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Tumor Cell Complexity and Metabolic Flexibility in Tumorigenesis and Metastasis

  • Chapter
Tumor Cell Metabolism

Abstract

Most cancers originate in a particular cell type within a tissue by accumulating both mutations and epigenetic changes that alter the hierarchical balance of cells within the affected tissue. These changes result in greater self-renewal and proliferation capacity and a tendency to immortalization at the expense of differentiation, senescence, and cell death. Over time, subpopulations of these aberrant cells break tissue boundaries, invade adjacent tissues, suppress the immune system, and spread to other parts of the body. These changes are associated with metabolic remodeling to support a predominantly glycolytic metabolism. This metabolic remodeling occurs while interacting with normal cells in the microenvironment including stromal, vascular, and neural cells and cells of the immune system. Complex tumor biology demands strategic therapeutic approaches that address different aspects of this biology simultaneously and that can be adapted to the ongoing changes in metabolism that underpin tumor progression.

A previous version of this chapter included an incorrect figure (Fig. 2.1. was represented incorrectly). For this reason an erratum has been published, correcting the mistake in the previous version and showing the correct figure (see DOI 10.1007/978-3-7091-1824-5_16).

The version readers currently see is the corrected version with the figure in chapter 2 shown correctly. The reader sees the chapter in its intended form. The Publisher would like to apologize for the earlier mistake.

An erratum to this chapter can be found at http://dx.doi.org/10.1007/978-3-7091-1824-5_16

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Correspondence to Michael V. Berridge .

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Berridge, M.V., Herst, P.M. (2015). Tumor Cell Complexity and Metabolic Flexibility in Tumorigenesis and Metastasis. In: Mazurek, S., Shoshan, M. (eds) Tumor Cell Metabolism. Springer, Vienna. https://doi.org/10.1007/978-3-7091-1824-5_2

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