Br J Cancer  1998 Mar;77(5):720-3 

K-ras point mutation occurs in the early stage of carcinogenesis in lung cancer.

Sagawa M, Saito Y, Fujimura S, Linnoila RI.

Biomarkers and Prevention Research Branch, National Cancer Institute, Rockville,
Maryland 20850, USA.

In order to determine the topographical distribution of the K-ras codon 12
mutations in carcinoma and preneoplastic lesions of the lung, selective
ultraviolet radiation fractionation, as well as microdissection followed by
polymerase chain reaction-restriction fragment length polymorphism (PCR-RELP),
was performed. Fourteen of 61 samples amplified (23.0%) had a mutation in the
K-ras codon 12. Of 41 adenocarcinoma, 12 samples (29.3%) had a mutation, whereas
none of the squamous cell carcinomas had a mutation. One of six large-cell
carcinomas, one of three carcinoid tumours and none of three other carcinomas
had a mutation. Direct sequencing revealed that K-ras codon 12 of six samples
were TGT (Cys), five samples were GTT (Val), two samples were GCT (Ala) and one
sample was TTT (Phe). A total of 113 lesions of 13 cases covered by dot were
amplified after UV radiation. All of 74 carcinoma lesions had the mutation, and
intratumour heterogeneity was not observed. Of 39 non-malignant lesions, one
type II cell hyperplasia had the mutation, which suggests that the K-ras
mutation occurs in the early stage of carcinogenesis. The lack of intratumour
heterogeneity supports the hypothesis.

PMID: 9514049 [PubMed - indexed for MEDLINE]