BCL7A is silenced by hypermethylation to promote acute myeloid leukemia.

ABSTRACT:

Background

Recent massive sequencing studies have revealed that SWI/SNF complexes are among the most frequently altered functional entities in solid tumors. However, the role of SWI/SNF in acute myeloid leukemia is poorly understood. To date, SWI/SNF complexes are thought to be oncogenic in AML or, at least, necessary to support leukemogenesis. However, mutation patterns in SWI/SNF genes in AML are consistent with a tumor suppressor role. Here, we study the SWI/SNF subunit BCL7A, which has been found to be recurrently mutated in lymphomas, but whose role in acute myeloid malignancies is currently unknown.

Methods

Data mining and bioinformatic approaches were used to study the mutational status of BCL7A and the correlation between BCL7A expression and promoter hypermethylatio

SUBMITTER: Patino-Mercau JR 

PROVIDER: S-EPMC10026484 | biostudies-literature | 2023 Mar

REPOSITORIES: biostudies-literature