Abstract
The biologic and epidemiologic study of acute myeloid leukaemia (AML) in the elderly is in its infancy. Most epidemiologic data attempting to ascertain the etiology of AML have been obtained from younger cohorts or patients with therapy-related AML. The increasing prevalence of deletional and complex karyotypes in elderly AML patients implies a cumulative genotoxicity over time for this subgroup, given the similar spectrum of abnormalities following exposure to known genotoxic agents such as alkylating chemotherapeutic drugs. Exposure to benzene, radiation, and tobacco smoke are clear but weak risk factors for AML. Polymorphic variants in several genes responsible for genomic protection and integrity are now also weak risk factors for AML. Future epidemiologic studies should correlate exposure data with well-defined biologic subtypes of AML.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
