Pathogenesis, Diagnosis and Treatment of Melanoma

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 30 April 2026 | Viewed by 834

Special Issue Editor


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Guest Editor
The Shraga Segal Department of Microbiology-Immunology and Genetics, Faculty of Health Sciences, Ben Gurion University of the Negev, Beer Sheva 84105, Israel
Interests: molecular cancer; metastasis; protein kinase C; micro peptide; breast cancer; cancer stem cells; melanoma; tumor biology; targeted therapy
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Special Issue Information

Dear Colleagues, 

Melanoma is the most aggressive of all skin cancers due to its metastatic nature. Potential advancements in melanoma therapy rely on advanced research that addresses the molecular complexity of this cancer. The current scenario requires both advanced scientific knowledge coupled with empirical evidence in identifying new therapeutic targets in order to improve drug sensitivity and overcome secondary resistance. Innovative research approaches focusing on the molecular mechanisms of the tumor microenvironment provides key insights into either reducing or eliminating melanoma. The aim of this Special Issue is to present a unified collection of the latest research articles and findings on melanoma, focusing on identifying new realms of molecular mechanisms and biomarkers and hopefully prompting the invention of significant molecular targeted therapies. This Special Issue includes the latest research articles on the mutations, signaling pathways, and immune responses that determine melanoma progression. This unified collection aims to describe how the latest findings are proving beneficial in developing innovative therapies, including targeted treatments and immunotherapies for melanoma patients. These research findings can pave the way for transforming preclinical trials into clinical practices. We welcome original research articles and reviews that address the molecular mechanisms behind melanoma and novel therapies related to the disease.

Dr. Vijayasteltar B. Liju
Guest Editor

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Keywords

  • melanoma
  • metastasis
  • targeted therapies
  • immunotherapy
  • tumor microenvironment
  • combination therapies
  • molecular pathways

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Published Papers (1 paper)

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Research

11 pages, 1809 KB  
Communication
Apoptosis, Cell Growth, and Glycogen Synthase Kinase 3β Phosphorylation in Caffeic Acid-Treated Human Malignant Melanoma Cells
by Yoon-Jin Lee, Ki Dam Kim, Min Hyuk Choi, Sukh Que Park, Yu Sung Choi, Youin Bae, Hae Seon Nam, Sang Han Lee and Moon Kyun Cho
Biomedicines 2025, 13(10), 2389; https://doi.org/10.3390/biomedicines13102389 - 29 Sep 2025
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Abstract
Objectives: Caffeic acid (CA), a naturally occurring phenolic compound exhibiting antioxidant and anti-inflammatory effects, has demonstrated anticancer activity against several tumor types. Nevertheless, its involvement in melanoma and its effects on the GSK3β signaling pathway have not been fully elucidated. This study aimed [...] Read more.
Objectives: Caffeic acid (CA), a naturally occurring phenolic compound exhibiting antioxidant and anti-inflammatory effects, has demonstrated anticancer activity against several tumor types. Nevertheless, its involvement in melanoma and its effects on the GSK3β signaling pathway have not been fully elucidated. This study aimed to assess the expression of p-GSK3β in melanoma tissues and to evaluate the anti-melanoma efficacy of CA. Methods: Western blot analysis was performed to determine the expression levels of p-GSK3β in melanoma and normal skin samples. G361 melanoma cells were exposed to CA, after which cell viability, apoptotic induction, cell cycle distribution, and related signaling molecules were examined. Results: Significantly increased p-GSK3β levels were identified in melanoma tissues. CA exposure decreased cell viability, triggered apoptosis, and elevated p-GSK3β levels in G361 melanoma cells. Moreover, CA induced the upregulation of p53 and p21 while concomitantly downregulating cyclin D1 and Bcl-2. Conclusions: These results suggest that CA inhibits melanoma cell growth through activation of a pathway involving the tumor suppressor p53, rather than through modulation of GSK3β signaling. Full article
(This article belongs to the Special Issue Pathogenesis, Diagnosis and Treatment of Melanoma)
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