International Journal of Molecular Sciences

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Dear Colleagues,

Skin cancer is the most common form of cancer, globally accounting for at least 40% of cancer cases. The most common SC type is nonmelanoma skin cancer, occurring in at least 2–3 million people per year. In the past few decades, significant advances have been made in SC screening, staging, treatment, and molecular characterization.

A significant challenge in SC is the development of curative treatment options for these patients. Recent advancements in molecular biological techniques and analyses have led to a much better understanding of the biology of SC. Genetic aberrations appear to be shared in SC. In addition, different subtypes of SCs have been defined based on molecular pathways involved and on specific DNA mutations. Furthermore, accumulating evidence proved that the tumor microenvironment, including the immune system, plays an essential role in SC development.

New treatment modalities become available that interfere in specific molecular pathways. Therefore, future treatment will be based on the underlying biology in specific cases of SCs.

The genetic and epigenetic instability, as a driving force, results in tumor heterogeneity. It has also become clear that therapeutic interventions can result in selective outgrowth of resistant subtypes. Cure outcome depends on the volume and unique characteristics of the tumor and depends on the competition between treatment efficacy and the outgrowth of escape variants.

In this Special Issue of IJMS, the focus will be on this competition by considering SC's biology about new treatment options.

Dr. Jànos Hunyadi
Prof. Dr. Liszkay Gabriella
Guest Editors

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Keywords

skin cancer
molecular pathway
tumor microenvironment
immunotherapy
biological
genetics
epigenetics

Published Papers (2 papers)

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Research

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11 pages, 1646 KiB

Open AccessArticle

Discovery of Small Molecule Activators of Chemokine Receptor CXCR4 That Improve Diabetic Wound Healing

by Junwang Xu, Junyi Hu, Shaquia Idlett-Ali, Liping Zhang, Karly Caples, Satyamaheshwar Peddibhotla, Morgan Reeves, Carlos Zgheib, Siobhan Malany and Kenneth W. Liechty

Int. J. Mol. Sci. 2022, 23(4), 2196; https://doi.org/10.3390/ijms23042196 - 16 Feb 2022

Cited by 10 | Viewed by 2080

Abstract

Diabetes produces a chronic inflammatory state that contributes to the development of vascular disease and impaired wound healing. Despite the known individual and societal impacts of diabetic ulcers, there are limited therapies effective at improving healing. Stromal cell-derived factor 1α (SDF-1α) is a CXC chemokine that functions via activation of the CXC chemokine receptor type 4 (CXCR4) receptor to recruit hematopoietic cells to locations of tissue injury and promote tissue repair. The expression of SDF-1α is reduced in diabetic wounds, suggesting a potential contribution to wound healing impairment and presenting the CXCR4 receptor as a target for therapeutic investigations. We developed a high-throughput β-arrestin recruitment assay and conducted structure–activity relationship (SAR) studies to screen compounds for utility as CXCR4 agonists. We identified CXCR4 agonist UCUF-728 from our studies and further validated its activity in vitro in diabetic fibroblasts. UCUF-728 reduced overexpression of miRNA-15b and miRNA-29a, negative regulators of angiogenesis and type I collagen production, respectively, in diabetic fibroblasts. In vivo, UCUF-728 reduced the wound closure time by 36% and increased the evidence of angiogenesis in diabetic mice. Together, this work demonstrates the clinical potential of small molecule CXCR4 agonists as novel therapies for pathologic wound healing in diabetes. Full article

(This article belongs to the Special Issue Molecular Diagnosis and Treatment of Skin Cancers)

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Review

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14 pages, 399 KiB

Open AccessReview

Molecular Pathology of Skin Melanoma: Epidemiology, Differential Diagnostics, Prognosis and Therapy Prediction

by József Tímár and Andrea Ladányi

Int. J. Mol. Sci. 2022, 23(10), 5384; https://doi.org/10.3390/ijms23105384 - 11 May 2022

Cited by 32 | Viewed by 5759

Abstract

Similar to other malignancies, TCGA network efforts identified the detailed genomic picture of skin melanoma, laying down the basis of molecular classification. On the other hand, genome-wide association studies discovered the genetic background of the hereditary melanomas and the susceptibility genes. These genetic studies helped to fine-tune the differential diagnostics of malignant melanocytic lesions, using either FISH tests or the myPath gene expression signature. Although the original genomic studies on skin melanoma were mostly based on primary tumors, data started to accumulate on the genetic diversity of the progressing disease. The prognostication of skin melanoma is still based on staging but can be completed with gene expression analysis (DecisionDx). Meanwhile, this genetic knowledge base of skin melanoma did not turn to the expected wide array of target therapies, except the BRAF inhibitors. The major breakthrough of melanoma therapy was the introduction of immune checkpoint inhibitors, which showed outstanding efficacy in skin melanoma, probably due to their high immunogenicity. Unfortunately, beyond BRAF, KIT mutations and tumor mutation burden, no clinically validated predictive markers exist in melanoma, although several promising biomarkers have been described, such as the expression of immune-related genes or mutations in the IFN-signaling pathway. After the initial success of either target or immunotherapies, sooner or later, relapses occur in the majority of patients, due to various induced genetic alterations, the diagnosis of which could be developed to novel predictive genetic markers. Full article

(This article belongs to the Special Issue Molecular Diagnosis and Treatment of Skin Cancers)

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