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Skin Cancer and Melanoma

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (28 February 2022) | Viewed by 34842

Special Issue Editors

Department of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan
Interests: skin cancer; dermatopathology; skin surgery
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The skin is the outermost part of the body, and is an area where various external and internal stimuli interact. Various malignant tumors may arise from epidermal keratinocytes, melanocytes, skin appendages, and dermal mesenchymal cells. The malignant tumors include cutaneous squamous cell carcinoma, basal cell carcinoma, melanoma, sebaceous carcinoma, hidradenocarcinoma, extramammary Paget disease, Merkel cell carcinoma, angiosarcoma, and dermatofibrosarcoma protuberans. Recent developments in immunotherapy and molecular targeted therapy have revolutionized the treatment of skin cancers and dramatically improved patient survival. Dysregulated signaling pathways are crucial factors of uncontrolled tumor proliferation and malignant transformation in skin cancer.

In this Special Issue of IJMS, we will publish cutting-edge information regarding diagnosis, therapy, and prevention, especially related to skin cancer and melanoma. We will also shed light on skin cancer signaling pathways. We warmly welcome submissions, including original papers and reviews.

Dr. Takamichi Ito
Prof. Dr. Masutaka Furue
Guest Editors

Manuscript Submission Information

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Keywords

  • Melanoma
  • Cutaneous squamous cell carcinoma
  • Basal cell carcinoma
  • Sebaceous carcinoma
  • Hidradenocarcinoma
  • Extramammary paget disease
  • Merkel cell carcinoma
  • Angiosarcoma and dermatofibrosarcoma protuberans;
  • Treatment
  • Diagnosis
  • Prevention
  • Immunotherapy
  • Target therapy
  • Radiotherapy
  • Chemotherapy

Published Papers (11 papers)

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Research

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13 pages, 7243 KiB  
Article
IL-17A Is the Critical Cytokine for Liver and Spleen Amyloidosis in Inflammatory Skin Disease
by Shohei Iida, Takehisa Nakanishi, Fumiyasu Momose, Masako Ichishi, Kento Mizutani, Yoshiaki Matsushima, Ai Umaoka, Makoto Kondo, Koji Habe, Yoshifumi Hirokawa, Masatoshi Watanabe, Yoichiro Iwakura, Yoshihiro Miyahara, Yasutomo Imai and Keiichi Yamanaka
Int. J. Mol. Sci. 2022, 23(10), 5726; https://doi.org/10.3390/ijms23105726 - 20 May 2022
Cited by 7 | Viewed by 2020
Abstract
Systemic amyloidosis is recognized as a serious complication of rheumatoid arthritis or inflammatory bowel disease, but also of inflammatory skin disease. However, the detailed molecular mechanism of amyloidosis associated with cutaneous inflammation remains unclear, and therapeutic approaches are limited. Here, we investigated the [...] Read more.
Systemic amyloidosis is recognized as a serious complication of rheumatoid arthritis or inflammatory bowel disease, but also of inflammatory skin disease. However, the detailed molecular mechanism of amyloidosis associated with cutaneous inflammation remains unclear, and therapeutic approaches are limited. Here, we investigated the pathophysiology of amyloidosis secondary to cutaneous inflammation and the therapeutic effects of Janus kinase (JAK) inhibitors by examining a mouse model of spontaneous dermatitis (KCASP1Tg mice). Moreover, KCASP1Tg mice were crossed with interleukin-17A (IL-17A) knockout mice to generate IL-17A-/KCASP1Tg and examine the role of IL-17A in amyloidosis under cutaneous inflammation. KCASP1Tg mice showed severe amyloid deposition in the liver and spleen. Increased serum-neutral fat levels and decreased lymphocyte production were observed in the spleen. Overproduction of amyloidosis was partially ameliorated by the administration of JAK inhibitors and was further improved in IL-17A-/KCASP1Tg mice. IL-17A-producing cells included CD4, gamma delta, and CD8 T cells. In summary, our results from the analysis of a mouse model of dermatitis revealed that skin-derived inflammatory cytokines can induce amyloid deposition in the liver and spleen, and that the administration of JAK inhibitors and, even more, IL-17A ablation, reduced amyloidosis. This study demonstrates that active control of skin inflammation is essential to prevent internal organ amyloidosis. Full article
(This article belongs to the Special Issue Skin Cancer and Melanoma)
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15 pages, 8433 KiB  
Article
Expression of NGF/proNGF and Their Receptors TrkA, p75NTR and Sortilin in Melanoma
by Mark Marsland, Amiee Dowdell, Chen Chen Jiang, James S. Wilmott, Richard A. Scolyer, Xu Dong Zhang, Hubert Hondermarck and Sam Faulkner
Int. J. Mol. Sci. 2022, 23(8), 4260; https://doi.org/10.3390/ijms23084260 - 12 Apr 2022
Cited by 8 | Viewed by 2459
Abstract
There is increasing evidence that nerve growth factor (NGF) and its receptors, the neurotrophic receptor tyrosine kinase 1 (NTRK1/TrkA), the common neurotrophin receptor (NGFR/p75NTR) and the membrane receptor sortilin, participate in cancer growth. In melanoma, there have been some reports suggesting [...] Read more.
There is increasing evidence that nerve growth factor (NGF) and its receptors, the neurotrophic receptor tyrosine kinase 1 (NTRK1/TrkA), the common neurotrophin receptor (NGFR/p75NTR) and the membrane receptor sortilin, participate in cancer growth. In melanoma, there have been some reports suggesting that NGF, TrkA and p75NTR are dysregulated, but the expression of the NGF precursor (proNGF) and its membrane receptor sortilin is unknown. In this study, we investigated the expression of NGF, proNGF, TrkA, p75NTR and sortilin by immunohistochemistry in a series of human tissue samples (n = 100), including non-cancerous nevi (n = 20), primary melanomas (n = 40), lymph node metastases (n = 20) and distant metastases (n = 20). Immunostaining was digitally quantified and revealed NGF and proNGF were expressed in all nevi and primary melanomas, and that the level of expression decreased from primary tumors to melanoma metastases (p = 0.0179 and p < 0.0001, respectively). Interestingly, TrkA protein expression was high in nevi and thin primary tumors but was strongly downregulated in thick primary tumors (p < 0.0001) and metastases (p < 0.0001). While p75NTR and sortilin were both expressed in most nevi and melanomas, there was no significant difference in expression between them. Together, these results pointed to a downregulation of NGF/ProNGF and TrkA in melanoma, and thus did not provide evidence to support the use of anti-proNGF/NGF or anti-TrkA therapies in advanced and metastatic forms of melanoma. Full article
(This article belongs to the Special Issue Skin Cancer and Melanoma)
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17 pages, 3425 KiB  
Article
Hyperthermia Enhances Doxorubicin Therapeutic Efficacy against A375 and MNT-1 Melanoma Cells
by Diana Salvador, Verónica Bastos and Helena Oliveira
Int. J. Mol. Sci. 2022, 23(1), 35; https://doi.org/10.3390/ijms23010035 - 21 Dec 2021
Cited by 11 | Viewed by 2698
Abstract
Melanoma is the deadliest form of skin cancer, and its incidence has alarmingly increased in the last few decades, creating a need for novel treatment approaches. Thus, we evaluated the combinatorial effect of doxorubicin (DOX) and hyperthermia on A375 and MNT-1 human melanoma [...] Read more.
Melanoma is the deadliest form of skin cancer, and its incidence has alarmingly increased in the last few decades, creating a need for novel treatment approaches. Thus, we evaluated the combinatorial effect of doxorubicin (DOX) and hyperthermia on A375 and MNT-1 human melanoma cell lines. Cells were treated with DOX for 24, 48, and 72 h and their viabilities were assessed. The effect of DOX IC10 and IC20 (combined at 43 °C for 30, 60, and 120 min) on cell viability was further analyzed. Interference on cell cycle dynamics, reactive oxygen species (ROS) production, and apoptosis upon treatment (with 30 min at 43 °C and DOX at the IC20 for 48 h) were analyzed by flow cytometry. Combined treatment significantly decreased cell viability, but not in all tested conditions, suggesting that the effect depends on the drug concentration and heat treatment duration. Combined treatment also mediated a G2/M phase arrest in both cell lines, as well as increasing ROS levels. Additionally, it induced early apoptosis in MNT-1 cells, while in A375 cells this effect was similar to the one caused by hyperthermia alone. These findings demonstrate that hyperthermia enhances DOX effect through cell cycle arrest, oxidative stress, and apoptotic cell death. Full article
(This article belongs to the Special Issue Skin Cancer and Melanoma)
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15 pages, 6991 KiB  
Article
Cabozantinib Is Effective in Melanoma Brain Metastasis Cell Lines and Affects Key Signaling Pathways
by Trond Are Mannsåker, Tuyen Hoang, Synnøve Nymark Aasen, Ole Vidhammer Bjørnstad, Himalaya Parajuli, Terje Sundstrøm and Frits Alan Thorsen
Int. J. Mol. Sci. 2021, 22(22), 12296; https://doi.org/10.3390/ijms222212296 - 14 Nov 2021
Cited by 2 | Viewed by 2691
Abstract
Melanomas have a high potential to metastasize to the brain. Recent advances in targeted therapies and immunotherapies have changed the therapeutical landscape of extracranial melanomas. However, few patients with melanoma brain metastasis (MBM) respond effectively to these treatments and new therapeutic strategies are [...] Read more.
Melanomas have a high potential to metastasize to the brain. Recent advances in targeted therapies and immunotherapies have changed the therapeutical landscape of extracranial melanomas. However, few patients with melanoma brain metastasis (MBM) respond effectively to these treatments and new therapeutic strategies are needed. Cabozantinib is a receptor tyrosine kinase (RTK) inhibitor, already approved for the treatment of non-skin-related cancers. The drug targets several of the proteins that are known to be dysregulated in melanomas. The anti-tumor activity of cabozantinib was investigated using three human MBM cell lines. Cabozantinib treatment decreased the viability of all cell lines both when grown in monolayer cultures and as tumor spheroids. The in vitro cell migration was also inhibited and apoptosis was induced by cabozantinib. The phosphorylated RTKs p-PDGF-Rα, p-IGF-1R, p-MERTK and p-DDR1 were found to be downregulated in the p-RTK array of the MBM cells after cabozantinib treatment. Western blot validated these results and showed that cabozantinib treatment inhibited p-Akt and p-MEK 1/2. Further investigations are warranted to elucidate the therapeutic potential of cabozantinib for patients with MBM. Full article
(This article belongs to the Special Issue Skin Cancer and Melanoma)
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13 pages, 2487 KiB  
Article
Prognostic Role of Tumoral PD-L1 and IDO1 Expression, and Intratumoral CD8+ and FoxP3+ Lymphocyte Infiltrates in 132 Primary Cutaneous Merkel Cell Carcinomas
by Piotr Donizy, Cheng-Lin Wu, Janusz Kopczynski, Malgorzata Pieniazek, Przemyslaw Biecek, Janusz Ryś and Mai P. Hoang
Int. J. Mol. Sci. 2021, 22(11), 5489; https://doi.org/10.3390/ijms22115489 - 23 May 2021
Cited by 7 | Viewed by 1889
Abstract
The association of immune markers and clinicopathologic features and patient outcome has not been extensively studied in Merkel cell carcinoma (MCC). We correlated tumoral PD-L1 and IDO1 expression, and intratumoral CD8+ and FoxP3+ lymphocytes count with clinicopathologic variables, Merkel cell polyomavirus (MCPyV) status, [...] Read more.
The association of immune markers and clinicopathologic features and patient outcome has not been extensively studied in Merkel cell carcinoma (MCC). We correlated tumoral PD-L1 and IDO1 expression, and intratumoral CD8+ and FoxP3+ lymphocytes count with clinicopathologic variables, Merkel cell polyomavirus (MCPyV) status, and patient outcomes in a series of 132 MCC. By univariate analyses, tumoral PD-L1 expression >1% and combined tumoral PD-L1 >1% and high intratumoral FoxP3+ lymphocyte count correlated with improved overall survival (OS) (p = 0.016, 0.0072), MCC-specific survival (MSS) (p = 0.019, 0.017), and progression-free survival (PFS) (p = 0.043, 0.004, respectively). High intratumoral CD8+ and FoxP3+ lymphocyte count correlated with longer MSS (p = 0.036) and improved PFS (p = 0.047), respectively. Ulceration correlated with worse OS and worse MSS. Age, male gender, and higher stage (3 and 4) significantly correlated with worse survival. MCPyV positivity correlated with immune response. By multivariate analyses, only ulceration and age remained as independent predictors of worse OS; gender and stage remained for shorter PFS. Tumoral PD-L1 expression and increased density of intratumoral CD8+ lymphocytes and FoxP+ lymphocytes may represent favorable prognosticators in a subset of MCCs. Tumoral PD-L1 expression correlated with intratumoral CD8+ and FoxP3+ lymphocytes, which is supportive of an adaptive immune response. Full article
(This article belongs to the Special Issue Skin Cancer and Melanoma)
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11 pages, 2470 KiB  
Communication
Targeting SIRT2 Sensitizes Melanoma Cells to Cisplatin via an EGFR-Dependent Mechanism
by Iwona Karwaciak, Anna Sałkowska, Kaja Karaś, Jarosław Dastych and Marcin Ratajewski
Int. J. Mol. Sci. 2021, 22(9), 5034; https://doi.org/10.3390/ijms22095034 - 10 May 2021
Cited by 6 | Viewed by 2559
Abstract
Melanoma cells are resistant to most anticancer chemotherapeutics. Despite poor response rates and short-term efficacy, chemotherapy remains the main approach to treating this cancer. The underlying mechanisms of the intrinsic chemoresistance of melanoma remain unclear, but elucidating these mechanisms is important to improve [...] Read more.
Melanoma cells are resistant to most anticancer chemotherapeutics. Despite poor response rates and short-term efficacy, chemotherapy remains the main approach to treating this cancer. The underlying mechanisms of the intrinsic chemoresistance of melanoma remain unclear, but elucidating these mechanisms is important to improve the efficacy of chemotherapy regimens. Increasing evidence suggests that sirtuin 2 (SIRT2) plays a key role in the response of melanoma cells to chemotherapeutics; thus, in the present study, we evaluated the impact of shRNA-mediated and pharmacological inhibition of SIRT2 on the sensitivity of melanoma cells to cisplatin, which is used in several regimens to treat melanoma patients. We found that cells with SIRT2 inhibition revealed increased sensitivity to cisplatin and exhibited increased accumulation of γ-H2AX and reduced EGFR-AKT-RAF-ERK1/2 (epidermal growth factor receptor-protein B kinase–RAF kinase-extracellular signal-regulated kinase 1/2) pathway signaling compared to control cells. Thus, our results show that sirtuin 2 inhibition increased the in vitro efficacy of cisplatin against melanoma cells. Full article
(This article belongs to the Special Issue Skin Cancer and Melanoma)
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20 pages, 18690 KiB  
Article
Celecoxib as a Valuable Adjuvant in Cutaneous Melanoma Treated with Trametinib
by Diana Valentina Tudor, Ioana Bâldea, Diana Elena Olteanu, Eva Fischer-Fodor, Virag Piroska, Mihai Lupu, Tudor Călinici, Roxana Maria Decea and Gabriela Adriana Filip
Int. J. Mol. Sci. 2021, 22(9), 4387; https://doi.org/10.3390/ijms22094387 - 22 Apr 2021
Cited by 10 | Viewed by 2980
Abstract
Background: Melanoma patients stop responding to targeted therapies mainly due to mitogen activated protein kinase (MAPK) pathway re-activation, phosphoinositide 3 kinase/the mechanistic target of rapamycin (PI3K/mTOR) pathway activation or stromal cell influence. The future of melanoma treatment lies in combinational approaches. To address [...] Read more.
Background: Melanoma patients stop responding to targeted therapies mainly due to mitogen activated protein kinase (MAPK) pathway re-activation, phosphoinositide 3 kinase/the mechanistic target of rapamycin (PI3K/mTOR) pathway activation or stromal cell influence. The future of melanoma treatment lies in combinational approaches. To address this, our in vitro study evaluated if lower concentrations of Celecoxib (IC50 in nM range) could still preserve the chemopreventive effect on melanoma cells treated with trametinib. Materials and Methods: All experiments were conducted on SK-MEL-28 human melanoma cells and BJ human fibroblasts, used as co-culture. Co-culture cells were subjected to a celecoxib and trametinib drug combination for 72 h. We focused on the evaluation of cell death mechanisms, melanogenesis, angiogenesis, inflammation and resistance pathways. Results: Low-dose celecoxib significantly enhanced the melanoma response to trametinib. The therapeutic combination reduced nuclear transcription factor (NF)–kB (p < 0.0001) and caspase-8/caspase-3 activation (p < 0.0001), inhibited microphthalmia transcription factor (MITF) and tyrosinase (p < 0.05) expression and strongly down-regulated the phosphatidylinositol-3-kinase/protein kinase B (PI3K/AKT) signaling pathway more significantly than the control or trametinib group (p < 0.0001). Conclusion: Low concentrations of celecoxib (IC50 in nM range) sufficed to exert antineoplastic capabilities and enhanced the therapeutic response of metastatic melanoma treated with trametinib. Full article
(This article belongs to the Special Issue Skin Cancer and Melanoma)
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17 pages, 3284 KiB  
Article
NECTIN4: A Novel Therapeutic Target for Melanoma
by Yuka Tanaka, Maho Murata, Che-Hung Shen, Masutaka Furue and Takamichi Ito
Int. J. Mol. Sci. 2021, 22(2), 976; https://doi.org/10.3390/ijms22020976 - 19 Jan 2021
Cited by 21 | Viewed by 4203
Abstract
Malignant melanoma is the most common lethal skin cancer and causes death in a short time when metastasized. Although BRAF inhibitors (BRAFi) have greatly improved the prognosis of BRAF-mutated melanoma, drug resistance is a major concern even when they are combined with MEK [...] Read more.
Malignant melanoma is the most common lethal skin cancer and causes death in a short time when metastasized. Although BRAF inhibitors (BRAFi) have greatly improved the prognosis of BRAF-mutated melanoma, drug resistance is a major concern even when they are combined with MEK inhibitors. Alternative treatments for BRAFi-resistant melanoma are highly anticipated. Nectin cell adhesion molecule 4 (NECTIN4) is highly expressed and associated with progression in tumors. We aimed to investigate the role of NECTIN4 in melanoma and its potency as a therapeutic target using 126 melanoma samples and BRAFi-resistant cells. Immunohistochemically, most of the clinical samples expressed NECTIN4, at least in part. NECTIN4 was highly expressed in BRAF-mutated melanoma and its high expression was associated with disease-free survival. In BRAFi-resistant melanoma cells, NECTIN4 and the PI3K/Akt pathway were upregulated, along with the acquisition of BRAFi resistance. Monomethyl auristatin E, a cytotoxic part of NECTIN4-targeted antibody–drug conjugate, was effective for BRAF-mutated or BRAFi-resistant melanoma cells. NECTIN4 inhibition increased the sensitivity of BRAFi-resistant cells to BRAFi and induced apoptosis. In conclusion, we revealed the expression and roles of NECTIN4 in melanoma. Targeted therapies against NECTIN4 can be a novel treatment strategy for melanoma, even after the acquisition of BRAFi resistance. Full article
(This article belongs to the Special Issue Skin Cancer and Melanoma)
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15 pages, 1016 KiB  
Article
In Cellulo Evaluation of the Therapeutic Potential of NHC Platinum Compounds in Metastatic Cutaneous Melanoma
by Elsa Charignon, Mathilde Bouché, Caroline Clave-Darcissac, Georges Dahm, Gabriel Ichim, Anthony Clotagatide, Hichem C. Mertani, Philippe Telouk, Julie Caramel, Jean-Jacques Diaz, Stéphane Bellemin-Laponnaz, Philippe Bouvet and Claire Billotey
Int. J. Mol. Sci. 2020, 21(21), 7826; https://doi.org/10.3390/ijms21217826 - 22 Oct 2020
Cited by 3 | Viewed by 2219
Abstract
We describe here the evaluation of the cytotoxic efficacy of two platinum (II) complexes bearing an N-heterocyclic carbene (NHC) ligand, a pyridine ligand and bromide or iodide ligands on a panel of human metastatic cutaneous melanoma cell lines representing different genetic subsets including [...] Read more.
We describe here the evaluation of the cytotoxic efficacy of two platinum (II) complexes bearing an N-heterocyclic carbene (NHC) ligand, a pyridine ligand and bromide or iodide ligands on a panel of human metastatic cutaneous melanoma cell lines representing different genetic subsets including BRAF-inhibitor-resistant cell lines, namely A375, SK-MEL-28, MeWo, HMCB, A375-R, SK-MEL-5-R and 501MEL-R. Cisplatin and dacarbazine were also studied for comparison purposes. Remarkably, the iodine-labelled Pt-NHC complex strongly inhibited proliferation of all tested melanoma cells after 1-h exposure, likely due to its rapid uptake by melanoma cells. The mechanism of this inhibitory activity involves the formation of DNA double-strand breaks and apoptosis. Considering the intrinsic chemoresistance of metastatic melanoma cells of current systemic treatments, these findings are promising and could give research opportunities in the future to improve the prognosis of patients suffering from unresectable metastatic melanoma that are not eligible or that do not respond to the most effective drugs available to date, namely BRAF inhibitors and the anti-PD-1 monoclonal antibody (mAb). Full article
(This article belongs to the Special Issue Skin Cancer and Melanoma)
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10 pages, 1829 KiB  
Article
NECTIN4 Expression in Extramammary Paget’s Disease: Implication of a New Therapeutic Target
by Maho Murata, Takamichi Ito, Yuka Tanaka, Yumiko Kaku-Ito and Masutaka Furue
Int. J. Mol. Sci. 2020, 21(16), 5891; https://doi.org/10.3390/ijms21165891 - 16 Aug 2020
Cited by 20 | Viewed by 2709
Abstract
Extramammary Paget’s disease (EMPD) is a rare skin cancer arising in the anogenital area. Most EMPD tumors remain dormant as in situ lesions, but the outcomes of patients with metastatic EMPD are poor because of the lack of effective systemic therapies. Nectin cell [...] Read more.
Extramammary Paget’s disease (EMPD) is a rare skin cancer arising in the anogenital area. Most EMPD tumors remain dormant as in situ lesions, but the outcomes of patients with metastatic EMPD are poor because of the lack of effective systemic therapies. Nectin cell adhesion molecule 4 (NECTIN4) has attracted attention as a potential therapeutic target for some cancers. Urothelial cancer is one such cancer, and clinical trials of enfortumab vedotin, a drug-conjugated anti-NECTIN4 antibody, are ongoing. However, little is known regarding the role of NECTIN4 in EMPD. In this study, we conducted immunohistochemical analysis of NECTIN4 expression in 110 clinical EMPD samples and normal skin tissue. In normal skin, positive signals were observed in epidermal keratinocytes (particularly in the lower part of the epidermis), eccrine and apocrine sweat glands, inner and outer root sheaths, and matrix of the hair follicles. The most EMPD lesions exhibited strong NECTIN4 expression, and high NECTIN4 expression was significantly associated with increased tumor thickness, advanced TNM stage, and worse disease-specific survival. These results support the potential use of NECTIN4-targeted therapy for EMPD. Our report contributes to the better understanding of the pathobiology of NECTIN4 in the skin and the skin-related adverse effects of NECTIN4-targeted therapy. Full article
(This article belongs to the Special Issue Skin Cancer and Melanoma)
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Review

Jump to: Research

28 pages, 1386 KiB  
Review
Molecular Mechanisms of Cutaneous Squamous Cell Carcinoma
by Matthew L. Hedberg, Corbett T. Berry, Ata S. Moshiri, Yan Xiang, Christopher J. Yeh, Cem Attilasoy, Brian C. Capell and John T. Seykora
Int. J. Mol. Sci. 2022, 23(7), 3478; https://doi.org/10.3390/ijms23073478 - 23 Mar 2022
Cited by 24 | Viewed by 6530
Abstract
Non-melanoma skin cancers are cutaneous malignancies representing the most common form of cancer in the United States. They are comprised predominantly of basal cell carcinomas and squamous cell carcinomas (cSCC). The incidence of cSCC is increasing, resulting in substantial morbidity and ever higher [...] Read more.
Non-melanoma skin cancers are cutaneous malignancies representing the most common form of cancer in the United States. They are comprised predominantly of basal cell carcinomas and squamous cell carcinomas (cSCC). The incidence of cSCC is increasing, resulting in substantial morbidity and ever higher treatment costs; currently in excess of one billion dollars, per annum. Here, we review research defining the molecular basis and development of cSCC that aims to provide new insights into pathogenesis and drive the development of novel, cost and morbidity saving therapies. Full article
(This article belongs to the Special Issue Skin Cancer and Melanoma)
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