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Bone morphogenetic proteins and cancer

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Part of the book series: Progress in Inflammation Research ((PIR))

Abstract

During early embryonic development several bone morphogenetic proteins (BMPs) are involved in processes such as determination, morphogenesis, proliferation, differentiation and apoptosis [1]. The interplay between BMPs, especially BMP-2 and BMP-4 with its antagonists Noggin and Chordin, is fundamental for mesoderm induction and further formation and thus overcoming the default state of neuroectoderm formation [2, 3]. Constantly high levels of BMPs in early Xenopus embryos maintain the ventral phenotype and keep the embryos alive for a long time. This is one hint that BMPs are necessary and sufficient for cell survival. The regular interplay between the processes of proliferation, apoptosis and differentiation is no longer correctly regulated during tumor initiation and progression (Fig. 1). Biology of tumor cells changes and they become more and more dedifferentiated and/or transdifferentiated. Finally, the tumor cells gain new functions and lose tissue-specific behavior and common restrictions, like proliferation control. It is generally accepted that the initial events of tumor formation occur at the genome level. Alterations in the DNA sequence of genes involved in the control of proliferation, cell-cycle regulation or apoptosis lead to malfunctions of the gene products and the beginning of a multi-step process ending in the formation of a tumor with the ability to form metastases (Fig. 2).

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Clement, J.H., Wölfl, S. (2004). Bone morphogenetic proteins and cancer. In: Vukicevic, S., Sampath, K.T. (eds) Bone Morphogenetic Proteins: Regeneration of Bone and Beyond. Progress in Inflammation Research. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-7857-9_12

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  • DOI: https://doi.org/10.1007/978-3-0348-7857-9_12

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