Titlebook: Apoptosis in Carcinogenesis and Chemotherapy; Apoptosis in cancer George G. Chen,Paul B.S. Lai Book 2009 Springer Science+Business Media B.

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neue betriebswirtschaftliche forschung (nbf)such as TGF-β, VEGF, bFGF, IL-6, and BAFF. These growth factors have also been shown to be involved in dysregulated apoptosis. Once a hematopoietic cell becomes malignant, these growth factors can be produced by both the tumor cell as well as by cells surrounding the tumor. These surrounding cells,

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,Informationsüberfluss? Wissensknappheit!,alities to survive. Alterations in apoptotic pathways may result in resistance to drugs and radiation. Such alterations might serve as predictors of chemotherapy- and radiotherapy-sensitivity and, most importantly, as new treatment targets. The proteins p53, bcl-2 and clusterin influence the apoptot

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https://doi.org/10.1007/978-3-322-91862-8s. COX-2 and some of its metabolites have been regarded as markers for diagnosis and prognosis for lung cancer prevention and therapy. There is increasing evidence indicating that the inhibition of the expression or/and the activity of COX-2 can sensitize tumor cells to anti-tumor treatments by prom

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https://doi.org/10.1007/978-3-322-89145-7ould be through re-direction into other death pathways, such as necrosis. However, necrosis is a non-specific, non-targeted process resulting in cell lysis and inflammation of both cancer and normal cells and therefore, not a viable alternative. However, if the necrosis could be targeted only to can

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https://doi.org/10.1007/978-3-322-89145-7irradiation, chemical carcinogenic agents, are involved in the development of thyroid cancer. These factors can cause molecular abnormalities of signaling pathways involved in proliferation, differentiation, and apoptosis, which eventually lead to the development and progression of various thyroid n

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https://doi.org/10.1007/978-1-4020-9597-9apoptosis; cancer; cancer therapy; carcinogenesis; carcinoma; cell; cell death; chemotherapy; melanoma; progr