作者: Craig E. Litz , Joan Etzell
DOI: 10.3109/10428199809050924
关键词: Mechanism (biology) 、 Acute promyelocytic leukemia 、 Aberrant DNA Methylation 、 Genetics 、 Myeloid leukemia 、 Chromosomal translocation 、 Myeloid 、 Biology
摘要: The mechanism of aberrant genetic recombinatorial events in neoplasia is vaguely understood. One hypothesis that DNA methylation may some way predispose genomic regions to recombination. Using the t(9;22) chronic myeloid leukemia (CML) and t(15;17) acute promyelocytic (APL) as models, our laboratory others have gathered data supporting this hypothesis. These are reviewed.