High Frequency of Codon 12 but not Codon 13 and 61 K-ras Gene Mutations in Invasive Ductal Carcinoma of Breast in a South Indian Population

Background: Ras genes are thought to play an important role in human cancer since they have been found to be activated frequently in several types of tumors including breast cancer, where the overall incidence of K-RAS oncogene activation is 0-10%. Evaluation of K-RAS gene not only for mutational fr...

Full description

Saved in:
Bibliographic Details
Published inAsian Pacific journal of cancer prevention : APJCP Vol. 16; no. 8; pp. 3505 - 3508
Main Authors Sushma, C, Prasad, Shiva, Devi, Rudrama, Murthy, Sudha, Rao, TS, Naidu, CK
Format Journal Article
LanguageKorean
Published 2015
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Background: Ras genes are thought to play an important role in human cancer since they have been found to be activated frequently in several types of tumors including breast cancer, where the overall incidence of K-RAS oncogene activation is 0-10%. Evaluation of K-RAS gene not only for mutational frequency but also for mutation types in this downstream signaling gene pathway is necessary to determine the mechanisms of action. The present study was conducted to test the hypothesis that K-RAS activation is involved in breast cancer risk of south Indian population. Materials and Methods: A total of 70 paired pathologically confirmed tumor and non-tumor tissues from the same breast cancer patients were analysed for most common K-RAS mutations of codon 12,13 and 61 by polymerase chain reaction followed by restriction digestion and direct nucleotide sequencing method. Results: We found that a high rate of homozygous and heterozygous mutations of codon 12, but not codon 13 and 61, may influence the invasive ductal carcinoma of breast risk in this study. Conclusions: Our study indicated that only codon 12 may be involved in initiating breast carcinogenesis in India.
Bibliography:KISTI1.1003/JNL.JAKO201528551641091
ISSN:1513-7368
2476-762X