Article
Version 1
Preserved in Portico This version is not peer-reviewed
Analysis for Mitochondrial Encoded Trna leucine2 (MT-TL2) Gene in Breast Cancer Patients
Version 1
: Received: 23 November 2023 / Approved: 23 November 2023 / Online: 23 November 2023 (05:44:55 CET)
How to cite: Ullah, A. Analysis for Mitochondrial Encoded Trna leucine2 (MT-TL2) Gene in Breast Cancer Patients. Preprints 2023, 2023111474. https://doi.org/10.20944/preprints202311.1474.v1 Ullah, A. Analysis for Mitochondrial Encoded Trna leucine2 (MT-TL2) Gene in Breast Cancer Patients. Preprints 2023, 2023111474. https://doi.org/10.20944/preprints202311.1474.v1
Abstract
(1) Background: Breast cancer (BC) is the second largest cause of mortality in female worldwide. Besides from basic risk factors, there are several hereditary variables that contribute to BC. Breast cancer has been linked to a variety of nuclear DNA changes as well as mitochondrial DNA alterations. The aim of this study was to analysis the association of mitochondrial tRNA leucine2 gene with BC. (2) Material and methods: In the current study, 24 samples have been collected from various families in Peshawar. DNA was extracted from Blood. PCR was used to amplify the mitochondrial tRNA MT-TL2 gene, and 22 samples were sequenced. The sequence was compared with accession #NC-012920.1 of the revised Cambridge Reference Sequence (rCRS). (3) Results: The results (Chromatograph, nucleotide sequence and rCRS alignment) shows mutations in mitochondrial tRNA MT-TL2 gene in our participants is not the cause of Breast cancer. (4) Conclusion: Yet, a significant number of BC patients must be studied, and their full mitochondrial DNA must be analyzed. This will provide an indication of the potential DNA marker that might be used to prevent BC deaths at the earliest stages.
Keywords
breast cancer; mitochondrial gene; MT-TL2 gene; mutation; sequencing
Subject
Biology and Life Sciences, Biochemistry and Molecular Biology
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Comments (0)
We encourage comments and feedback from a broad range of readers. See criteria for comments and our Diversity statement.
Leave a public commentSend a private comment to the author(s)
* All users must log in before leaving a comment