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Special Issue Editors

Dr. Dmitry V. Bulavin

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Guest Editor

Institute for Research on Cancer and Aging of Nice (IRCAN), INSERM, Université Côte d'Azur, CNRS, Nice, France
Interests: DNA damage signaling; stress-induced signaling; tumor heterogeneity; stemness; senescence; epigenetic reprogramming; tumor microenvironment; autophagy; apoptosis

Dr. Alexander Emelyanov

E-Mail Website
Guest Editor

Institute for Research on Cancer and Aging of Nice (IRCAN), INSERM, Université Côte d'Azur, CNRS, Nice, France
Interests: DNA damage signaling in cancer and aging

Special Issue Information

Dear Colleagues,

Therapies with broad targeting anticancer activity have significant favorable effects. Nevertheless, the presence of resistant cancer cells or acquisition of resistance in response to drug treatment represent major barriers to a full cure. Activation of DNA damage response (DDR) remains the main route for efficient cancer treatment in response to chemo- and radiotherapy. It is well documented, however, that under certain conditions, DDR can promote tumorigenesis. The mechanisms of this phenomenon are not completely understood but generally attributed to an increased mutation rate that is believed to either activate oncogenes or disable tumor suppressors, thus favoring tumorigenesis. Increasing evidence, however, suggests that chemo- and radiotherapy exert numerous tumor-promoting effects that cannot be exclusively explained by genetic alterations in cancer cells.

This Special Issue will highlight the emerging role of DNA damage and stress responses as important drivers of cancer evolution at the level of epigenetic reprogramming, modulation of senescence, induction of cancer cell plasticity, regulation of immune responses and tumor microenvironment, as well as other non-genetic changes. These novel basic and translational aspects could advance our understanding of targeting DNA damage and stress responses, ultimately improving our current anticancer therapeutic regimes.

Dr. Dmitry V. Bulavin
Dr. Alexander Emelyanov
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. Cancers 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 2900 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

DNA damage signaling
stress-induced signaling
tumor heterogeneity
stemness
senescence
epigenetic reprogramming
tumor microenvironment
autophagy
apoptosis

Published Papers (2 papers)

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Research

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20 pages, 1896 KiB

Open AccessArticle

Modulation of DNA Damage Response by SAM and HD Domain Containing Deoxynucleoside Triphosphate Triphosphohydrolase (SAMHD1) Determines Prognosis and Treatment Efficacy in Different Solid Tumor Types

by Eudald Felip, Lucía Gutiérrez-Chamorro, Maica Gómez, Edurne Garcia-Vidal, Margarita Romeo, Teresa Morán, Laura Layos, Laia Pérez-Roca, Eva Riveira-Muñoz, Bonaventura Clotet, Pedro Luis Fernandez, Ricard Mesía, Anna Martínez-Cardús, Ester Ballana and Mireia Margelí

Cancers 2022, 14(3), 641; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers14030641 - 27 Jan 2022

Cited by 8 | Viewed by 3008

Abstract

SAMHD1 is a deoxynucleotide triphosphate (dNTP) triphosphohydrolase with important roles in the control of cell proliferation and apoptosis, either through the regulation of intracellular dNTPs levels or the modulation of the DNA damage response. However, SAMHD1′s role in cancer evolution is still unknown. We performed the first in-depth study of SAMHD1′s role in advanced solid tumors, by analyzing samples of 128 patients treated with chemotherapy agents based on platinum derivatives and/or antimetabolites, developing novel in vitro knock-out models to explore the mechanisms driving SAMHD1 function in cancer. Low (or no) expression of SAMHD1 was associated with a positive prognosis in breast, ovarian, and non-small cell lung cancer (NSCLC) cancer patients. A predictive value was associated with low-SAMHD1 expression in NSCLC and ovarian patients treated with antimetabolites in combination with platinum derivatives. In vitro, SAMHD1 knock-out cells showed increased γ-H2AX and apoptosis, suggesting that SAMHD1 depletion induces DNA damage leading to cell death. In vitro treatment with platinum-derived drugs significantly enhanced γ-H2AX and apoptotic markers expression in knock-out cells, indicating a synergic effect of SAMHD1 depletion and platinum-based treatment. SAMHD1 expression represents a new strong prognostic and predictive biomarker in solid tumors and, thus, modulation of the SAMHD1 function may constitute a promising target for the improvement of cancer therapy. Full article

(This article belongs to the Special Issue Tumor-Promoting Functions of DNA Damage and Stress Response Signaling)

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Review

Jump to: Research

19 pages, 2454 KiB

Open AccessReview

Homologous Recombination Repair Deficiency and Implications for Tumor Immunogenicity

by Sandra van Wilpe, Sofie H. Tolmeijer, Rutger H. T. Koornstra, I. Jolanda M. de Vries, Winald R. Gerritsen, Marjolijn Ligtenberg and Niven Mehra

Cancers 2021, 13(9), 2249; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13092249 - 07 May 2021

Cited by 27 | Viewed by 8546

Abstract

Homologous recombination repair deficiency (HRD) can be observed in virtually all cancer types. Although HRD sensitizes tumors to DNA-damaging chemotherapy and poly(ADP-ribose) polymerase (PARP) inhibitors, all patients ultimately develop resistance to these therapies. Therefore, it is necessary to identify therapeutic regimens with a more durable efficacy. HRD tumors have been suggested to be more immunogenic and, therefore, more susceptible to treatment with checkpoint inhibitors. In this review, we describe how HRD might mechanistically affect antitumor immunity and summarize the available translational evidence for an association between HRD and antitumor immunity across multiple tumor types. In addition, we give an overview of all available clinical data on the efficacy of checkpoint inhibitors in HRD tumors and describe the evidence for using treatment strategies that combine checkpoint inhibitors with PARP inhibitors. Full article

(This article belongs to the Special Issue Tumor-Promoting Functions of DNA Damage and Stress Response Signaling)

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