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Sporadic Cancers

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The Molecular Basis of Human Cancer

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Abstract

The majority of cancers develop sporadically. In contrast to hereditary cancers with a single genetic factor of high penetrance, the reason why sporadic cancer develops seems to be multifold. In a minority of sporadic cancers, a single etiologic factor can be identified. However, in most sporadic cancers an unknown number of factors, which are alone neither necessary nor sufficient to cause malignant transformation, act together and increase the susceptibility to one or more specific malignancies. This may be achieved by direct interaction such as DNA damage through ionizing radiation or genotoxic compounds or by indirect interaction such as reduced immunocompetence and subsequently limited immunoclearance of malignant cells or cancerogenic viruses such as the Human Papilloma Virus (HPV). In the end, all of these factors influence malignant transformation by genetic and/or epigenetic events and subsequently cause loss of cell proliferation control. In this respect, gatekeeping genes, i.e., those genes that are directly regulating the growth of cells, are frequently mutated in sporadic cancers through somatic mutations, as well as through germ-line mutations in predisposed individuals. Thus, there seems to be a gradual, but not a principal difference between cancerogenic pathways in sporadic and hereditary cancers.

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Authors and Affiliations

  1. Department of Obstetrics and Gynecology, Ruhr University Bochum, Hoelkeskampring 40, 44625, Herne, Germany

    Clemens B. Tempfer M.D., M.B.A.

  2. Department of Surgery, University of Tübingen, Tübingen, Germany

    Marc-André Reymond M.D., M.B.A.

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  1. Clemens B. Tempfer M.D., M.B.A.
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Correspondence to Clemens B. Tempfer M.D., M.B.A. .

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Editors and Affiliations

  1. Department of Pathology and Laboratory Medicine, Curriculum in Toxicology, UNC Program in Translational Medicine, UNC Lineberger Comprehensive Center, University of North Carolina School of Medicine, Chapel Hill, North Carolina, USA

    William B. Coleman

  2. Laboratory for Clinical Genomics and Advanced Technology (CGAT), Department of Pathology and Laboratory Medicine, Dartmouth-Hitchcock Medical Center, Norris Cotton Cancer Center, Geisel School of Medicine at Dartmouth, Lebanon, Hanover, New Hampshire, USA

    Gregory J. Tsongalis

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Tempfer, C.B., Reymond, MA. (2017). Sporadic Cancers. In: Coleman, W., Tsongalis, G. (eds) The Molecular Basis of Human Cancer. Humana Press, New York, NY. https://doi.org/10.1007/978-1-59745-458-2_21

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