Endocrine Abstracts

Medullar thyroid cancer (MTK) approximately constitutes 5% of thyroid cancer, over the 25% cases it progresses in familial form. In charge of genetic inherited clinical features in RET protooncogene ‘germ-line’ makes up activating mutations. In post RET mutation in association with tyrosine kinase activation oncogenic cell proliferation is increased. In medullary thyroid cancer persistent and recurrence disease management is complicated, because it is unresponsive toward chemotherapy, radiotherapy, and radioactive iodine therapy. In these cases, RET and tyrosine are termed as the agents targeting kinase receptor activity. Tyrosine kinas inhibitors may be potential to stabilize metastatic disease, but in terms of survival time period they do not lead to any variation and due to widespread of side effects their clinical administration remains difficult. Stains inhibiting mevolanat channel by HMG Co A reductase inhibition, based on proapoptotic, antiangiogenetic, and immunomodulatuar effect were identified to be able to cancer cell growth in previous plenty of studies. In the present study, throughout TT cell line we investigated atorvastatin’s apoptotic impact in cancer cells and calcitonin’s variation gene expression.

TT cell’s administered in atorvastatin varying doses (12.5–25–50–60–70–80–90–100–125–150–200 μM) and at 24. Hours IC 50 ratio accounted 90 μM, 48. Time IC 50 value 80 μM and at 72. Hours IC 50 value calculated as 80 μM. Atorvastatin’s apoptotic effect; evaluated in correlation with caspase 9 activity. In comparison with atorvastatin’s control cohort at 24. Hours 1.273-fold, at 48. Hours 1.660-fold and at 72 h 1.716-fold caspase 9 activity found to proliferate. In post atorvastatin calcitonin gene expression, compare to control cohort at 24. Hours identified to attenuate 1.377-fold, at 48. Hours identified to attenuate 7.290-fold and at 72. Hours identified to attenuate 8.494-fold. Eventually; atorvastatin along the TT cell line as dependent on dose and time increase apoptosis and calcitonin alleviate gene expression. Owing to atorvastatin easy clinical use and lesser side effects in the therapy of progressed MTK cases it may be deemed as a promising new agent.