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      Cutaneous Squamous Cell Carcinoma: From Biology to Therapy

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          Abstract

          Cutaneous squamous cell carcinoma (CSCC) is the second most frequent cancer in humans and its incidence continues to rise. Although CSCC usually display a benign clinical behavior, it can be both locally invasive and metastatic. The signaling pathways involved in CSCC development have given rise to targetable molecules in recent decades. In addition, the high mutational burden and increased risk of CSCC in patients under immunosuppression were part of the rationale for developing the immunotherapy for CSCC that has changed the therapeutic landscape. This review focuses on the molecular basis of CSCC and the current biology-based approaches of targeted therapies and immune checkpoint inhibitors. Another purpose of this review is to explore the landscape of drugs that may induce or contribute to the development of CSCC. Beginning with the pathogenetic basis of these drug-induced CSCCs, we move on to consider potential therapeutic opportunities for overcoming this adverse effect.

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          Combined vemurafenib and cobimetinib in BRAF-mutated melanoma.

          James Larkin, Paolo Ascierto, Brigitte Dréno … (2014)
          The combined inhibition of BRAF and MEK is hypothesized to improve clinical outcomes in patients with melanoma by preventing or delaying the onset of resistance observed with BRAF inhibitors alone. This randomized phase 3 study evaluated the combination of the BRAF inhibitor vemurafenib and the MEK inhibitor cobimetinib. We randomly assigned 495 patients with previously untreated unresectable locally advanced or metastatic BRAF V600 mutation-positive melanoma to receive vemurafenib and cobimetinib (combination group) or vemurafenib and placebo (control group). The primary end point was investigator-assessed progression-free survival. The median progression-free survival was 9.9 months in the combination group and 6.2 months in the control group (hazard ratio for death or disease progression, 0.51; 95% confidence interval [CI], 0.39 to 0.68; P<0.001). The rate of complete or partial response in the combination group was 68%, as compared with 45% in the control group (P<0.001), including rates of complete response of 10% in the combination group and 4% in the control group. Progression-free survival as assessed by independent review was similar to investigator-assessed progression-free survival. Interim analyses of overall survival showed 9-month survival rates of 81% (95% CI, 75 to 87) in the combination group and 73% (95% CI, 65 to 80) in the control group. Vemurafenib and cobimetinib was associated with a nonsignificantly higher incidence of adverse events of grade 3 or higher, as compared with vemurafenib and placebo (65% vs. 59%), and there was no significant difference in the rate of study-drug discontinuation. The number of secondary cutaneous cancers decreased with the combination therapy. The addition of cobimetinib to vemurafenib was associated with a significant improvement in progression-free survival among patients with BRAF V600-mutated metastatic melanoma, at the cost of some increase in toxicity. (Funded by F. Hoffmann-La Roche/Genentech; coBRIM ClinicalTrials.gov number, NCT01689519.).
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            T Cell Dysfunction in Cancer.

            Daniela S Thommen, Ton Schumacher (2018)
            Therapeutic reinvigoration of tumor-specific T cells has greatly improved clinical outcome in cancer. Nevertheless, many patients still do not achieve durable benefit. Recent evidence from studies in murine and human cancer suggest that intratumoral T cells display a broad spectrum of (dys-)functional states, shaped by the multifaceted suppressive signals that occur within the tumor microenvironment. Here we discuss the current understanding of T cell dysfunction in cancer, the value of novel technologies to dissect such dysfunction at the single cell level, and how our emerging understanding of T cell dysfunction may be utilized to develop personalized strategies to restore antitumor immunity.
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              PD-1 Blockade with Cemiplimab in Advanced Cutaneous Squamous-Cell Carcinoma

              Victor Moreno, Michael Migden, Danny Rischin … (2018)
              No systemic therapies have been approved for the treatment of advanced cutaneous squamous-cell carcinoma. This cancer may be responsive to immune therapy, because the mutation burden of the tumor is high and the disease risk is strongly associated with immunosuppression. In the dose-escalation portion of the phase 1 study of cemiplimab, a deep and durable response was observed in a patient with metastatic cutaneous squamous-cell carcinoma.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Mol Sci
                Journal ID (iso-abbrev): Int J Mol Sci
                Journal ID (publisher-id): ijms
                Title: International Journal of Molecular Sciences
                Publisher: MDPI
                ISSN (Electronic): 1422-0067
                Publication date (Electronic): 22 April 2020
                Publication date Collection: April 2020
                Volume: 21
                Issue: 8
                Electronic Location Identifier: 2956
                Affiliations
                [1 ]Instituto de Biología Molecular y Celular del Cáncer (IBMCC)-Centro de Investigación del cáncer (CIC)-CSIC, Laboratory 7, 37007 Salamanca, Spain; rober.corchado@ 123456usal.es (R.C.-C.); nataliagarciasancha@ 123456usal.es (N.G.-S.); jperezlosada@ 123456usal.es (J.P.-L.)
                [2 ]Instituto de Investigación Biomédica de Salamanca (IBSAL), Complejo Asistencial Universitario de Salamanca, Hospital Virgen de la Vega, 37007 Salamanca, Spain; gonzalez@ 123456usal.es
                [3 ]Molecular Medicine Unit, Department of Medicine, University of Salamanca, 37007 Salamanca, Spain
                [4 ]Department of Dermatology, Complejo Asistencial Universitario de Salamanca, 37007 Salamanca, Spain
                Author notes
                [* ]Correspondence: jcanueto@ 123456usal.es ; Tel.: +34-923-291-100 (ext. 55574)
                [†]

                These authors contributed equally to this work.

                Author information
                https://orcid.org/0000-0002-2726-6795
                https://orcid.org/0000-0003-0037-7353
                Article
                Publisher ID: ijms-21-02956
                DOI: 10.3390/ijms21082956
                PMC ID: 7216042
                PubMed ID: 32331425
                SO-VID: e1c70d05-0b11-40b1-8600-a5b5ff7055f4
                Copyright © © 2020 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 02 March 2020
                Date accepted : 20 April 2020
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular biology
                Keywords: cutaneous squamous cell carcinoma,immunotherapy,epidermal growth factor receptor (egfr) inhibitors,braf inhibitors,azathioprine,cyclosporine
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: cutaneous squamous cell carcinoma, immunotherapy, epidermal growth factor receptor (egfr) inhibitors, braf inhibitors, azathioprine, cyclosporine

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