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Mutations in the tumor suppressor genes TSC1 and TSC2 in Tuberous Sclerosis Complex (TSC) and pulmonary Lymphangioleiomyomatosis (LAM) lead to aberrant activation of the AKT/mTOR pathway, frequently dysregulated also in other forms of cancer. Our goal is to elucidate novel mechanisms and signaling pathways leading to mTOR-dependent tumor formation with the potential for therapeutic intervention. Our work focuses on the functions of the proteins involved in TSC/LAM pathogenesis with regards to cell division. |
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©2007-2013 Aristotelis Astrinidis |
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