Abstract:
Renal Cell Carcinoma (RCC) also called renal adenocarcinoma and accounts for 90 à 95% of primary malignant kidney tumors. It's the 14th most common cancer in the world, and the third of urological malignant tumors after prostate cancer and bladder cancer. Several environmental and genetic risk factors are potentially involved in renal carcinogenesis. Recently, several genome-wide association studies (GWAS) were conducted in the aim to identify additional new risk loci for RCC. In this sense, the objective of our work was to identify, through two statistical studies, some risk factors and histopathological parameters, as well as the possible involvement of genes encoding angiogenesis (VHL, VEGF and EPAS1), DNA repair (ATM, LRRIQ4), metabolism (ALDH9A1), apoptosis (FAF1, RHOBTB and LRRIQ4), chromatin remodeling complex (DPF3), telomere length regulation (OBFC1), and the occurrence of kidney cancer after molecular analysis using the sequenom iPLEX. The statistical study demonstrated an increase in the rate of renal cancer from the age 50years old with means age of 56.37±13.70. Higher incidences were reported in men than women (odds ratio: 1.35). Also, the sporadic form is the most common form in renal cancers. Furthermore, the most common type of RCC is clear cell renal carcinoma. On the other hand, the genetic analysis of patients and controls for the studied genes presented by the p-value indicates that no association between gene polymorphisms (VEGF, VHL, FAF1, LRRIQ4, RHOBTB2, OBFC1, DPF3 and EPSA1) and renal carcinogenesis. However, the results of the ATM rs1800057 variant showed a significant difference with susceptibility to kidney cancer. Thus, the polymorphism rs3845536 of the ALDH9A1 gene seems to have a protective effect against the RCC in our population.
