Consequently, the role of multiple mechanisms of drug resistance was identified, including decreased sensitivity to apoptosis, enhanced metabolism, and extrusion of drugs, and, for the first time, the role of estrogen receptor in drug resistance of leukemia cells.
We assessed the relation of first-degree family history of breast, prostate, lung, colorectal, ovarian, and cervical cancer and lymphoma or leukemia, to the risk of estrogen receptor-positive (ER(+)), ER(-), and triple-negative breast cancer in data from the African American Breast Cancer Epidemiology and Risk Consortium.
Hypermethylation within the promoters of some genes appear to be an early event in the pathogenesis of neoplasia (ER, P15), while other genes seem to become methylated during the progression of leukemias (HIC1, c-abl).
In addition, rat and mouse leukemia cell line also exhibited this change, indicating that ER CpG island methylation in leukemias is conserved among species.
The abnormal juxtaposition of DNA control elements close to the promoter of the ESR gene may be one mechanism by which aberrant synthesis of estrogen-receptor protein can occur to provide a growth advantage for leukemia cell clones.