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 patway, frequently dusregulated 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.

©2007-2009 Aristotelis Astrinidis
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