Inactivation of the MAL gene in breast cancer is a common event that predicts benefit from adjuvant chemotherapy.

ABSTRACT: Dysregulation of MAL (myelin and lymphocyte protein) has been implicated in several malignancies including esophageal, ovarian, and cervical cancers. The MAL protein functions in apical transport in polarized epithelial cells; therefore, its disruption may lead to loss of organized polarity characteristic of most solid malignancies. Bisulfite sequencing of the MAL promoter CpG island revealed hypermethylation in breast cancer cell lines and 69% of primary tumors analyzed compared with normal breast epithelial cells. Differential methylation between normal and cancer DNA was confined to the proximal promoter region. In a subset of breast cancer cell lines including T47D and MCF7 cells, promoter methylation correlated with transcriptional silencing that was reversible with the methylation in

SUBMITTER: Horne HN 

PROVIDER: S-EPMC2700346 | biostudies-literature | 2009 Feb

REPOSITORIES: biostudies-literature