PT  - JOURNAL ARTICLE
AU  - Omer Saeed
AU  - Antonio Lopez-Beltran
AU  - Kurt W Fisher
AU  - Marina Scarpelli
AU  - Rodolfo Montironi
AU  - Alessia Cimadamore
AU  - Francesco Massari
AU  - Matteo Santoni
AU  - Liang Cheng
TI  - RAS genes in colorectal carcinoma: pathogenesis, testing guidelines and treatment implications
AID  - 10.1136/jclinpath-2018-205471
DP  - 2019 Feb 01
TA  - Journal of Clinical Pathology
PG  - 135--139
VI  - 72
IP  - 2
4099  - http://jcp.bmj.com/content/72/2/135.short
4100  - http://jcp.bmj.com/content/72/2/135.full
SO  - J Clin Pathol2019 Feb 01; 72
AB  - The RAS family is among the most commonly mutated genes in all human malignancies including colon cancer. In normal cells, RAS proteins act as a link in the intracellular signal transduction initiated by binding of growth factors to cell membrane receptors mediating cell survival. RAS isoproteins have great morphological similarities, but despite that, they are thought to have different functions in different tissues. RAS mutations, as supported by several studies including animal models, have a role in the development and progression of colorectal cancer. The detection of RAS mutations in patients with colorectal carcinoma, specifically KRAS and NRAS, has significant clinical implications. It is currently recommended that patients with colon cancer who are considered for antiepidermal growth factor receptor monoclonal antibodies, get RAS mutation testing since only those with wildtype-RAS genes benefit from such treatment. Despite decades of research, there is currently no effective and safe treatment that directly targets RAS-mutated neoplasms. Multiple therapeutic approaches directed against RAS mutations are currently experimental, including a promising immunotherapy study using T-cells in patients with metastatic colon cancer.