Mutations Driving Human Solid Tumors
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 4547
Special Issue Editor
2. MAP Kinase Resource, Bioinformatics, Melchiorstrasse 9, CH-3027 Bern, Switzerland
Interests: breast cancer; prostate cancer; acute myeloid leukemia (AML); kinases
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Most known cancers (at least 90%) have gene modifications, such as amplifications, deletions, translocations, inversions, frameshifts, and substitutions. The mutation of genes can either enhance the function of proteins, sometimes even making them permanently active, or decrease their functioning or even abolish them completely. Later on, changes in protein function can cause uncontrolled proliferation, survival, motility, and adhesion of cells as well as DNA repair problems, microsatellite instability, and other processes, which can lead to the development, growth, and spread of cancer. Compared to protein-truncating mutations and fusions, missense mutations induce delicate changes, which are often difficult to explain at the phenotypic level. Therefore, distinguishing missense driver mutations based on their impact on molecular protein function is challenging. Nevertheless, focusing on important functional elements, such as protein domains, post-translational modification sites, and protein interaction sites, has been shown to be an effective way to identify malignant mutations. In this Special Issue of Cancers, experts are invited to contribute original research papers or review articles that will provide further insights on the various consequences of gene missense mutations in cancers, their role as biomarkers as well as possible drug targets.
Dr. Jonas Cicenas
Guest Editor
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Keywords
- somatic missense mutations
- genetic variant
- missense mutations and cancer
- mutations in oncogenes
- mutations in tumor suppressors
- mutations as biomarkers
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