Special Issue "Skin Cancer"

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A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (30 November 2012)

Special Issue Editor

Guest Editor
Dr. Chyi-Chia Richard Lee

Laboratory of Pathology, National Cancer Institute, Building 10, Room 2S235J, 10 Center Drive, Bethesda, MD 20892, USA
Website | E-Mail
Fax: +1 301 480 9488
Interests: melanoma; skin cancers; dermatopathology; skin pathology; melanocytic skin lesions

Special Issue Information

Dear Colleagues,

Melanoma and non-melanoma skin cancers are the most common form of cancer in the United States and many other countries.  This special issue of Cancers is an opportunity to report orgininal research and discoveries in the field of skin cancer, such as dermatopathology, treatment, epidemiology, and cancer prevention.

Dr. Chyi-Chia Richard Lee
Guest Editor

Keywords

  • skin cancer
  • cutaneous neoplasm
  • squamous cell carcinoma
  • basal cell carcinoma
  • melanoma
  • adnexal tumors
  • dermatopathology
  • skin cancer diagnosis and treatment
  • skin cancer epidemiology and prevention
  • cutaneous tumor biology
  • skin cancer genetics

Published Papers (2 papers)

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Review

Open AccessReview The Role of the Immune Response in Merkel Cell Carcinoma
Cancers 2013, 5(1), 234-254; doi:10.3390/cancers5010234
Received: 7 December 2012 / Revised: 30 January 2013 / Accepted: 6 February 2013 / Published: 28 February 2013
Cited by 12 | PDF Full-text (1408 KB) | HTML Full-text | XML Full-text
Abstract
Merkel cell carcinoma (MCC) is an aggressive neuroendocrine skin cancer. The Merkel cell polyomavirus (MCPyV) is implicated in its pathogenesis. Immune mechanisms are also implicated. Patients who are immunosuppressed have an increased risk. There is evidence that high intratumoral T-cell counts and immune
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Merkel cell carcinoma (MCC) is an aggressive neuroendocrine skin cancer. The Merkel cell polyomavirus (MCPyV) is implicated in its pathogenesis. Immune mechanisms are also implicated. Patients who are immunosuppressed have an increased risk. There is evidence that high intratumoral T-cell counts and immune transcripts are associated with favorable survival. Spontaneous regressions implicate immune effector mechanisms. Immunogenicity is also supported by observation of autoimmune paraneoplastic syndromes. Case reports suggest that immune modulation, including reduction of immune suppression, can result in tumor regression. The relationships between MCPyV infection, the immune response, and clinical outcome, however, remain poorly understood. Circulating antibodies against MCPyV antigens are present in most individuals. MCPyV-reactive T cells have been detected in both MCC patients and control subjects. High intratumoral T-cell counts are also associated with favorable survival in MCPyV-negative MCC. That the immune system plays a central role in preventing and controlling MCC is supported by several observations. MCCs often develop, however, despite the presence of humoral and cellular immune responses. A better understanding on how MCPyV and MCC evade the immune response will be necessary to develop effective immunotherapies. Full article
(This article belongs to the Special Issue Skin Cancer)
Open AccessReview Mouse Genetic Models Reveal Surprising Functions of IkB Kinase Alpha in Skin Development and Skin Carcinogenesis
Cancers 2013, 5(1), 170-183; doi:10.3390/cancers5010170
Received: 21 November 2012 / Revised: 25 January 2013 / Accepted: 6 February 2013 / Published: 15 February 2013
Cited by 4 | PDF Full-text (503 KB) | HTML Full-text | XML Full-text
Abstract
Gene knockout studies unexpectedly reveal a pivotal role for IkB kinase alpha (IKKa) in mouse embryonic skin development. Skin carcinogenesis experiments show that Ikka heterozygous mice are highly susceptible to chemical carcinogen or ultraviolet B light (UVB) induced benign and malignant skin
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Gene knockout studies unexpectedly reveal a pivotal role for IkB kinase alpha (IKKa) in mouse embryonic skin development. Skin carcinogenesis experiments show that Ikka heterozygous mice are highly susceptible to chemical carcinogen or ultraviolet B light (UVB) induced benign and malignant skin tumors in comparison to wild-type mice. IKKa deletion mediated by keratin 5 (K5).Cre or K15.Cre in keratinocytes induces epidermal hyperplasia and spontaneous skin squamous cell carcinomas (SCCs) in Ikka floxed mice. On the other hand, transgenic mice overexpressing IKKa in the epidermis, under the control of a truncated loricrin promoter or K5 promoter, develop normal skin and show no defects in the formation of the epidermis and other epithelial organs, and the transgenic IKKa represses chemical carcinogen or UVB induced skin carcinogenesis. Moreover, IKKa deletion mediated by a mutation, which generates a stop codon in the Ikka gene, has been reported in a human autosomal recessive lethal syndrome. Downregulated IKKa and Ikka mutations and deletions are found in human skin SCCs. The collective evidence not only highlights the importance of IKKa in skin development, maintaining skin homeostasis, and preventing skin carcinogenesis, but also demonstrates that mouse models are extremely valuable tools for revealing the mechanisms underlying these biological events, leading our studies from bench side to bedside. Full article
(This article belongs to the Special Issue Skin Cancer)

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