Molecular architecture of the tumor microenvironment caused by BRCA1 and BRCA2 somatic mutations in lung adenocarcinoma
This study utilizes single-cell and multi-omics analyses to reveal that while BRCA1 and BRCA2 somatic mutations in lung adenocarcinoma drive distinct transcriptional programs and immune microenvironment alterations—such as differential T cell activation and tissue-resident memory T cell expansion—they collectively predict improved responses to immune checkpoint blockade despite being associated with genomic instability and poor prognosis.