Researchers at NYU Langone Health have identified the CK1 protein as a key player in cancer cell development. Inhibiting this enzyme may provide a new approach to treating cancer cells, particularly those with malfunctioning mTOR signaling pathways.
Researchers identify hyperactive c-Met protein as key player in ADPKD cyst growth, leading to potential therapeutic target. Pharmacological inhibition of c-Met decreases mTOR activity and blocks cyst formation in mouse model.
Researchers found that transforming growth factor-β1 contributes to kidney disease by inducing fibrosis and nephron degeneration. Meanwhile, a new diagnostic criteria for T-cell lymphoma was discovered using mast cells and Th17 cells. Additionally, a novel peptide ASARM may implicate in impaired dentin mineralization in rickets.
Researchers link PMSE syndrome to mTOR pathway, a complex network implicated in common neurological disorders with autism-like symptoms. The study reveals clues about TSC, a relatively common disorder, and its connection to PMSE and other neurological conditions.
Researchers at Burnham Institute for Medical Research discovered that the REDD1 protein is degraded under hypoxic conditions, enabling cells to rapidly restore mTOR signaling. This regulation mechanism plays a crucial role in cellular stress response and may be linked to tumor growth in cancer.
Scientists at the University of California, San Francisco, have created a new drug that blocks cancer's main source of growth and has proven effective in mice. The drug succeeds where similar compounds fail by blocking both mTOR signal pathways, making it a major advance over existing rapamycin-based drugs.
Simultaneous inhibition of two signaling pathways, mTOR and MAPK, resulted in enhanced antitumor effects in mouse models of prostate and breast cancer. This combination therapy may improve the treatment of human cancers, particularly for patients with advanced, hormone-refractory prostate cancer.
Research led by Beth Israel Deaconess Medical Center identifies a previously unrecognized problem faced by mTORC1 inhibitors: activating the MAPK pathway, which encourages cancer cell survival. Scientists found that combining mTORC1 and MAPK inhibitors may offer a new treatment option for cancer patients.
Researchers found that simultaneously inhibiting the mTOR and MAPK signaling pathways enhanced antitumor effects in mouse models of prostate and breast cancer. This dual inhibition was particularly effective against aggressive forms of the disease, leading to a potential breakthrough for combination therapy.