Role of Genomic Instability in Cancer and Microenvironment

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Nuclei: Function, Transport and Receptors".

Deadline for manuscript submissions: 15 July 2024 | Viewed by 136

Special Issue Editor


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Guest Editor
Center for Genomics and Precision Medicine, Texas A&M College of Medicine, Houston, TX 77030, USA
Interests: DNA damage repair; epigenetics; cancer

Special Issue Information

Dear Colleagues,

In order to achieve the long-term goal of improving therapeutic outcomes, especially for resistant tumors, we need to close critical gaps in our understanding of how cells repair DNA damage is required before tumor cell repair capacity can be specifically targeted for drug development. More than two-thirds of cancer-causing mutations result from replication, and failure to protect or properly restart stalled replication forks causes DNA double-strand breaks and mutations, leading to genomic aberrations and cancer. So, oncogene- and chemotherapy-induced replication stress, which stalls DNA replication forks, requires efficient repair and restart to avoid cell death or mutagenesis. There is a need to evaluate and compare the DNA damage repair mechanism to identify specific factors and post-translational chromatin modifications that account for robust DSB repair and oncogenesis. The answers to these questions will help us to better understand DNA damage repair mechanisms and their pathogenesis, as well as the role of chromatin in disease cure.

The purpose of this Special Issue is to highlight the most recent findings regarding the mechanism of DNA damage repair, the role of genomic instability in oncogenesis, and drug resistance in vitro and in vivo. This Special Issue will provide a broad scope of the studies in DNA damage repair pathways and how these are regulated by chromatin status in connection with oncogenesis. Furthermore, we invite papers to submit to this Special Issue which focus on how DNA damage repair and chromatin status could be exploited for tailoring therapy, specifically for patients of cancer or age-related diseases.

Prof. Dr. Tej K. Pandita
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • DNA damage repair
  • HR
  • NHEJ
  • chromatin
  • oncogenesis

Published Papers

This special issue is now open for submission.
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