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In the majority of genetic tumor syndromes and sporadic cancers, oncogenic signaling pathways lead to dysregulation of the heterotrimeric TSC1/TSC2/TBC1D7 (TSC) complex, which in turn, activates mTORC1 and renders it insensitive to perturbations by cellular growth conditions.  While it is widely believed that uncontrolled mTORC1 signaling plays a key role in tumor initiation and progression, the molecular consequences of mTORC1 activation are still not fully defined. In the lab, we are taking advantage of cells and tumor models lacking the TSC complex to understand the consequences of aberrant mTORC1 signaling common to genetic tumor syndromes (LAM, TSC) and sporadic cancers.

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