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Hedgehog signaling regulates bladder cancer growth and tumorigenicity - Research Paper Example

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Instructor Institution Date Hedgehog Signaling Regulates Bladder Cancer Growth And Tumorigenicity. The issue of hedgehog regulating bladder cancer growth and tumorigenicity still remains controversial and questionable despite the immeasurable efforts by the medics to coming up with a justifying answer…
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Hedgehog signaling regulates bladder cancer growth and tumorigenicity
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For the embryo cells to develop properly they receive the information they require from the hedgehog signaling pathway. The concentration of these proteins differs from one part of the embryo to the other. Hedgehogs homologous are three in mammals’ .Scientists have majorly progressed in the study of the Sonic Hedgehog. The other hedgehogs include the Desert hedgehog and the Indian hedgehog. Recently more advanced studies and research show that hedgehog signaling is involved in regeneration and maintenance of adult tissues in regulation of adult stem cells.

Analyses have also shown that the pathway is also involved in the development of certain cancer cells. Emerging concepts indicate that tumors are an analogous to these adult tissues which are self renewing. Their maintainer is a group of unique stem cells. Cancer cells have their unique characteristics which easily define them. The best defined characteristics are tumorigenic properties with high differentiating potential and are self renewing hence regenerating cellular heterogeneity of original patient tumors.

In order to maintain their self renewal and differentiating potential adult stem and embryonic cells with respect to their inherent nature keep their pathways active which are always down regulated on differentiation. The following are some of the pathways involved; Signal transducer, Sonic Hedgehog, Notch Signaling, Stat3 Signaling and Wnt catenin. However research shows that all the above pathways are also activated by various cancers. This indicates that they take part in the renewal of cancer stem cells.

Human cancer is extremely complex in its development in that heterogeneity is rather common in the active pathways amongst patients. Laboratory results by some of the professionals reveal that only a group of related patients correlate to activation of a certain pathway. Wnt signaling pathway is a complex network of protein s that works with the receptors. In both embryotic and adult cells it regulates communication between the cells. In the mouse it was identified as one of the genes involved in breast cancer.

Mutations in this pathway can be terribly dangerous since they can contribute to the development of cancer in adults. The normal state of Wnt pathway is default repression, under its association with axin, APC complex and GSK-3 to target bete-catenin leading to ubiquitination degradation. In any case when mutations damage this pathway it no longer controls beta-catenin. Research proves that beta-catenin is found in breast and lung cancer. It also confers self renewal of granulocyte-macrophage progenitors in blood cancer.

The Notch receptor has a large extracellular domain, a single transmembrane domain, and a cytoplasmic domain. Ligands for the Notch receptors are proteins being expressed in the surface of the adjacent cells, and the primary target of notch signaling is activation of the transcription factor SuH in Drosophila species or CBF-1 in mammals. Though the mechanism by which the Notch transmits signals has not been worked out positively, it appears to be fairly different from other receptors. Current evidence suggest that the cytoplasmic domain of the notch is proteolytically cleaved and the translocated to nucleus, where it interacts directly with transcription factors.

The tumor neclosis factor family of receptors has a conserved cysteine-rich region found in the extracellular do

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