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Esophageal cancer is caused due to many reasons such as obesity, smoking, gastro esophageal reflex disease but it can also be due to the genetic factors or hereditary. The ancestors may be affected and so due to their genes, their family is also affected. When compared to other ways, the percentage of people affected by esophageal cancer due to genetic factors is comparatively less.

A familial correlation, commingling and complex segregation analyses of nearly 224 families from the Chaos Han population and 403 families from the Taichung population using FPMM program was conducted. Then a second analysis was also conducted and it focused on specific families which have a large number of affected individuals or early onset of the disease.

The heritability of the esophageal cancer among the first degree relatives was 52.6% and that among the second degree relatives was 31.2% and also the weighted average heritability was 49.2% the relative risks among first degree relatives were 10.49 for males, 7.69 for females and 9.17 for both male and female.

The esophageal cancer occurring due to genetic alteration in SSC and ADC of the esophagus and on their possible implications for the elucidation of the pathogenesis and etiology of these cancers . In esophageal cancers, the most common alterations include allelic losses at chromosomes 3p, 5q, 9p, 13q, 17p, 17q and 18q as well as mutations of p53 (mostly missense), Rb (deletions), cyclin DI (amplifications) and c-myc (amplifications). These alterations may occur in some sequence with respect to histopathological tumor progression.

Genomic DNA samples were assayed for restriction fragment length polymorphisms in the CYP2E1 and GSTP1 loci by PCR amplification followed by digestion with Rsal and Alw261 the deletion of the genes such as GSTM1 and GSTT1 were detected by multiplex PCR. Also the distribution of CYP2E1 c1/c1 allele frequency was found to be significantly different between the controls and cases with esophageal cancer.

The individuals who have c1/c1 genotype were at a 3.1 fold increased risk of developing dysphasia and a 3.2 fold increased risk of developing squamous cell carcinoma of the esophagus. The frequency of the GSTM1 non null genotypes appeared to be over represented in cases with cancer compared to controls. A joint effect of CYP2E1 c1/c1 genotype and GSTM1 non null genotype on the cancer risk was observed. The final results demonstrate that CYP2E1 and perhaps GSTM1 are the genetic determinants in the development of squamous cell carcinoma of the esophagus.

However, among the alcohol drinkers, the XRC1399Arg/gin was most frequently found in patients with esophageal cancer. After adjustment with other environmental confounders, the OR genotype of XRC1399Arg was 2.78 as compared with the XRCC1399Gin/Gin and XRC1399Arg/Gin genotypes in the alcohol drinkers. Similar trends were observed among cigarette smokers and areca chewers. Genetic polymorphism in enzymes involved in carcinogen metabolism has been shown to influence susceptibility to cancer.