Abstract
Over time, up to 30 percent of differentiated thyroid cancer become de-differentiated and do not respond to traditional therapeutic modalities, posing a therapeutic challenge. Thyroid cancer is characterized by genetic alterations with both, activation of proto oncogenes, and inactivation of tumour suppressors. Over expression and/ or uncontrolled activation of receptor tyrosine kinases, downstream signaling molecules, and inhibition of programmed cell death (apoptosis) are other moleculer mechanisms. Currently a number of various therapeutic approaches are being tested in preclinical and clinical studies based on the pathogenesis of the dedifferentiation and target the altered genes or intracellular molecules involved in these processes. It is hoped that same of novel strategies will probably extend the current therapeutic options and provide a hope for otherwise untreatable patients.
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