Minireviews
Copyright ©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Hepatol. Jun 27, 2021; 13(6): 662-672
Published online Jun 27, 2021. doi: 10.4254/wjh.v13.i6.662
Role of chromosome 1q copy number variation in hepatocellular carcinoma
Nathan R Jacobs, Pamela A Norton
Nathan R Jacobs, Pamela A Norton, Department of Microbiology and Immunology, Drexel University College of Medicine, Philadelphia, PA 19102, United States
Author contributions: Norton PA designed the project; Jacobs NR and Norton PA performed the research and wrote the paper.
Conflict-of-interest statement: The authors declare no conflicts of interests for this article.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Pamela A Norton, PhD, Associate Professor, Department of Microbiology and Immunology, Drexel University College of Medicine, 245 N 15th Street, Room 14307, Philadelphia, PA 19102, United States. pan29@drexel.edu
Received: February 24, 2021
Peer-review started: February 24, 2021
First decision: May 3, 2021
Revised: May 13, 2021
Accepted: June 4, 2021
Article in press: June 4, 2021
Published online: June 27, 2021
Abstract

Chromosome 1q often has been observed to be amplified in hepatocellular carcinoma. This review summarizes literature reports of multiple genes that have been proposed as possible 1q amplification drivers. These largely fall within 1q21-1q23. In addition, publicly available copy number alteration data from The Cancer Genome Atlas project were used to identify additional candidate genes involved in carcinogenesis. The most frequent location for gene amplification was 1q22, consistent with the results of the literature search. The genes TPM3 and NUF2 were found to be candidates whose amplification and/or mRNA up-regulation was most highly associated with poorer hepatocellular carcinoma outcomes.

Keywords: Liver cancer, Chromosomal amplification, Hepatocellular carcinoma, The Cancer Genome Atlas

Core Tip: A list of candidate chromosome 1q amplification driver genes was compiled from the existing literature by PubMed search. Bioinformatics tools were used to identify additional candidates using publicly available genomics and transcriptomics data. Genes identified this way were largely distinct from those identified from the literature. Thus, these two strategies can be used in a complementary manner.