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Biomolecules
Special Issues
Recent Advance of Melanoma
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Recent Advance of Melanoma

A special issue of Biomolecules (ISSN 2218-273X).

Deadline for manuscript submissions: closed (31 August 2020) | Viewed by 3389

Special Issue Editor

Prof. Dr. Iris Helfrich

E-Mail Website
Guest Editor
1. Department of Dermatology and Allergy of the Ludwig Maximilian University Munich, German Cancer Consortium (DKTK), Partner Munich, Essen, Germany
2. Skin Cancer Unit of the Dermatology Department, Medical Faculty Essen & German Cancer Consortium (DKTK), Partner Site Essen/Düsseldorf, Essen, Germany
Interests: melanoma metastasis; tumor microenvironment; tumor cell plasticity; cancer immunotherapy; therapy resistance

Special Issue Information

Dear Colleagues,

Malignant melanoma is the most treatment resistant type of skin cancer, characterized by continuously rising incidence and a high mortality. The recent clinical success of cancer immunotherapies in patients suffering from malignant melanoma and other cancer types has revolutionized the therapeutic landscape of metastatic cancer. The approval of antibodies against the so-called “immune checkpoints” has rapidly changed the standard of care, and has emphasized the essential role of the dynamic interplay of tumor cells with the cells of the immune system. The inflammation and massive infiltration of leukocytes is a hallmark of various tumor entities. Moreover, the recruitment of immune cells into the tumor microenvironment has been shown to contribute to patients’ clinical outcomes in certain types of cancer, including melanoma. In contrast to conventional cancer therapies, the immunotherapeutic approach specifically targets the different subtypes of the immune cells, and thus orchestrates a systemic response against tumors. However, depending on the context of the reciprocal interaction between cancer cells and their surrounded stromal composition, the tumor microenvironment can both dampen or enhance immune responses, directing a patient’s survival.

The Special Issue, “Recent Advance of melanoma”, will shed light on novel molecular targets and microenvironmental modulators in the field of melanoma therapy and resistance.  I strongly encourage you and/or your colleagues to submit manuscripts that match the objectives and topic of this Special Issue.

Dr. Iris Helfrich
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. Biomolecules is an international peer-reviewed open access monthly 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

  • malignant melanoma
  • immunotherapy
  • tumor cell plasticity

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Published Papers (1 paper)

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Research

12 pages, 1767 KiB  
Article
Loss of ADAM9 Leads to Modifications of the Extracellular Matrix Modulating Tumor Growth
by Anna N. Abety, Elke Pach, Nives Giebeler, Julia E. Fromme, Lavakumar Reddy Aramadhaka, Cornelia Mauch, Jay W. Fox and Paola Zigrino
Biomolecules 2020, 10(9), 1290; https://doi.org/10.3390/biom10091290 - 7 Sep 2020
Cited by 3 | Viewed by 2961
Abstract
ADAM9 is a metalloproteinase strongly expressed at the tumor-stroma border by both tumor and stromal cells. We previously showed that the host deletion of ADAM9 leads to enhanced growth of grafted B16F1 melanoma cells by a mechanism mediated by TIMP1 and the TNF-α/sTNFR1 [...] Read more.
ADAM9 is a metalloproteinase strongly expressed at the tumor-stroma border by both tumor and stromal cells. We previously showed that the host deletion of ADAM9 leads to enhanced growth of grafted B16F1 melanoma cells by a mechanism mediated by TIMP1 and the TNF-α/sTNFR1 pathway. This study aimed to dissect the structural modifications in the tumor microenvironment due to the stromal expression of ADAM9 during melanoma progression. We performed proteomic analysis of peritumoral areas of ADAM9 deleted mice and identified the altered expression of several matrix proteins. These include decorin, collagen type XIV, fibronectin, and collagen type I. Analysis of these matrices in the matrix producing cells of the dermis, fibroblasts, showed that ADAM9−/− and wild type fibroblasts synthesize and secreted almost comparable amounts of decorin. Conversely, collagen type I expression was moderately, but not significantly, decreased at the transcriptional level, and the protein increased in ADAM9−/− fibroblast mono- and co-cultures with melanoma media. We show here for the first time that ADAM9 can release a collagen fragment. Still, it is not able to degrade collagen type I. However, the deletion of ADAM9 in fibroblasts resulted in reduced MMP-13 and -14 expression that may account for the reduced processing of collagen type I. Altogether, the data show that the ablation of ADAM9 in the host leads to the altered expression of peritumoral extracellular matrix proteins that generate a more favorable environment for melanoma cell growth. These data underscore the suppressive role of stromal expression of ADAM9 in tumor growth and call for a better understanding of how protease activities function in a cellular context for improved targeting. Full article
(This article belongs to the Special Issue Recent Advance of Melanoma)
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