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The 1996 report which concluded that Ptc is the receptor for shh also noted that genetic mutations in the Ptc protein are often associated with basal cell carcinoma. This finding suggested that shh provides mitogenic and differentiative signals to basal cells throughout one�s lifetime, giving the protein novel functions aside from embryonic development. A 2004 experiment revisiting the actions of the hedgehog signaling pathway found that shh activity is required in the regeneration of the prostate epithelia. It was concluded that continuous activation of the shh gene renders the prostate progenitor cells tumorigenic. Studies based upon medulloblastoma, the most common form of malignant brain tumor in young children, showed that various inhibitors of the shh signaling pathway such as cyclopamine (found in various plants) trigger the regression of medullobastoma. These results confirm the involvement of shh in this specific type of brain tumor, although similar tests failed to show shh involvement in other brain tumors.
Another group concurrently investigated the participation of shh in the carcinogenesis of airway epithelia due to injury. It was found that the injury triggered the expression of shh, which launched a signaling pathway aimed towards the proliferation of target cells; but once the injury healed, shh continued to be expressed, inducing the formation of a tumor.
Overall, shh and related proteins in the shh pathway are responsible for countless varieties of cancer development. Research has been underway for several years in attempt to create pharmaceuticals with the ability of appropriately reducing pathway activity to cure such cancers (OMIM, 2008).
This web page was produced as an assignment for an AP Biology course at Montgomery High School. |
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