its relationship to cancer. Nat Genet. 2012;44(6):642–50. 5. Sahin E, Depinho RA. Linking functional decline of telomeres, n this issue, the Hematology, Transfusion and Cell Therapy ournal is publishing a… Click to show full abstract
its relationship to cancer. Nat Genet. 2012;44(6):642–50. 5. Sahin E, Depinho RA. Linking functional decline of telomeres, n this issue, the Hematology, Transfusion and Cell Therapy ournal is publishing a paper of Alves et al. coordinated by Dr. ayão from the Medical School of Marilia, São Paulo, Brazil, iscussing an interesting aspect of cytogenetic abnormalities CA) in respect to aging. In a retrospective analysis of a large ample (746 patients) over 18 years of observation and includng several types of onco-hematological diseases in patients f all ages, the authors investigated the influence of age on he frequency of CA.1 The authors found a higher frequency f hematological malignancies among elderly patients, about 1%, followed by adult (38%) and young patients (about of 11%). he authors reported that “it is possible to conclude that failres in genomic mechanisms and hematopoiesis with aging ead to the formation of cells with the chromosomal altertions found in hematological malignancies”. From the 1960s ith the description of Philadelphia chromosome in chronic yeloid leukemia (CML),2 CA have been recognized as imporant prognostic factors in acute promyelocytic leukemia (APL), cute myeloid leukemia (AML), myelodysplastic syndromes MDS) and in a great number of onco-hematological diseases nd syndromes.3 These abnormalities became diagnostic and rognostic markers and they are very useful in the monitorng of minimal residual disease (MDR). Data from the literature upports the higher frequency of onco-hematological diseases n the elderly population.4 Particularly in AML, elderly patients ave a poor prognosis compared to young and adult patients, espite the development of different therapeutic approaches. he authors emphasize that the higher aggressiveness in he elderly is probably due to bone marrow and immune ystem impairment. Genomic and somatic mutations, inadquate cytokine production, and impairment of modulation
               
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