The cold immunological landscape of ATM-deficient cancers.

ABSTRACT:

Background

Mutations in genes encoding DNA repair factors, which facilitate mismatch repair, homologous recombination, or DNA polymerase functions, are known to enhance tumor immunogenicity. Ataxia telangiectasia mutated (ATM) is a central regulator of DNA double-strand break repair and is frequently affected by somatic or germline mutations in various cancer types, including breast, prostate, pancreatic, and lung cancer. However, the consequences of ATM loss on tumor immunogenicity are poorly understood.

Methods

We generated isogenic ATM-null models using CRISPR in murine triple-negative breast (4T1) and colorectal (CT26) cancer cell lines. ATM inactivation was confirmed by PCR and western blot. Immune cell infiltrates were assessed by flow cytometry and immun

SUBMITTER: Sinha S 

PROVIDER: S-EPMC12067784 | biostudies-literature | 2025 May

REPOSITORIES: biostudies-literature