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Tumor Angiogenesis

  • Chapter
Melanoma

Part of the book series: Current Clinical Oncology ((CCO))

Abstract

As early as the 1960s, the observation of hyperemia and increased vascularity of tumors was considered to be due to a dilation of pre-existing host vessels stimulated by necrotic tumor products (1,2). Despite early reports, that suggested this phenomenon could result from induction of new vessels rather than vasodilation (3,4),a debate persisted about whether tumors were supplied by existing vessels or by neovascularization. Subsequent experiments, in which a transparent chamber was implanted into a rabbit ear, permitted the observation of angiogenesis in vivo (5).Critical experiments which marked a turning point in the field were initiated in 1963 by Folkman and his collaborators (6, 7). They showed that tumors, implanted into isolated perfused organs, were restricted in their growth to spheroids of about 1 mm3 or less. This limited growth was accompanied by a complete absence of angiogenesis, due to a degeneration of capillary endothelium following prolonged perfusion. However, when the tumor spheroid was transplanted to the mouse strain from which it originated, the tumors became vascularized and grew rapidly beyond the 1 mm3 limit and killed their hosts.

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Authors
  1. Bela Anand-Apte MBBS,PhD
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  2. Paul L. Fox PhD
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Editors and Affiliations

  1. Center for Cancer Drug Discovery and Development, Taussig Cancer Center, The Cleveland Clinic Foundation, Cleveland, OH, USA

    Ernest C. Borden MD (Director) (Director)

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© 2002 Humana Press Inc.,Totowa, NJ

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Anand-Apte, B., Fox, P.L. (2002). Tumor Angiogenesis. In: Borden, E.C. (eds) Melanoma. Current Clinical Oncology. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-159-6_12

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  • DOI: https://doi.org/10.1007/978-1-59259-159-6_12

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