apoptose nessas células.6,7 Dessa forma, essa hemopatia caracteriza-se por hematopoese ineficaz, com displasia de uma ou mais linhagens celulares da medula óssea (MO), citopenias periféricas, 2,3 aumento do número de mieloblastos no sangue periférico (SP) e/ou MO 8,9 e instabilidade genética.2,3,5

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Progression of myelodysplasia to acute lymphoblastic leukaemia: Implications for disease biology

Cited by 68 publications

References 52 publications

High-resolution whole genome tiling path array CGH analysis of CD34+ cells from patients with low-risk myelodysplastic syndromes reveals cryptic copy number alterations and predicts overall and leukemia-free survival

High-resolution whole genome tiling path array CGH analysis of CD34+ cells from patients with low-risk myelodysplastic syndromes reveals cryptic copy number alterations and predicts overall and leukemia-free survival

Safety and efficacy of azacitidine in Belgian patients with high-risk myelodysplastic syndromes, acute myeloid leukaemia, or chronic myelomonocytic leukaemia: results of a real-life, non-interventional post-marketing survey

Síndromes mielodisplásicas: aspectos moleculares, laboratoriais e a classificação OMS 2008

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