Abstract

Colorectal cancer (CRC) is one of the globally prevalent and virulent types of cancer with a distinct alteration in chromosomes. Often, any alterations in the adenomatosis polyposis coli (APC), a tumor suppressor gene, and methylenetetrahydrofolate reductase (MTHFR) gene are related to surmise colorectal cancer significantly. In this study, we have investigated chromosomal and gene variants to discern a new-fangled gene and its expression in the southern populations of India by primarily spotting the screened APC and MTHFR variants in CRC patients. An equal number of CRC patients and healthy control subjects (n = 65) were evaluated to observe a chromosomal alteration in the concerted and singular manner for APC and MTHFR genotypes using standard protocols. The increasing prognosis was observed in persons with higher alcoholism and smoking (P < 0.05) with frequent alterations in chromosomes 1, 5, 12, 13, 15, 17, 18, 21, and 22. The APC Asp 1822Val and MTHFR C677T genotypes provided significant results, while the variant alleles of this polymorphism were linked with an elevated risk of CRC. Chromosomal alterations can be the major cause in inducing carcinogenic outcomes in CRCs and can drive to extreme pathological states.

Highlights

  • Increased westernization and its cultural influence have exalted colorectal cancer (CRC) spread in industrialized countries [1]

  • CRC progresses from single crypt lesions “adenomatous polyps” to carcinomas [13, 14] by following varying stages of invasion, lymph node involvement, site, and migration characterized by tumor-node-metastasis classification [15, 16]

  • The study group consists of 130 subjects comprising of each 65 CRC patients and controls with the inclusion of the characteristics linked to lifestyle, site of a tumor, grade of tumor, family history, follow-up checkups, and clinical analysis

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Summary

Introduction

Increased westernization and its cultural influence have exalted colorectal cancer (CRC) spread in industrialized countries [1]. The prevalence of CRC is majorly sporadic 65-80% with few familial 15-30% modes of spread, implicating the major involvement of shared genes and environmental factors [2]. Worldwide intensive increase of cases (about two million) and mortality (about one million) was registered in 2018 [4], with the shooting of two to five times CRC rates in the urbanized countries when compared to developing countries, suggesting a contrasting variation assortment in risk factors and analytical practices [5, 6]. The influence of sedentary lifestyle and western diet patterns, like food rich in animal proteins and fats, are the presumptive causes of elevated CRC cases in the current scenario. CRC progresses from single crypt lesions “adenomatous polyps” to carcinomas [13, 14] by following varying stages of invasion, lymph node involvement, site, and migration characterized by tumor-node-metastasis classification [15, 16]

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