Expression data from Tsc2-null cell line ELT3, and the ELT3-derivative rapamycin-resistant cell line ELT3-245

TSC2 loss leads to mTORC1 hyperactivation in Tuberous Sclerosis Complex (TSC) and Lymphangioleiomyomatosis (LAM), and rapamycin or analogues Life-long use of rapalogs are proposed for the treatment of Tuberous Sclerosis Complex (TSC) and Lymphangioleiomyomatosis (LAM), which increases the chances for the development of rapalog resistance. Moreover, a percentage of patients do not respond to rapalogs. Understanding the signaling perturbations leading to rapalog resistance in TSC and LAM is critical for the development of better therapeutic strategies. We developed a Tsc2-null cell line, ELT3-245, that is highly tumorigenic and are refractory to rapamycin treatment.

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