Genomic Instability and Cancer: Insights into DNA Repair Pathway Dysregulation

Dear Colleagues,

Genomic instability, characterized by an increased number of alterations in the genome, is a hallmark of cancer and a driving force behind tumorigenesis. The intricate balance between DNA damage and repair mechanisms is paramount for maintaining genomic integrity. Hence, the dysregulation of this delicate equilibrium can lead to the accumulation of genetic aberrations, fostering the development and progression of various cancers. Although cancer-driving mutations such as BRCA1 and BRCA2 are the Achilles heels of cancer cells, some are vulnerable to inhibitors of poly(ADP-ribose) polymerase (PARP), an exciting class of drugs that have transformed the clinical management of some cancers.

Current research efforts have unveiled the profound impact of DNA repair dysregulation on genomic stability and its consequences for cancer cells. Studies exploring the molecular intricacies of DNA repair pathways, such as homologous recombination, base excision repair, and mismatch repair, have shed light on how alterations in these processes contribute to the acquisition of somatic mutations and chromosomal aberrations observed in cancer genomes.

This Special Issue of the journal Biology aims to provide a comprehensive overview of the current state of research on genomic instability in cancer, emphasizing the molecular insights into DNA repair dysregulation. Through a collection of cutting-edge articles, we will explore the multifaceted roles of DNA repair pathways in cancer initiation and progression.

In this Special Issue, we invite fellow researchers to contribute their latest research findings, theories, and experimental approaches to enhance our understanding of genomic instability and propel the field towards transformative therapeutic breakthroughs. Original research articles and reviews are welcome, and we look forward to receiving your contributions.

Dr. Xiangbing Meng
Guest Editor

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• homologous recombination
• base excision repair
• mismatch repair
• somatic mutations
• chromosomal aberrations
• BRCA1
• BRCA2
• poly(ADP-ribose) polymerase (PARP)
• cancer initiation