The Tumor Suppressor TP53 in Colorectal Carcinoma
A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Therapy".
Deadline for manuscript submissions: closed (31 May 2021) | Viewed by 45168
Special Issue Editors
Interests: genotoxic stress response; tumor suppressors; cell death mechanisms; regulation of senescence and DNA repair; chemotherapy resistance; CRC; glioblastoma
Interests: natural products; molecular pharmacology; cancer; drug resistance; genome-wide profiling
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Despite the tremendous gain of knowledge in colorectal cancer (CRC) biology during the past years, this tumor type is still the second most common cancer worldwide, characterized by complex genetic, epigenetic, and biochemical defects. A few crucial intracellular signaling pathways, including Wnt/β-catenin, Ras, and p53 signaling, are often deregulated in CRC. The tumor suppressor TP53 is mutated in more than 60% of CRC, and there is no doubt that TP53 is one of the most crucial players in this deadly disease. As a guardian of genome stability, upon genotoxic stress, this multifaceted transcription factor is involved in the regulation of cell cycle arrest, senescence, apoptosis, non-apoptotic cell death, and DNA repair. Critical mutations (hot spots) in the TP53 gene are key drivers of the transition from adenoma to adenocarcinoma. Thus, exploring the functional roles of TP53 gain-of-function (GOF) mutations in tumor development is of utmost importance, since patients with mutant p53 are often resistant to current chemotherapies, experiencing a short lifespan upon diagnosis.
For this Special Issue, we welcome contributions from all preclinical areas that elaborate on the eminent importance of TP53 in CRC:
Basic CRC biology:
- Chronic inflammation and colorectal carcinogenesis
- Cell cycle and proliferation
- Invasion and metastasis
- Cell death mechanisms
- Senescence
- Stemness
- Microenvironment
- Signal transduction pathways
- Genetic instability
- DNA repair
- Mutational analyses
- “Omics” analyses, including single-cell analyses
- Epigenetic dysregulation
Prevention and therapy:
- Chemoprevention
- Drug resistance
- Network pharmacology
- Novel drugs and targeted chemotherapy
- Immunotherapy
- Novel experimental therapy strategies
Dr. Maja T. Tomicic
Prof. Dr. Thomas Efferth
Guest Editors
Manuscript Submission Information
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Keywords
- p53
- tumor suppressor
- colorectal cancer
- p53 mutations
- therapy