Skin cancer represents the most frequent cancer in humans and includes different entities, based on the cell types and tissues affected. Next to epithelial tumors, such as keratinocyte-derived basal cell carcinomas (BCC) and squamous cell carcinomas (SCC), and neuroendocrine Merkel cell carcinoma (MCC), skin malignancies also include neuroectodermal malignant melanoma (MM), as well as tumors of skin-associated tissues, lipomas, angiosarcomas, tumors of connective tissue, and cutaneous lymphomas. Ultraviolet (UV) radiation is an important risk factor for epithelial tumors and MM, because most of the tumor lesions occur in sun-exposed skin areas and contain UV signature mutations [1, 2]. However, some tumors are located in sun-protected body areas, indicating other factors involved in carcinogenesis.
Access provided by Autonomous University of Puebla. Download to read the full chapter text
Chapter PDF
Similar content being viewed by others
Keywords
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
Reference
Ziegler A, Leffell DJ, Kunala S et al. (1993) Mutation hotspots due to sunlight in the p53 gene of nonmelanoma skin cancer. Proc Natl Acad Sci USA 90:4216–4220.
Popp S, Waltering S, Herbst C et al (2002) UV-B-type mutations and chromosomal imbalances indicate common pathways for the development of Merkel and squamous cell carcinomas. Int J Cancer 99:352–360.
Rubin AI, Chen EH, Ratner D (2005) Basal cell carcinoma. N Engl J Med 353:2262–2269.
Harwood CA, Proby CM (2002) Human papillomaviruses and non-melanoma skin cancer. Curr Opin Infect Dis 15:101–114.
Cleaver JE (1968) Defective repair replication of DNA in xeroderma pigmentosum. Nature (Lond) 218:652–656.
Millikan RC, Hummer A, Begg C et al. (2006) Polymorphisms in nucleotide excision repair genes and risk of multiple primary melanoma: the genes environment and melanoma study. Carcinogenesis (Oxf) 27:610–618.
Gailini MR, Stahle-Backdahl M, Leffell DJ (1996) The role of the human homologue of Drosophila patched in sporadic basal cell carcinomas. Nat Genet 14:78–81.
Crawson AN (2006) Basal cell carcinoma: biology, morphology, and clinical implications. Mod Pathol 19:S127–S147.
Xie J, Murone M, Luoh SM et al. (1996) Activating smoothened mutations in sporadic basal cell carcinomas. Nature (Lond) 391:90–92.
Chin L (2003) The genetics of malignant melanoma: lessons from mouse and man. Nat Rev Cancer 3:559–570.
Landi MT, Kanetsky PA, Tsang S et al. (2005) MC1R, ASIP, and DNA repair in sporadic and familial melanoma in a Mediterranean population. J Natl Cancer Inst 97:998–1007.
Liboutet M, Portela M, Delestaing G et al. (2006) MC1R and PTCH gene polymorphism in French patients with basal cell carcinoma. J Invest Dermatol 126:1510–1517.
Cho KR, Hedrick L (1997) Genetic alterations in human tumors. Curr Top Microbiol Immunol 221:149–176.
Kumar R, Angelini S, Snellman E, Hemminki K (2004) BRAF-mutations ar common somatic events in melanocytic nevi. J Invest Dermatol 122:342–348.
Wu H, Goel V, Haluska FG (2003) PTEN signaling pathways in melanoma. Oncogene 22:3113–3122.
Kraehn GM, Utikal J, Udart M et al. (2001) Extra c-myc oncogene copies in high risk cutaneous malignant melanoma metastases. Br J Cancer 84:72–79.
Li G, Schaider H, Satyamoorthy K et al. (2001) Downregulation of E-cadherin and Desmoglein 1 by autocrine hepatocyte growth factor during melanoma development. Oncogene 20:8125–8135.
Jin Y, Jin C, Salemark L et al. (2002) Clonal chromosome abnormalities in premalignant lesions of the skin. Cancer Genet Cytogenet 136:48–52.
Ashton KJ, Weinstein SR, Maguire DJ, Griffith LR (2003) Chromosomal aberrations in squamous cell carcinomas and solar keratoses revealed by genomic hybridization. Arch Dermatol 139:876–882.
Boukamp P, Popp S, Altmeyer S et al. (1997) Sustained nontumorigenic phenotype correlates with a largely stable chromosome content during long-term culture of the human keratinocyte line HaCaT. Genes Chromosomes Cancer 19:201–214.
Boukamp P (2005) UV-induced skin cancer: similarities – variations. JDDG (J German Soc Dermatol) (J Dtsch Dermatol Ges)3:493–503.
Burnworth B, Popp S, Stark HJ et al. (2006) Gain of 11q/cyclin D1 overexpression is an essential early step in skin cancer development and causes abnormal tissue organization and differentiation. Oncogene 25:4399–4412.
Obermueller E, Vosseler S, Fusenig NE, Mueller MM (2004) Cooperative autocrine and paracrine functions of granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor in the progression of skin cancer cells. Cancer Res 64:7801–7812.
Good DJ, Polverini PJ, Rastinejad F et al. (1990) A tumor suppressor dependent inhibitor of angiogenesis is immunologically and functionally indistinguishable from a fragment of thrombospondin. Proc Natl Acad Sci U S A 87:6624–6628.
Bleuel K, Popp S, Fusenig NE et al. (1999) Tumor suppression in human skin carcinoma cells by chromosome 15 transfer or thrombospondin-1 overexpression through halted tumor vascularization. Proc Natl Acad Sci U S A 96:2065–2070.
Mueller MM, Peter W, Mappes M et al. (2001) Tumor progression of skin carcinoma cells in vivo promoted by clonal selection, mutagenesis, and autocrine growth regulation by granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor. Am J Pathol 159:1567–1569.
Nindl I, Dang C, Forschner T et al. (2006) Identification of differentially expressed genes in cutaneous squamous cell carcinoma by microarray expression profiling. Mol Cancer 5:30.
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2009 Springer Science+Business Media, LLC
About this chapter
Cite this chapter
Meyer, T. (2009). Molecular Events in Skin Cancer. In: Stockfleth, E., Ulrich, C. (eds) Skin Cancer after Organ Transplantation. Cancer Treatment and Research, vol 146. Springer, Boston, MA. https://doi.org/10.1007/978-0-387-78574-5_16
Download citation
DOI: https://doi.org/10.1007/978-0-387-78574-5_16
Publisher Name: Springer, Boston, MA
Print ISBN: 978-0-387-78573-8
Online ISBN: 978-0-387-78574-5
eBook Packages: MedicineMedicine (R0)