Abstract
Heat shock proteins (Hsp) participate in many events related to cancer as molecular chaperones, starting from the very beginning of carcinogenesis. Several etiological factors involve the Hsp family in their mechanisms of action, including oncogenic viruses, hereditary and non hereditary alterations in tumor suppressors or oncoproteins, hypermethylation, radiation and carcinogenic agents. All of them produce changes in the Hsp response with consequences in cell proliferation, differentiation, inflammation, apoptosis, DNA repair, angiogenesis, metastasis, and drug resistance and in the immunological response mounted by the host. In this chapter we will examine the participation of the Hsp response in tumor cell transformation, either by up-regulation or down-regulation of specific Hsp. This can explain the variations in Hsp expression found in pre-neoplastic and neoplastic human tumors in different tissues and organs. These variations have important clinical consequences in cancer progression, and the exploitation of such knowledge may improve anticancer treatment strategies
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Ciocca, D.R., Fanelli, M.A., Cuello-CarriĆ³n, F.D., Calderwood, S.K. (2007). Implications of Heat Shock Proteins in Carcinogenesis and Cancer Progression. In: Calderwood, S.K., Sherman, M.Y., Ciocca, D.R. (eds) Heat Shock Proteins in Cancer. Heat Shock Proteins, vol 2. Springer, Dordrecht. https://doi.org/10.1007/978-1-4020-6401-2_2
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