The discovery of somatic mutations in cancer-related genes has been applied to understand the genetic basis of cancer. Here we report somatic mutations of two tumor suppressor genes:
LKB1 (exons 1, 4, and 8) and
TP16 (
CDKN2A) (exons 1 and 2); and two oncogenes: epidermal growth factor receptor
EGFR (exons 18-21) and
KRAS (exon 2) in 97 lung adenocarcinoma tissues in a cohort from the Kujukuri coast area of Chiba, Japan. In the
LKB1 gene, only F354L substitutions were observed in 14 of the 97 tissue samples (14.4%). In the
TP16 gene, only two deletions were observed in contrast to previous reports. On the other hand, the
EGFR gene was highly mutated (38.1%) and mainly L858R substitutions occurred (23.7%) as well as insertions and deletions. In the
KRAS gene, 10 substitutions at codon 12 were observed (10.3%). Co-occurrence of
EGFR and
KRAS somatic mutations was identified in one patient, those of
EGFR and
LKB1 were in three patients, and those of
KRAS and
LKB1 were in four patients. The lower rates of
LKB1,
TP16, and
KRAS somatic mutations in lung adenocarcinomas are characteristic of the Kujukuri cohort as compared to Caucasians. while being infrequent in NSCLC Another review (were observed in 20.18% of lung adenocarcinoma byanalyzing the Catalog of Somatic Mutations in Cancer(COSMIC) (the W(
CDKN2Aa tumor suppressor gene and has been reported to show a high rate of deletions as a major type of somatic mutation in cancerin the COSMIC database (suppressor genes, central role in tumorigenesis. EGFR phosphorylates tyrosine residues of tarincluding KRAS, to initiate multiple signaling pathwaysresulting in cell proliferation, migration, metastasis,resistance to apoptosis, and angiogenesis (molecule inhibitors of EGFR tyrosine kinase activity (TKIs) such as gefitinib and erlotinib provide a good concept for anticancer drugs. Howeversignificant variability in the
EGFR
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