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Oncogenes in Renal Cell Carcinoma

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Biology of Renal Cell Carcinoma

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Abstract

Recent molecular studies have demonstrated that the accumulation of a variety of genetic aberrations is necessary for the initiation and progression of human cancers. This is consistent with the “multistep carcinogenesis” hypothesis, and accounts for the exponential relationship between the incidence rate and the age of onset of human cancers (1,2). Two types of genes have been implicated in the development of human cancers: oncogenes and tumor suppressor genes. The former can promote tumorigenesis by gene activation in a dominant mode. The latter contributes to tumor formation in a recessive or a dominant- present, 70 to 80 oncogenes and about 10 tumor suppressor genes have been identified. Although the activation of certain oncogenes definitely has an important role in the genesis of leukemias or lymphomas, it is widely accepted that the more frequently mutated genes are tumor suppressor genes in most human cancers (3). However, since tumor suppressor genes, like oncogenes, encode the proteins essential for cell differentiation and proliferation, both genes may be involved in the same control mechanism which regulates normal cell growth.

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Authors and Affiliations

  1. Kyoto University, Kyoto, Japan

    Osamu Yoshida M.D., Tomonori Habuchi M.D., Hidefumi Kinoshita M.D. & Osamu Ogawa M.D.

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  1. Osamu Yoshida M.D.
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  2. Tomonori Habuchi M.D.
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  3. Hidefumi Kinoshita M.D.
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  4. Osamu Ogawa M.D.
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© 1995 Springer-Verlag New York Inc.

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Yoshida, O., Habuchi, T., Kinoshita, H., Ogawa, O. (1995). Oncogenes in Renal Cell Carcinoma. In: Biology of Renal Cell Carcinoma. Springer, New York, NY. https://doi.org/10.1007/978-1-4612-2536-2_3

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  • DOI: https://doi.org/10.1007/978-1-4612-2536-2_3

  • Publisher Name: Springer, New York, NY

  • Print ISBN: 978-1-4612-7571-8

  • Online ISBN: 978-1-4612-2536-2

  • eBook Packages: Springer Book Archive

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