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Skin Cancer: From Molecular Pathophysiology to Novel Treatment
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Skin Cancer: From Molecular Pathophysiology to Novel Treatment

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 25 December 2025 | Viewed by 1442

Special Issue Editor

Prof. Dr. Soon-Hyo Kwon

E-Mail Website
Guest Editor
Department of Dermatology, Kyung Hee University Hospital at Gangdong, Kyung Hee University College of Medicine, Seoul, Republic of Korea
Interests: solar lentigo; RNA-seq data; inflammation; oxidative stress; dermatology; skin; photoaging

Special Issue Information

Dear Colleagues,

We invite researchers to submit original studies and reviews focusing on the molecular mechanisms underlying skin cancer, including genetic mutations, epigenetic modifications, and dysregulated signaling pathways. Special emphasis is placed on tumor microenvironment interactions, immune evasion, and resistance mechanisms. We particularly welcome studies identifying novel molecular targets and developing innovative therapeutic strategies, such as targeted therapies, immunotherapies, and nanomedicine-based approaches. Additionally, research on biomarkers for early detection, prognosis, and treatment response is encouraged.

This collection aims to bridge fundamental molecular research with translational and clinical applications, providing insights into next-generation skin cancer therapies. Contributions from various disciplines, including molecular biology, bioinformatics, and pharmaceutical sciences, are highly encouraged.

By bringing together cutting-edge research, we hope to advance our understanding of skin cancer pathophysiology and foster the development of more effective treatments. Submit your work to contribute to this growing field and shape the future of skin cancer therapy.

Prof. Dr. Soon-Hyo Kwon
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • basal cell carcinoma
  • malignant melanoma
  • molecular genetics
  • epigenetics
  • signaling pathways
  • tumor microenvironment
  • tumor resistance
  • biomarkers
  • molecular target
  • multiomics
  • genomics
  • transcriptomics
  • proteomics
  • metabolomics
  • skin cancer
  • squamous cell carcinoma

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Published Papers (2 papers)

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Research

19 pages, 1145 KB  
Article
Checkpoint Blockade Efficacy in Uveal Melanoma Is Linked to Tumor Immunity, CD28, and CCL8
by Elias A. T. Koch, Renato Liguori, Alejandro Afonso Castro, Stefan Schliep, Anne Petzold, Anja Wessely, Waltraud Fröhlich, Fulvia Ferrazzi, Julio Vera, Markus Eckstein, Carola Berking and Markus V. Heppt
Int. J. Mol. Sci. 2025, 26(20), 9964; https://doi.org/10.3390/ijms26209964 - 13 Oct 2025
Viewed by 381
Abstract
For patients with metastatic uveal melanoma (UM), tebentafusp is currently the only systemic therapy approved by the EMA and FDA, but its use is limited to HLA-A*02:01-positive individuals. Immune checkpoint blockade (ICB) represents another option, though only a small subgroup of patients benefits, [...] Read more.
For patients with metastatic uveal melanoma (UM), tebentafusp is currently the only systemic therapy approved by the EMA and FDA, but its use is limited to HLA-A*02:01-positive individuals. Immune checkpoint blockade (ICB) represents another option, though only a small subgroup of patients benefits, and no reliable predictive biomarkers are available to date. The aim of this study was therefore to identify parameters associated with favorable ICB response. Tumor samples and clinical data from 30 patients were analyzed. Group A (n = 16) showed clinical benefit, while Group B (n = 14) experienced disease progression. NanoString® analyses revealed 258 upregulated genes in Group A, including IDO1, CD28, and CCL8. The enriched pathways were predominantly linked to immune activation, leukocyte adhesion, and responses to external stimuli. Immunohistochemistry confirmed significantly higher CD28 expression on infiltrating immune cells in Group A, while a machine learning approach identified CCL8 as a predictive marker with ~78% accuracy. Overall survival differed significantly between the groups. These findings indicate that patients responding to ICB display tumors with enhanced immune activation. CD28 and CCL8 emerged as promising candidates and should be validated in prospective studies to determine their clinical utility. Full article
(This article belongs to the Special Issue Skin Cancer: From Molecular Pathophysiology to Novel Treatment)
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13 pages, 1527 KB  
Article
Ethnic-Specific and UV-Independent Mutational Signatures of Basal Cell Carcinoma in Koreans
by Ye-Ah Kim, Seokho Myung, Yueun Choi, Junghyun Kim, Yoonsung Lee, Kiwon Lee, Bark-Lynn Lew, Man S. Kim and Soon-Hyo Kwon
Int. J. Mol. Sci. 2025, 26(14), 6941; https://doi.org/10.3390/ijms26146941 - 19 Jul 2025
Viewed by 798
Abstract
Basal cell carcinoma (BCC), the most common skin cancer, is primarily driven by Hedgehog (Hh) and TP53 pathway alterations. Although additional pathways were implicated, the mutational landscape in Asian populations, particularly Koreans, remains underexplored. We performed whole-exome sequencing of BCC tumor tissues from [...] Read more.
Basal cell carcinoma (BCC), the most common skin cancer, is primarily driven by Hedgehog (Hh) and TP53 pathway alterations. Although additional pathways were implicated, the mutational landscape in Asian populations, particularly Koreans, remains underexplored. We performed whole-exome sequencing of BCC tumor tissues from Korean patients and analyzed mutations in 11 established BCC driver genes (PTCH1, SMO, GLI1, TP53, CSMD1/2, NOTCH1/2, ITIH2, DPP10, and STEAP4). Mutational profiles were compared with Caucasian cohort profiles to identify ethnicity-specific variants. Ultraviolet (UV)-exposed and non-UV-exposed tumor sites were compared; genes unique to non-UV-exposed tumors were further analyzed with protein–protein interaction analysis. BCCs in Koreans exhibited distinct features, including fewer truncating and more intronic variants compared to Caucasians. Korean-specific mutations in SMO, PTCH1, TP53, and NOTCH2 overlapped with oncogenic gain-of-function/loss-of-function (GOF/LOF) variants annotated in OncoKB, with some occurring at hotspot sites. BCCs in non-exposed areas showed recurrent mutations in CSMD1, PTCH1, and NOTCH1, suggesting a UV-independent mechanism. Novel mutations in TAS1R2 and ADCY10 were exclusive to non-exposed BCCs, with protein–protein interaction analysis linking them to TP53 and NOTCH2. We found unique ethnic-specific and UV-independent mutational profiles of BCCs in Koreans. TAS1R2 and ADCY10 may contribute to tumorigenesis of BCC in non-exposed areas, supporting the need for population-specific precision oncology. Full article
(This article belongs to the Special Issue Skin Cancer: From Molecular Pathophysiology to Novel Treatment)
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