AccScience Publishing / EJMO / Volume 1 / Issue 1 / DOI: 10.14744/ejmo.2017.22931
REVIEW

Frequency of Ras Mutations (Kras, Nras, Hras) in Human Solid Cancer

Hilmi Kodaz1 Osman Kostek2 Muhammet Bekir Hacioglu2 Bulent Erdogan2 Cagnur Elpen Kodaz3 Ilhan Hacibekiroglu4 Esma Turkmen2 Sernaz Uzunoglu2 Irfan Cicin2
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1 Department of Medical Oncology, Acibadem Eskisehir Hospital, Eskisehir, Turkey
2 Department of Medical Oncology, Trakya University Faculty of Medicine, Edirne, Turkey
3 Department of Health, Acibadem Eskisehir Hospital, Eskisehir, Turkey
4 Department of Medical Oncology, Sakarya University Faculty of Medicine, Sakarya, Turkey
Submitted: 21 May 2017 | Accepted: 3 July 2017 | Published: 26 July 2017
© 2017 by the Author(s). This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution -Noncommercial 4.0 International License (CC-by the license) ( https://creativecommons.org/licenses/by-nc/4.0/ )
Abstract

RAS oncogene affects numerous cellular functions including growth, proliferation, apoptosis, migration, division and differentiation of the cells. It has 3 known isoforms as Harvey- RAS (HRAS), Kirsten - RAS (KRAS) and NeuroblastomaRAS (NRAS). RAS has an intrinsic GTPase activity. It encodes proteins binding the guanine nucleotides. KRAS and HRAS were discovered in studies carried out on viruses leading to cancer. Retroviral oncogenes related to murine sarcoma virus genes (Kristen Rat Sarcoma Virus and Murine Sarcoma Virus) were discovered in 1982. These two oncogenes are similar to human KRAS. Approximately 30% of all human cancers have ras genes. Mutations in KRAS account for about 85% for all RAS mutations in human tumors, NRAS is about 11–15%, and HRAS is about 1%.

Keywords
KRAS
NRAS
HRAS
cancer
Conflict of interest
None declared.
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