Researchers in Dr. Mark Kay's lab have developed a patented approach to inducing apoptosis that could represent a new strategy against cancer and other diseases.
Researchers at Stanford have developed a combination therapy to treat neuroblastoma, the most common and deadly solid tumor in childhood. Neuroblastoma derives from neural crest cells that fail to exit the cell cycle and differentiate.
Researchers at Stanford have developed methods of using CRISPR/Cas9-mediated genome editing to treat patients with EGFR-mutant non-small-cell lung cancer (NSCLC). Approximately 85% of lung cancers are NSCLC.
Researchers at Stanford and their colleagues have developed easily expressed Wnt agonist and antagonists. Wnts are central mediators of development as they influence cell proliferation, differentiation and migration.
Researchers at Stanford have developed methods to classify and treat MYC-driven hematopoietic cancers. The MYC oncogene drives the proliferation and survival of many hematopoietic cancers. These cancers are highly aggressive and do not respond to conventional chemotherapies.
Researchers in Prof. Gerald Crabtree's laboratory have identified the pathological mechanism for synovial sarcoma (SS) that could be used to develop targeted therapeutics. This approach aims to reverse the effects of the SS18-SSX fusion protein (the hallmark of human SS).
Researchers in Prof. Gerald Crabtree's laboratory have developed a method for identifying cancer patients that are likely to benefit from treatment with topoisomerase IIa (TOP2A) inhibitors.
Stanford researchers have developed a method that can tune the ratio between reversible (RE) and irreversible (IRE) electroporation through waveform adjustments.
Stanford researchers have proposed antibody-based reduction of Neuromedin (NMU) signaling as a therapeutic strategy to improve glucose metabolism in multiple physiological or disease states, including obesity, diabetes, and cancer where NMU levels are elevated.
Researchers in Prof. Michelle Monje-Deisseroth's laboratory have discovered a previously unknown mechanism for glioma tumor growth and invasion that defines a novel set of therapeutic targets.
Stanford researchers have identified small molecules that can intercept cancerous or pre-cancerous cells by activating DNA repair in cells damaged by oxidative stress.
A method of using neuregulin antagonists to delay the time of tumor recurrence in cancer patients has been developed by Dr. Sweet-Cordero and collaborators. This technology is available for non-exclusive license.