Single Nucleotide Polymorphism in SMAD7 and CHI3L1 and Colorectal Cancer Risk

Table 2

Risk factors of CRC.

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Nonmodifiable

(i) Age: the incidence of CRC diagnosis increases after the age of 40 and rises sharply after age 50, but there is an increase in the young-onset rate due to the adoption of a Westernized lifestyle and diet [9]
(ii) Family history of CRC (especially a first-degree relative diagnosed at age 49 or younger) [10]
(iii) Hereditary predisposition
  (a) Hereditary nonpolyposis colorectal cancer (HNPCC, Lynch syndrome)
  (b) Familial adenomatous polyposis (FAP) [4, 9]
(iv) Inflammatory bowel disease (IBD): chronic inflammation is assumed to underlie the cause of colitis-associated cancer, which is associated with oxidative stress-induced DNA damage resulting in the activation of procarcinogenic genes and silencing of tumor-suppressor pathways [11]
(v) Adenomatous polyp: polyps are abnormal growths of the large intestine lining that protrude into the intestinal lumen. Polyps greater than one centimeter in diameter are associated with a greater risk of cancer [12]

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Modifiable

(i) Diets: Western diet rich in red meat, refined grains, desserts, and low in fiber was reported to be associated with increased CRC risk [10, 13, 14]
(ii) Cigarette smoking: carcinogens as aromatic amines, nitrosamines, and polycyclic aromatic hydrocarbons in tobacco smoke produce metabolites that can react with DNA or other macromolecules to form DNA adducts inducing genetic mutations [15]
(iii) Obesity: obese women have higher risk of CRC than obese men due to higher abdominal visceral adipose tissue volume [16, 17]
(iv) High alcohol consumption (>2 glasses per day): ethanol increases the activation of various procarcinogens present in tobacco smoke, diets, and industrial chemicals to carcinogens through the induction of CYP2E1 [18]

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