Acute myeloblastic leukaemias and myelodysplastic syndromes in adult patients: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up.

Department of Medical Oncology, Inselspital and University of Bern, Switzerland.
Annals of Oncology (Impact Factor: 6.58). 05/2010; 21 Suppl 5:v158-61. DOI: 10.1093/annonc/mdq179
Source: PubMed
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    ABSTRACT: Over the last several decades, advancements in the understanding of genetic and molecular origins of acute myeloid leukemia (AML) have brought about significant changes in how the disease is classified, diagnosed, and treated. The change from the traditional French-American-British classification system to that of the World Health Organization redefined how the disease is diagnosed not only morphologically but genetically. With genetic information proving to have prognostic value, the newer classification system, which incorporates results of cytogenetic and molecular analyses, allows better definition of disease and risk stratification, ultimately guiding treatment choices. As understanding and advancements in the molecular basis of AML continue to grow and influence patient management, the importance of an accurate and thorough initial patient evaluation is paramount. We performed a review of AML cases diagnosed at Baylor Charles A. Sammons Cancer Center from February 2010 to December 2012 to assess the thoroughness of initial diagnostic evaluations based on current guidelines, including up-to-date molecular analyses for mutations in NPM1, CEBPA, FLT3, and C-KIT. Results showed that patients newly diagnosed with AML undergo thorough diagnostic evaluation in keeping with current recommendations, and many had further genetic and molecular evaluations, which although considered optional or investigational, have prognostic significance. We identified potential areas of improvement for making this diagnostic evaluation more specific to the patient and the patient's disease. Currently, we are investigating having patients undergo reflex genetic testing if they meet certain criteria to better define their specific disease while avoiding unnecessary genetic evaluations that come at increased cost.
    Proceedings (Baylor University. Medical Center) 10/2014; 27(4):299-304.
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    ABSTRACT: In a Phase III trial, 485 patients (≥65 years) with newly diagnosed acute myeloid leukemia received decitabine 20 mg/m(2) intravenously for 5 days every 4 weeks or a treatment choice (supportive care or cytarabine 20 mg/m(2) subcutaneously for 10 days every 4 weeks). We summarized overall and progression-free survival by baseline white blood cell count using two analyses: <1, 1-5, >5×10(9)/L; ≤10 or >10×10(9)/L. There were 446 deaths (treatment choice, n=227; decitabine, n=219). Median overall survival was 5.0 (treatment choice) versus 7.7 months (decitabine; nominal P=0.037). Overall survival differences between white blood cell groups were not significant; hazard ratios (HRs) favored decitabine. Significant progression-free survival differences favored decitabine for groups 1-5×10(9)/L (P=0.005, HR =0.67), greater than 5×10(9)/L (P=0.027, HR =0.71), and up to 10×10(9)/L (P=0.003, HR =0.72). There was a trend toward improved outcome with decitabine, regardless of baseline white blood cell count.
    Hematology Research and Reviews 01/2015; 6:25. DOI:10.2147/JBM.S64067
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    ABSTRACT: 100 Definición Grupo heterogéneo de leucemias que se presen-tan en precursores de células mieloides, eritroides, megacariocíticos y monocíticos. Resultan de una transformación clonal de precursores hematopo-yéticos a través de la adquisición de rearreglos cro-mosómicos y múltiples mutaciones genéticas (1). Incidencia Cinco a 8 casos por cada 100,000 individuos al año. Seis mil quinientos niños y adolescentes por año, en Esta-dos Unidos. No hay diferencia entre varones y mujeres, ni en población blanca o negra. Mayor incidencia en población latinoamericana. La incidencia incrementa con la edad, exposición a quimioterapia, radioterapia y benceno (1-3). La mortalidad se estima en cuatro a seis casos por 100,000 habitantes por año. Algunas condi-ciones que predisponen al desarrollo de leucemia aguda mieloblástica (LAM) son: síndrome de Down; síndro-mes hereditarios y adquiridos de falla medular, donde destacan: la anemia aplásica; el síndrome mielodisplá-sico (SMD) y la hemoglobinuria paroxística nocturna (HPN). Algunos síndromes mieloproliferativos (SMP) podrán evolucionar a ciertas formas de LAM (4-6).