By Alvaro Macieira-Coelho
In this publication, tumour progress is perceived as a deviation from the traditional improvement of the human organism. The molecular, mobile, and tissue determinants of other tumours are mentioned exhibiting that every is a special sickness, usually reminiscent of a selected developmental degree. The traditional historical past of numerous cancers illustrates how medical prevalence will be simply the obvious a part of the iceberg, whereas the 1st alterations on the tissue point occasionally take place a number of years ahead of tumour progress turns into happen. numerous mechanisms are proposed to provide an explanation for the distribution of cancers through the human existence span and the decline of the prevalence of cancers in the course of human senescence.
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Thus, specific compounds may be without effect in specific patients, or the cancer cells may develop resistance against the compounds. However, these obstacles may be overcome by precise diagnostic classification of tumors, using expression profiling and combinatorial chemotherapy. 5 Future Prospects An impressive amount of knowledge about the involvement of Hh signaling in tumor formation and growth has accumulated since the discovery of PTCH as the disease gene in NBCCS. While the research so far has uncovered many important aspects and laid the foundation for the development of potential anti-cancer drugs, many questions are still unanswered and several surprises can probably be expected.
While the best characterized of these include regulation of the actin cytoskeleton and cell migraion, they have also been implicated in cell-cycle progression, cell survival, and gene expression. Given that Rho GTPases influence these processes in normal cells, it is likely that aberrant activation of Rho GTPase signaling contributes to their dysregulation in various cancers. In this chapter, we will discuss the evidence implicating Rho proteins in various stages of cancer development, including tumor initiation, invasion, and metastasis.
Science 274:255–259 Price MA, Kalderon D (2002) Proteolysis of the Hedgehog signaling effector Cubitus interruptus requires phosphorylation by Glycogen Synthase Kinase 3 and Casein Kinase 1. Cell 108:823–835 Qualtrough D, Buda A, Gaffield W, Williams AC, Paraskeva C (2004) Hedgehog signalling in colorectal tumour cells: induction of apoptosis with cyclopamine treatment. Int J Cancer 20(110):831–837 Raffel C, Jenkins RB, Frederick L, Hebrink D, Alderete B, Fults DW, James CD (1997) Sporadic medulloblastomas contain PTCH mutations.
Developmental Biology of Neoplastic Growth (Progress in Molecular and Subcellular Biology) by Alvaro Macieira-Coelho