P53, EMT and DNA Repair: Novel Links Impacting Cancer Progression and Drug Response
A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".
Deadline for manuscript submissions: closed (30 April 2024) | Viewed by 1614
Special Issue Editor
Special Issue Information
Dear Colleagues,
Major challenges in the treatment of carcinomas are metastatic spread and the development of therapeutic resistance. Much work has characterized the changes that tumor cells undergo in the process of metastasis, particularly epithelial to mesenchymal transition (EMT). This developmental program is often reactivated in cancers, leading to loss of cell polarity and adhesion and the adoption of an aggressive, motile phenotype. In recent years, EMT has been linked to resistance to several chemotherapeutic agents and to populations alternately dubbed tumor-initiating cells or cancer stem cells. The first aim of this Special Issue is to bring together the latest work on the role of EMT in cancer recurrence and resistance.
P53, a regulator of genomic integrity, is commonly mutated in cancers, with variants appearing in virtually all serous ovarian cancers, half of all non-small cell lung cancers, and a third of breast cancers, among others. In breast, ovarian, and prostate cancers, mutations in the BRCA genes can give rise to tumors but also leave these tumors vulnerable to inhibitors of Poly(ADP-ribose) polymerase. Determining how dysregulation of DNA repair via mutations in these and other genes impacts drug responses, and how the metastatic process and EMT factor in, will be essential for the design of new treatment strategies and comprises the second aim of this Special Issue.
I am pleased to invite original research articles, reviews, and commentaries, and I look forward to receiving your contributions.
Dr. Cai M. Roberts
Guest Editor
Manuscript Submission Information
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Keywords
- epithelial to mesenchymal transition
- metastasis
- DNA repair
- p53
- chemoresistance
- cancer stem cells
- drug discovery
