Drug Discov Ther. 2012;6(1):24-30. (DOI: 10.5582/ddt.2012.v6.1.24)

LKB1, TP16, EGFR, and KRAS somatic mutations in lung adenocarcinomas from a Chiba Prefecture, Japan cohort.

Suzuki Y, Oonishi T, Kudo T, Doi H

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.

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