Melanoma: From Molecular Mechanisms to Therapeutic Opportunities—Series 2
A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".
Deadline for manuscript submissions: 20 December 2024 | Viewed by 3489
Special Issue Editors
Interests: apoptosis; genotoxicity; skin biology; melanoma; cancer; cell proliferation
Special Issues, Collections and Topics in MDPI journals
Interests: apoptosis; genotoxicity; DNA damage; skin biology; wound healing; melanoma; cancer
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
We are pleased to announce the second edition of our Special Issue. The first edition attracted the interest of researchers around the world. The publications that are freely available for download are listed at the following:
Cells website: https://www.mdpi.com/journal/cells/special_issues/Melanoma_Molecular_Mechanism
Malignant melanoma remains a formidable challenge, with ~106,110 new cases and ~7,180 deaths in the United States in 2021. Drug and immune resistance, together with invasion and metastasis, determine tumor progression, and, ultimately, patient survival. With the highest mortality rate among skin cancers, cutaneous melanoma is associated with driver mutations in MAPK and other signaling pathways, including RAS/PI3K/AKT, p16INK4a/CDK4/RB, WNT, and p53. Activating mutations are primarily in the V600 or K601 of BRAF (50% of melanomas), Q61 of NRAS (>20%), and LOF mutations in NF1 (10%). Although combinations of targeted kinase inhibitors for BRAF and MEK, combined with immune checkpoint inhibitors, have improved progression-free and overall survival of melanoma patients, ~75% of melanomas recur after BRAF copy number gains, alternative splicing, MEK1/2, and NRAS gain-of-function mutations; 20% of BRAFi-resistant melanomas upregulate compensatory PI3K/AKT survival pathways. Although treatment for recalcitrant NRAS-mutant metastatic tumors has advanced, with immunotherapies anti–PD-1, anti-PD-L1, and/or anti-CTLA4 proving efficacious, many patients remain unresponsive, and chemotherapy with dacarbazine, temozolomide, or carboplatin shows limited success. There is a compelling rationale to examine unexploited pathways. Resistance has been attributed to subpopulations of “melanoma initiating cells”, highly tumorigenic cancer stem cells characterized by melanosphere formation, and expression of specific cancer stem cell markers.
This Special Issue will publish original articles and reviews focusing on novel targets for therapeutic intervention; biomarkers for screening, predicting treatment response, and monitoring disease progression; and mechanistic insights and advances in molecular and cellular pathways involved in melanomagenesis and progression. Topics of interest include mechanisms underlying melanoma progression and treatment response, signal transduction, melanoma-initiating cells, drug resistance, invasiveness, immune evasion, and metastasis. There remains an urgent need to identify novel targets and develop new combinatorial therapeutic approaches that can overcome drug resistance mechanisms.
We look forward to receiving your contributions to this Special Issue.
Prof. Dr. Cynthia Simbulan-Rosenthal
Dr. Dean S. Rosenthal
Guest Editors
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Keywords
- melanomagenesis
- treatment response
- signal transduction
- melanoma initiating cells
- drug resistance
- invasiveness
- immune evasion
- metastasis
- MAPK pathway
- PI3K/AKT survival pathways
- MEKi
- BRAFi
- trametinib
- dabrafenib
- immunotherapies
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