CCDC102B in 18q22.1 is associated with somatic mutations in lung cancer (1 mutated sample).
430 abstracts on EGFR and ALK mutations in lung cancer were annotated manually.
In this study, we set out to identify a panel of recurrent mutations in lung adenocarcinoma that would cover the majority of patients.
KRAS mutations in lung cancer occur primarily at codon 12 or 13, making the protein GAP insensitive and constitutively GTP bound leading to the activation of downstream effectors.
In this study, we sought to define a panel of common hotspot mutations in lung adenocarcinoma to allow molecular diagnostic laboratories to design and optimise primers to cover the majority of patients.
The identification of genotype phenotype associations as in the case of EGFR-TKI (Epidermal growth factor receptor-tyrosine kinase inhibitor) and EGFR mutations in lung cancer led to the restriction of drugs to patients for which tumor genotype predicts efficacy.
The classification results and the top features determined by the classifiers suggest that this scheme would be generalizable to other mutations in lung cancer, as well as studies on driver mutations in other cancer domains.
The results of our grouped testing approach with optimized biosensors were consistent with that of direct sequencing, suggesting that our proposed protocol can be excellent candidate for genotyping of EGFR mutations in lung cancer patients.
Two types of somatic mutations (in-frame deletions and point substitutions) in the EGFR gene were successfully identified within 3.5 h using this system, suggesting that this system could be used in clinical tests of EGFR gene mutations in lung cancer, and potentially other cancer, patients.
It is important to note, we have recently shown that MET mutations in lung cancer are in majority germline [31].
TP53 mutations in lung cancer are very closely spaced (≤30 nt) in 33% of doublets, and multiplets generally contain two or more very closely spaced mutations.
