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Understanding Melanoma Pathogenesis: Emerging Molecular Pathways and Targets in Melanoma...
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Understanding Melanoma Pathogenesis: Emerging Molecular Pathways and Targets in Melanoma Progression

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".

Deadline for manuscript submissions: closed (31 October 2021) | Viewed by 30252

Special Issue Editors

Dr. Ali R. Jazirehi

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Guest Editor
Department of Life Sciences, Los Angeles City College, Los Angeles, CA, USA
Interests: immunotherapy; NHL; ALL; apoptosis; signal transduction; adoptive cell therapy; resistance
Special Issues, Collections and Topics in MDPI journals
Dr. Shikhar Mehrotra

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Guest Editor
Medical University of South Carolina, Charleston, SC, USA
Interests: multiple myeloma; immunotherapy; melanoma; lymphoma
Dr. Negroiu Gabriela

E-Mail Website
Guest Editor
Institute of Biochemistry of the Romanian Academy, Bucharest, Romania
Interests: melanoma signaling pathways; diagnostic/prognostic biomarkers in melanoma; anti-tumor (melanoma) targeted therapy (nanostructures)

Special Issue Information

Dear Colleagues,

Melanoma is a dreaded disease. Even though only 4–7% of skin cancers are melanomas, it causes 80% of skin-cancer deaths. It is increasing, and unlike other solid tumors, it mostly affects young and middle-aged individuals.

The characteristics of melanoma are insidious and fast progression, heterogeneity, therapeutic resistance, and unexpected recurrence.

Melanoma represents the malignant transformation of melanocytes, the neural-crest-derived cells that principally populate the basal epidermis, and hair follicles, mucosal surfaces, meninges, and the choroidal layer of the eye. The transformation of melanocytes, cells normally programmed for melanin synthesis, into tumor cells that disseminate from the primary site and reach distal organs, where metastasis occurs through a complex plethora of molecular events, takes place. Over the past ten years, significant progress has been made in melanoma diagnosis and treatment, which has increased the duration and quality of the lives of patients with advanced stages. This has only been possible due to intense and continuous research devoted to understating how melanoma cells work, their versatility in bypassing the organism’s defense system, and their survival and proliferation under stressful conditions. However, the mechanisms of melanoma progression are not entirely understood and need to be controlled for the patient's full benefit.

This Special Issue aims to focus on the significant advancements in melanoma molecularity. We welcome any contributions such as research articles, reviews, communications, and concept papers that uncover the most recently validated or novel pathways and key players, primarily but not only in skin melanoma cells, related to mutations, therapeutic or environmental resistance, and cross-talk between tumor cells and the cellular environment or cells of the immune system. Due to the specific profile of the journal, we encourage contributions focused on experimental cytology rather than clinical and epidemiological studies.

We also expect that in addition to fundamental knowledge, this updated information will represent a foundation for the initiation of translational preclinical studies for more efficient diagnostic and therapeutic strategies.

Dr. Ali R. Jazirehi
Dr. Shikhar Mehrotra
Dr. Negroiu Gabriela
Guest Editors

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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • prognostic biomarkers in melanoma
  • signaling pathways in melanoma progression
  • melanoma microenvironment
  • immune response mechanisms
  • pathways in melanoma

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Published Papers (5 papers)

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Research

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16 pages, 2681 KiB  
Article
p53 Promotes Cytokine Expression in Melanoma to Regulate Drug Resistance and Migration
by Pinakin Pandya, Lyubov Kublo and Jacob Stewart-Ornstein
Cells 2022, 11(3), 405; https://doi.org/10.3390/cells11030405 - 25 Jan 2022
Cited by 9 | Viewed by 3300
Abstract
The transcription factor p53 is frequently lost during tumor development in solid tumors; however, most melanomas retain a wild type p53 protein. The presence of wild type p53 in melanoma has fueled speculation that p53 may play a neutral or pro-tumorigenic role in [...] Read more.
The transcription factor p53 is frequently lost during tumor development in solid tumors; however, most melanomas retain a wild type p53 protein. The presence of wild type p53 in melanoma has fueled speculation that p53 may play a neutral or pro-tumorigenic role in this disease. Here we show that p53 is functional in human melanoma cell lines, and that loss of p53 results in a general reduction in basal NF-kB regulated cytokine production. The reduced cytokine expression triggered by p53 loss is broad and includes key inflammatory chemokines, such as CXCL1, CXCL8, and the IL6 class cytokine LIF, resulting in a reduced ability to induce chemotactic-dependent migration of tumor cells and immune cells and increased sensitivity to BRAF inhibition. Taken together, this result indicates that wild type p53 regulates cytokine expression and induces cytokine-dependent phenotype on melanoma. Full article
(This article belongs to the Special Issue Understanding Melanoma Pathogenesis: Emerging Molecular Pathways and Targets in Melanoma Progression)
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Review

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28 pages, 2358 KiB  
Review
Interleukin-8 in Melanoma Pathogenesis, Prognosis and Therapy—An Integrated View into Other Neoplasms and Chemokine Networks
by Anca Filimon, Iulia A. Preda, Adina F. Boloca and Gabriela Negroiu
Cells 2022, 11(1), 120; https://doi.org/10.3390/cells11010120 - 30 Dec 2021
Cited by 18 | Viewed by 3703
Abstract
Cutaneous melanoma accounts for only about 7% of skin cancers but is causing almost 90% of deaths. Melanoma cells have a distinct repertoire of mutations from other cancers, a high plasticity and degree of mimicry toward vascular phenotype, stemness markers, versatility in evading [...] Read more.
Cutaneous melanoma accounts for only about 7% of skin cancers but is causing almost 90% of deaths. Melanoma cells have a distinct repertoire of mutations from other cancers, a high plasticity and degree of mimicry toward vascular phenotype, stemness markers, versatility in evading and suppress host immune control. They exert a significant influence on immune, endothelial and various stromal cells which form tumor microenvironment. The metastatic stage, the leading cause of mortality in this neoplasm, is the outcome of a complex, still poorly understood, cross-talk between tumor and other cell phenotypes. There is accumulating evidence that Interleukin-8 (IL-8) is emblematic for advanced melanomas. This work aimed to present an updated status of IL-8 in melanoma tumor cellular complexity, through a comprehensive analysis including data from other chemokines and neoplasms. The multiple processes and mechanisms surveyed here demonstrate that IL-8 operates following orchestrated programs within signaling webs in melanoma, stromal and vascular cells. Importantly, the yet unknown molecularity regulating IL-8 impact on cells of the immune system could be exploited to overturn tumor fate. The molecular and cellular targets of IL-8 should be brought into the attention of even more intense scientific exploration and valorization in the therapeutical management of melanoma. Full article
(This article belongs to the Special Issue Understanding Melanoma Pathogenesis: Emerging Molecular Pathways and Targets in Melanoma Progression)
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31 pages, 2393 KiB  
Review
Molecular Markers and Targets in Melanoma
by Cristina Teixido, Paola Castillo, Clara Martinez-Vila, Ana Arance and Llucia Alos
Cells 2021, 10(9), 2320; https://doi.org/10.3390/cells10092320 - 5 Sep 2021
Cited by 106 | Viewed by 11960
Abstract
Melanoma develops as a result of several genetic alterations, with UV radiation often acting as a mutagenic risk factor. Deep knowledge of the molecular signaling pathways of different types of melanoma allows better characterization and provides tools for the development of therapies based [...] Read more.
Melanoma develops as a result of several genetic alterations, with UV radiation often acting as a mutagenic risk factor. Deep knowledge of the molecular signaling pathways of different types of melanoma allows better characterization and provides tools for the development of therapies based on the intervention of signals promoted by these cascades. The latest World Health Organization classification acknowledged the specific genetic drivers leading to melanoma and classifies melanocytic lesions into nine distinct categories according to the associate cumulative sun damage (CSD), which correlates with the molecular alterations of tumors. The largest groups are melanomas associated with low-CSD or superficial spreading melanomas, characterized by frequent presentation of the BRAFV600 mutation. High-CSD melanomas include lentigo maligna type and desmoplastic melanomas, which often have a high mutation burden and can harbor NRAS, BRAFnon-V600E, or NF1 mutations. Non-CSD-associated melanomas encompass acral and mucosal melanomas that usually do not show BRAF, NRAS, or NF1 mutations (triple wild-type), but in a subset may have KIT or SF3B1 mutations. To improve survival, these driver alterations can be treated with targeted therapy achieving significant antitumor activity. In recent years, relevant improvement in the prognosis and survival of patients with melanoma has been achieved, since the introduction of BRAF/MEK tyrosine kinase inhibitors and immune checkpoint inhibitors. In this review, we describe the current knowledge of molecular pathways and discuss current and potential therapeutic targets in melanoma, focusing on their clinical relevance of development. Full article
(This article belongs to the Special Issue Understanding Melanoma Pathogenesis: Emerging Molecular Pathways and Targets in Melanoma Progression)
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17 pages, 631 KiB  
Review
Epigenetic Regulation in Melanoma: Facts and Hopes
by Emilio Francesco Giunta, Gianluca Arrichiello, Marcello Curvietto, Annalisa Pappalardo, Davide Bosso, Mario Rosanova, Anna Diana, Pasqualina Giordano, Angelica Petrillo, Piera Federico, Teresa Fabozzi, Sara Parola, Vittorio Riccio, Brigitta Mucci, Vito Vanella, Lucia Festino, Bruno Daniele, Paolo Antonio Ascierto, Margaret Ottaviano and On Behalf of SCITO YOUTH
Cells 2021, 10(8), 2048; https://doi.org/10.3390/cells10082048 - 11 Aug 2021
Cited by 24 | Viewed by 4086
Abstract
Cutaneous melanoma is a lethal disease, even when diagnosed in advanced stages. Although recent progress in biology and treatment has dramatically improved survival rates, new therapeutic approaches are still needed. Deregulation of epigenetics, which mainly controls DNA methylation status and chromatin remodeling, is [...] Read more.
Cutaneous melanoma is a lethal disease, even when diagnosed in advanced stages. Although recent progress in biology and treatment has dramatically improved survival rates, new therapeutic approaches are still needed. Deregulation of epigenetics, which mainly controls DNA methylation status and chromatin remodeling, is implied not only in cancer initiation and progression, but also in resistance to antitumor drugs. Epigenetics in melanoma has been studied recently in both melanoma preclinical models and patient samples, highlighting its potential role in different phases of melanomagenesis, as well as in resistance to approved drugs such as immune checkpoint inhibitors and MAPK inhibitors. This review summarizes what is currently known about epigenetics in melanoma and dwells on the recognized and potential new targets for testing epigenetic drugs, alone or together with other agents, in advanced melanoma patients. Full article
(This article belongs to the Special Issue Understanding Melanoma Pathogenesis: Emerging Molecular Pathways and Targets in Melanoma Progression)
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16 pages, 1712 KiB  
Review
CDK4/6 Inhibitors in Melanoma: A Comprehensive Review
by Mattia Garutti, Giada Targato, Silvia Buriolla, Lorenza Palmero, Alessandro Marco Minisini and Fabio Puglisi
Cells 2021, 10(6), 1334; https://doi.org/10.3390/cells10061334 - 28 May 2021
Cited by 40 | Viewed by 6251
Abstract
Historically, metastatic melanoma was considered a highly lethal disease. However, recent advances in drug development have allowed a significative improvement in prognosis. In particular, BRAF/MEK inhibitors and anti-PD1 antibodies have completely revolutionized the management of this disease. Nonetheless, not all patients derive a [...] Read more.
Historically, metastatic melanoma was considered a highly lethal disease. However, recent advances in drug development have allowed a significative improvement in prognosis. In particular, BRAF/MEK inhibitors and anti-PD1 antibodies have completely revolutionized the management of this disease. Nonetheless, not all patients derive a benefit or a durable benefit from these therapies. To overtake this challenges, new clinically active compounds are being tested in the context of clinical trials. CDK4/6 inhibitors are drugs already available in clinical practice and preliminary evidence showed a promising activity also in melanoma. Herein we review the available literature to depict a comprehensive landscape about CDK4/6 inhibitors in melanoma. We present the molecular and genetic background that might justify the usage of these drugs, the preclinical evidence, the clinical available data, and the most promising ongoing clinical trials. Full article
(This article belongs to the Special Issue Understanding Melanoma Pathogenesis: Emerging Molecular Pathways and Targets in Melanoma Progression)
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