Spots Global Cancer Trial Database for KRAS Mutation and Incidence of the Colorectal Carcinoma in Martinique Between 2007 and 2009

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Trial Identification

Brief Title: KRAS Mutation and Incidence of the Colorectal Carcinoma in Martinique Between 2007 and 2009

Official Title: Study of KRAS Mutation in 250 Cases of Colorectal Carcinoma and Study of the Incidence of the Disease in Martinique, From 2007 to 2009

Study ID: NCT01151007

Conditions

Colorectal Carcinoma

Interventions

Study Description

Brief Summary: * There is no data at present concerning the KRAS mutation in patients from Martinique with colorectal cancer. Despite the fact that the incidence of this disease continues to increase there is no recent data to confirm it. This study has a descriptive purpose, allowing a comparison of the population from Martinique to other populations. * A study of incidence of colorectal cancer, overseen by the Association from Martinique for the Epidemiological Search on Cancer (AMREC), also leads to a better knowledge of the local characteristics of the colorectal cancer. * These two descriptive characteristics of colorectal cancer in Martinique will be useful data for the health professionals to provide their patients better care.

Detailed Description: * The colorectal carcinogenesis is complex. It influences among others, the EGFR (Epidermal Growth Factor Receptor) which activation leads to tumoral proliferation, differentiation and invasion. The binding of the EGF (Epidermal Growth Factor) or of another ligand to the EGFR is responsible for the activation of the Ras- Raf and Pi3k pathways. * The mutation of the genes KRAS, BRAF or PIK3CA results in their continuous activation, independently of the activation or of the pharmacological blocking of EGFR. The most frequently found mutation affects the KRAS gene (20 to 50 % of the cases). 90 % of these mutations are situated on codons 12 and 13 of this gene (70 % codon 12 and 30 % codon 13). These mutations are responsible for a decrease of the GTPase activity of the ras protein, which stays then in active conformation bound to the GTP. This leads to the blocking of the pathway and to the inactivity of the pharmacological blocking of EGFR.