Abstract
BAT25 and BAT26 Microsatellite Mutations in Colorectal Cancer (CRC)
Ndiaye A*, Mbaye F, Kénémé B, Samba A, Thiam S, Soumah IY, Diedhiou F, Coly NF, Cissé F, Diallo F and Sembene M
Corresponding Author: Ndiaye A, Laboratory of Molecular Biochemistry-Biology, Cheikh Anta Diop University of Dakar, Laboratory of Biochemistry, Aristide Le Dantec Hospital, Senegal.
Revised: July 23, 2024; Available Online: July 23, 2024
Citation: Ndiaye A, Mbaye F, Kénémé B, Samba A, Thiam S, et al. (2024) BAT25 and BAT26 Microsatellite Mutations in Colorectal Cancer (CRC). BioMed Res J 8(S1): 09.
Copyrights: ©2024 Ndiaye A, Mbaye F, Kénémé B, Samba A, Thiam S, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Introduction: Colorectal cancer (CRC) is becoming more and more common. The diagnosis is essentially based on the demonstration of mutations in certain markers chosen at the international meeting in Bethesda (December, 1997). Among these markers we have BAT25 and BAT26; and because of their polymorphism, they have been implicated in the occurrence of this pathology.

Objective: The aim is to evaluate the degree of polymorphism of these two markers in a population of the population.

Methods: The study involved 29 patients with CRC. Patients were selected at the level of structures such as the main hospital, the general hospital of Grand Yoff and the Aristide Le Dantec hospital in Dakar. Each patient was sampled from healthy tissue and cancerous tissue. To serve as controls, blood samples were taken from subjects without CRC. The samples were then sent to the laboratory for DNA extraction, followed by PCR amplification of BAT25 and BAT26 markers and their sequencing. Dnasp version 5.10, MEGA version 6.06 and the Harlequin program version 3.5.1.3 were used to extract the parameters of variability, genetic distances and genetic structuring test according to the clinical parameters of the patients such as age, sex and tumor location.

Results: The comparison between healthy tissue and cancerous tissue of each patient reveals a high variability of the BAT25 and BAT26 loci with mutations specific to cancerous tissues. Among these mutations, the most frequent is the deletion of a thymine at position 72 (72delT). This variability between healthy tissue and cancerous tissue is further confirmed by Nei's genetic distance. On the other hand, no genetic structuring of the BAT25 and BAT26 loci according to clinico-pathological parameters was observed.

Conclusion: Our results showed a variable expressivity of the BAT25 and BAT26 loci between healthy tissue and cancerous tissue, indicating their involvement in the occurrence of CRCs in these patients.

Keywords: BAT25, BAT 26, Colorectal cancer