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<i>ATMIN</i> Is a Tumor Suppressor Gene in Lung Adenocarcinoma.


ABSTRACT: Tumor cells proliferate rapidly and thus are frequently subjected to replication stress and the risk of incomplete duplication of the genome. Fragile sites are replicated late, making them more vulnerable to damage when DNA replication fails to complete. Therefore, genomic alterations at fragile sites are commonly observed in tumors. FRA16D is one of the most common fragile sites in lung cancer, however, the nature of the tumor suppressor genes affected by FRA16D alterations has been controversial. Here, we show that the ATMIN gene, which encodes a cofactor required for activation of ATM kinase by replication stress, is located close to FRA16D and is commonly lost in lung adenocarcinoma. Low ATMIN expression was frequently observed in human lung adenocarcinoma tumors and was associa

SUBMITTER: Foster H 

PROVIDER: S-EPMC6797498 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature

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