Abstract: The present invention relates to methods of treating a condition associated with mTORC1 hyperactivation or TSC2-deficient cancer, the method comprising administering to a subject having the cancer a pharmaceutically-effective amount of a poly(ADP-ribose) polymerase 1 (PARP1) inhibitor. In some embodiments, the condition associated with mTORC1 hyperactivation is tuberous sclerosis complex (TSC). In some embodiments, the condition associated with mTORC1 hyperactivation is lymphangioleiomyomatosis (LAM). In some embodiments, the condition associated with mTORC1 hyperactivation is TSC2-deficient cancer.

Abstract: Embodiments disclosed herein provide compositions and methods for treating lymphangioleiomyomatosis (LAM) comprising inhibiting COX overexpression and prostaglandin over production by administering at least one COX inhibitor and/or prostaglandin biosynthetic pathway inhibitors.

Abstract: The present invention relates to methods of treating a condition associated with mTORC1 hyperactivation or TSC2-deficient cancer, the method comprising administering to a subject having the cancer a pharmaceutically-effective amount of a poly(ADP-ribose) polymerase 1 (PARP1) inhibitor. In some embodiments, the condition associated with mTORC1 hyperactivation is tuberous sclerosis complex (TSC). In some embodiments, the condition associated with mTORC1 hyperactivation is lymphangioleiomyomatosis (LAM). In some embodiments, the condition associated with mTORC1 hyperactivation is TSC2-deficient cancer.

Abstract: Embodiments disclosed herein provide compositions and methods for treating lymphangioleiomyomatosis (LAM) comprising inhibiting COX overexpression and prostaglandin over production by administering at least one COX inhibitor and/or prostaglandin biosynthetic pathway inhibitors. Lymphangioleiomyomatosis (LAM) is a rare lung disease. Some LAM occurances are associated with mutations in the tuberous sclerosis complex (TSC) locus. LAM occurs almost exclusively in women, usually of childbearing age.

Abstract: The present invention relates to methods of treating a condition associated with mTORC1 hyperactivation or TSC2-deficient cancer, the method comprising administering to a subject having the cancer a pharmaceutically-effective amount of a poly(ADP-ribose) polymerase 1 (PARP1) inhibitor. In some embodiments, the condition associated with mTORC1 hyperactivation is tuberous sclerosis complex (TSC). In some embodiments, the condition associated with mTORC1 hyperactivation is lymphangioleiomyomatosis (LAM). In some embodiments, the condition associated with mTORC1 hyperactivation is TSC2-deficient cancer.

Abstract: Embodiments disclosed herein provide compositions and methods for treating lymphangioleiomyomatosis (LAM) comprising inhibiting COX overexpression and prostaglandin over production by administering at least one COX inhibitor and/or prostaglandin biosynthetic pathway inhibitors. Lymphangioleiomyomatosis (LAM) is a rare lung disease. Some LAM occurances are associated with mutations in the tuberous sclerosis complex (TSC) locus. LAM occurs almost exclusively in women, usually of childbearing age.

Abstract: Treatment of lymphangioleiomyomatosis with the MEK1/2 inhibitor CI-1040 delayed the development of primary tumors and blocked the estrogen-induced lung metastases in treated animals. Such treatment also reduced the number of circulating ELT3 cells and decreased their lung colonization after intravenous injection.

Abstract: Treatment of lymphangioleiomyomatosis with the MEK1/2 inhibitor CI-1040 delayed the development of primary tumors and blocked the estrogen-induced lung metastases in treated animals. Such treatment also reduced the number of circulating ELT3 cells and decreased their lung colonization after intravenous injection.

Abstract: Methods for inhibiting estrogen hormone-induced pulmonary metastasis of smooth muscle cells that are capable of pulmonary metastasis comprise antagonizing the estradiol receptor on the smooth muscle cells such that pulmonary metastasis of the cells is inhibited.

Abstract: Treatment of lymphangioleiomyomatosis with the MEK1/2 inhibitor CI-1040 delayed the development of primary tumors and blocked the estrogen-induced lung metastases in treated animals. Such treatment also reduced the number of circulating ELT3 cells and decreased their lung colonization after intravenous injection.