Stanford researchers have discovered that tumors increase the risk of atherosclerosis by regulating expression of a specific gene that stimulates angiogenesis and intraplaque neovessel formation.
Stanford researchers have developed an innovative approach for accurate and automated cell classification on H&E-stained images using multiplexed immunofluorescence (mIF) imaging, eliminating human annotations, and enhancing biological interpretability in histopathology.
Stanford researchers have developed a high-affinity IL-11 decoy cytokine for super-agonism and antagonism of the IL-11 receptor, enabling the treatment of a wide variety of diseases from inflammatory disease to cancer as well as research into IL-11 signaling pathways.
Stanford researchers have formulated a first in line framework called EcoTyper which systematically profiles the tumor microenvironment (TME) cell states in multiple solid tumor types, providing a platform for effective personalized cancer decisions.
Stanford scientists have developed a new, better binder for the tumor-associated macrophage marker CD206. This binder can be conjugated to a variety of payloads, including an anti-immune checkpoint protein antibody for more selective immune checkpoint blockade.
A team of Stanford researchers has developed humanized and chimeric mouse anti-human CD99 monoclonal antibodies with demonstrated activity against AML (acute myeloid leukemia) cells in vitro and in vivo.
Researchers at Stanford have developed a nanoparticle-based platform to enhance activation of self-specific CD8+ T cells in the tumor microenvironment to fight cancer while minimizing toxic side effects.
Researchers at Stanford University have discovered that the absence of a long non coding RNA (lnc122) predisposed mice to high numbers of hepatocellular carcinomas (HCC), and its replacement decreased the risk of HCC.
Researchers at Stanford have developed a method using expressed genetic barcodes to enable simultaneous lineage tracing and single cell profiling. Intratumor heterogeneity fosters tumor evolution which is a key contributor to therapeutic failure and the lethality of cancer.
Stanford researchers have developed a platform for identifying highly specific modulators of cancer-associated mutant Histone Acetyltransferase 1 (HAT1) holoenzyme complexes.
Low doses of agents that activate BMP signaling (such as FK506) could be used to prevent the progression of bladder cancer and potentially treat breast, colon and other types of epithelial-derived cancer. This technology is based on the discovery by Prof.