Background: Germline mutations in the BRCA1 and BRCA2 DNA repair genes confer susceptibility to breast and ovarian cancer, and are targets for PARP inhibitors. The term “BRCAness” broadly refers to somatic molecular defects in the cellular DNA repair machinery, resulting in a phenotype similar to that caused by BRCA germline mutations. We evaluated data from The Cancer Genome Atlas (TCGA) for molecular alterations in double strand DNA repair genes in NSCLC. Methods: We examined somatic molecular alterations in 20 homologous recombination (HR) and 16 Fanconi anemia (FA) genes in 230 lung adenocarcinoma (LUAD) and 178 squamous cell carcinoma (SQCC) samples from TCGA data using cBio portal. Alterations were classified into homozygous deletion, mutation, and amplification. Tendency towards co-occurrence and mutual exclusivity of mutations in these genes was described using odds ratios (OR) and calculated by Fisher’s exact test using α = 0.05. Results: Somatic molecular alterations involving at least 1 HR or FA gene were observed in 121 (53%) of LUAD and 90 (51%) of SQCC respectively. The most common homozygous deletions noted were in RAD51 (3%) in LUAD and XRCC1 (1%) in SQCC. Frequent somatic gene mutations in BRCA2 (5%), BRCA1 (3%), RAD54B (3%) and BRIP1 (3%) were observed in LUAD, including the well-known nonsense S3376 and S2695 mutations in BRCA2. BRCA1 and RAD51D mutations tended to co-occur (OR >10; p=0.03), while BRCA2 mutations tended to co-occur with FANCB (OR >10; p=0.02) and RAD54L (OR >10; p=0.01) in LUAD. Commonly observed somatic mutations in SQCC included the following genes: BRCA1 (6%), BRCA2 (6%), FANCA (3%) and PALB2 (3%), including the known Q94 and K1160 nonsense mutations in BRCA1 and nonsense mutations Q499 and E187 in BRCA2. BRCA1 and PALB2 gene mutations tended to co-occur (OR>10; p=0.001) in SQCC. Amplifications were most commonly noted in XRCC2, NBN, RBBP8 and C19ORF40 in LUAD (2% each), and FANCG, FANCL, C19ORF40 in SQCC (4% each). Conclusions: BRCAness is commonly observed in NSCLC and may be a target for PARP inhibition in molecularly selected patient populations.