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Abstract

Cervical cancer is one of the most frequent cancers affecting women worldwide. Infection with human papilloma virus aided by several cofactors is causally related to cervical carcinogenesis. HPV infection is known to influence TGF-β signaling and TGF-β may stimulate normal cervical remodeling and limit HPV-immortalized cervical cell progression. Loss of heterozygosity of chromosomes that harbor Smads and/or TGF-β receptors reported in human cervical cancer suggests that inactivation of their genes may play a role in the progression of cervical carcinoma. Cervical cancer is associated with enhanced production of TGF-β, repression or mutation of TGF-β transmembrane receptors, or loss of expression and/or mutations in Smads. Therapeutic approaches should aim to inhibit the TGF-β-induced invasive phenotype, but also to retain its growth-inhibitory and apoptosis-inducing effects. Interrelationships between TGF-β signaling and HPV oncoproteins as well as latest developments on the molecular alterations in human cervical cancer associated with TGF-β signaling are described in this chapter.

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Karunagaran, D., Jinesh, G. (2008). TGF-β, Smads and Cervical Cancer. In: Jakowlew, S.B. (eds) Transforming Growth Factor-β in Cancer Therapy, Volume II. Cancer Drug Discovery and Development. Humana Press. https://doi.org/10.1007/978-1-59745-293-9_3

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