| Abstract: | Background Genetic variability in obesity-related genes and the resulting phenotypes are being recognized as major risk factors for colorectal
cancer and/or severity of the disease.
Materials and methods A total of 102 patients (aged 68 ± 10.2 years, 79 men and 23 women) and 101 age-matched (68.1 ± 5.4 years old) individuals
without colorectal cancer, 59 men and 42 women, were recruited. All the individuals were genotyped for the following subset
of polymorphisms in obesity-related genes: angiotensinogen gene (M235T and -6A/G), in IL-6 gene (-174 G/C and -596 A/G), in
leptin gene (-2548 A/G), and polymorphism Gln223Arg within the leptin receptor (LEPR) gene.
Results A significant increase in frequency of double heterozygote genotype (MTAG) of both angiotensinogen polymorphisms in males
with colorectal cancer was observed when compared to control men odds ratio (OR) = 3.77, P
corr = 0.001]. A marginally significant difference in genotype distribution of -174 G/C IL-6 polymorphism between the patients
in stage I–II compared to patients in III–IV was found (P
g = 0.05, P
a = 0.173). The GG genotype of -174 G/C IL-6 polymorphism in the patients in stage III–IV carries an increased risk compared
to those in stage I–II (OR = 2.83, P
corr = 0.06). Similarly, a difference in genotype distribution of Gln223Arg in LEPR gene between the patients staged I–II compared
to III–IV was observed (P
g = 0.05). The AA genotype was shown to be risky for the patients staged III–IV (OR = 3.35, P
corr = 0.06).
Conclusions The investigated single nucleotide polymorphisms within the genes encoding for obesity-related genes were observed to be associated
both with clinical manifestation of colorectal cancer and with severity of the disease. Thus, we suggest that defined genetic
variability in the genes might become DNA markers for colorectal cancer in the future. |
