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Distinct Metabolic States Guide Maturation of Inflammatory and Tolerogenic Dendritic Cells

Scientists at UCSF and the Parker Institute of Cancer Immunotherapy have developed methods for characterizing dendritic cells as well as methods for identifying a dendritic cell as either an inflammatory or a tolerogenic dendritic cell. Their results provide important insights into previously obscured metabolic heterogeneity impacting immune profiles of immunogenic and tolerogenic dendritic cells (DC).

Combinatorial Drug Therapy for Treating Resistant Glioblastoma Multiforme

Researchers at the University of California, Davis have discovered a new treatment target to attack and kill GBM cancer cells that evades macrophage phagocytosis and are resistant to radioimmunotherapy.

Human Antibody Targeting Cd146 And Uses Thereof

Brief description not available

(SD2020-085) Targeting RBP-Prss23 Binding Interaction For Myc-Dependent Cancer Therapy. Therapeutic for Myc-dependent cancer.

Considering the versatile functions of m6A in various physiological processes, it is thus not surprising to find links between m6A and numerous human diseases; many originated from mutations or single nucleotide polymorphisms (SNPs) of cognate factors of m6A. The linkages between m6A and numerous cancer types have been indicated in reports that include stomach cancer, prostate cancer, breast cancer, pancreatic cancer, kidney cancer, mesothelioma, sarcoma, and leukaemiaC-MYC(MYC) was among of the earliest described human oncogenes identified and is now recognized as the primary driver in oncogenic transformation and maintenance of cancer gene expression programs in a broad spectrum of cancer types where cells become “addicted” and dependent on MYC for survival. MYC transcript stability is coordinately regulated by RNA-binding proteins that both positively and negatively affect its half-life. Several RBPs interacting with m6A-modified RNA become upregulated in cancer, and are required for cellular growth, survival and invasion of cancer cells. Thus, Myc regulates cellular function and survival in part by modulating RNA metabolism and is itself controlled posttranscriptionally by RBPs.There have been conflicting findings regarding the function of YTHDF2 in cancer. For example, loss of YTHDF2 sensitizes acute myeloid leukemia (AML) cells to TNF-induced apoptosis, while overexpression of YTHDF2 in hepatocellular carcinoma (HCC) represses cell proliferation and growth by destabilizing EGFR mRNA [9, 10]. Moreover, the direct YTHDF2 target RNAs have yet to be defined in the mammary epithelial or in human breast cancer. It is unknown if the mechanism in other cancer types may be attributed to YTHDF2-Prss23 regulation. Existing art includes US20100104501A1 patent, characterizing Prss23 as a biomarker, therapeutic and diagnostic target. The invention involves compounds which bind to and/or inhibit the activity of PRSS23, which is the opposite of what we have determined is required to trigger apoptosis in Myc-dependent cancer.There are no current findings suggesting intervention of the YTHDF2-Prss23 binding interaction as a cancer therapeutic.

Eradication Of Human Cancer Cells By Antigen Specific Delivery Of Carbon Monxide With A Family Photoactivatable Antibobody Photocorm Conjugates

PhotoCORMs are compounds that release Carbon monoxide (CO) upon exposure to light. CO released from photoCORMs exposed to light is known to cause apoptotic cell death and can sensitize human cancer cells to chemotherapeutics. Drug resistance is often encountered in cancer chemotherapy. In addition, efforts to minimize toxicity from chemotherapy have met with little success. A UC Santa Cruz researcher has developed a system to specifically deliver photoCORMs to tumors and presensitize those tumors to conventional chemotherapy

Improving primary human NK cell expansion with a chimeric cytokine receptor

Natural Killer (NK) cells are innate lymphocytes with the ability to lyse tumor cells. One limitation of NK cells when encountering tumor cells is that they can’t control their own proliferation and expansion to increase their numbers at the tumor site. Current approaches to increase NK cell numbers and stimulate NK-cell anti-cancer functions include systemic administration of recombinant cytokines (IL-15, IL-2, or IL-12) that exhibit systemic or local toxicity or constitutive expression of IL-15 in transduced NK cells. Researchers at UCSF have engineered NK cells with a chimeric cytokine receptor (CCR) that provides autocrine signaling through the secretion of IFNγ, which subsequently enhances NK cell proliferation and function to support NK cell anti-cancer immune response specifically at the tumor site while avoiding recombinant cytokine- related toxicity. 

Compositions and Methods for Modification of Cells

New chemistries are emerging for the direct attachment of complex molecules to cell surfaces. Chemistries that modify cells must perform under a narrow set of conditions in order to maintain cell viability. They must proceed in buffered aqueous media at the optimal physiological pH—typically pH 7.4—and within a temperature range of 4 – 37 ºC. Furthermore, these reactions must have sufficiently rapid kinetics to achieve high conversion even when confronted with the limits of surface diffusion characteristics. Due to these requirements, few chemistries exist that can attach molecules and proteins to live cells.  There is a need for improved methods of attaching proteins to living cells.   UC researchers have developed a convenient enzymatic strategy for the modification of cell surfaces for targeted immunotherapy applications.  

Methods to Prevent and Treat Diffuse Large and Other B Cell Lymphomas

Professor Ameae Walker from the University of California, Riverside, Professor Srividya Swaminathan from the City of Hope Beckman Research Institute and their colleagues have developed a method for the prevention and treatment of B cell lymphomas. This technology works by systemically inhibiting expression of one form of the set of cell surface molecules that allow cells to respond to prolactin. This highly specific technology suppresses the deleterious downstream effects of prolactin that promote and sustain abnormal B cells. This invention is advantageous compared to existing technologies: all measures in mouse models and analysis of human cells suggest it is nontoxic and therefore will have significantly fewer, if any, side effects. It may also be used together with anti-psychotics that elevate prolactin. Finally, the technology includes a method for screening populations susceptible to development of DLBCL and other B lymphomas for early signs of disease. Antimaia Acts at Three Stages of B Lymphoma Development: 1) Antimaia, a splice modulating oligonucleotide (SMO) that decreases expression of the long form of the prolactin receptor, reduces the number of premalignant cells and the formation of abnormal antibody-producing cells. This also improves the symptomatology of autoimmune disease. 2) Antimaia prevents the conversion of premalignant to overt malignant B cells. 3) Antimaia kills B lymphoma cells. Antimaia works by reducing the number of long and intermediate form prolactin receptors (LF/IF PRLR) without effect on short receptors (SFPRLR). PRL, prolactin; Bcl2, B cell lymphoma 2; Myc, a proto-oncogene.

Recombinantly produced p27 for use in screening inhibitors of Cdk4/6;Cyc6/p27 kinase complex

Cyclin Dependent Kinases (Cdk) 4 and 6 promote cell proliferation through their kinase activity. The active cellular form of the Cdk 4 or 6 enzyme forms a complex with both cyclin D (CycD) and p27 in vivo. Current therapeutics that target Cdk4 or 6 were generated in a complex that lacked p27 because of difficulties in expressing a recombinant form of p27. This technology describes a recombinantly produced engineered form of p27 that forms stable complexes with Cdk4/6 and CycD in vitro.

Single-Cell Analysis of Somatic Mutation Burden

Brief description not available

Transformable Smart Peptides as Cancer Therapeutics

Researchers at the University of California, Davis have developed smart, supramolecular, materials that can assemble into nanoparticles. These particles can then be used to target tumor cells.

Integrin Binding to P-Selectin as a Treatment for Cancer and Inflammation

Researchers at the University of California, Davis have developed a potential drug target for cancer and inflammation by studying the binding of integrins to P-selectin.

Conjugates That Combine HDAC Inhibitors and Retinoids into Disease Preventatives/Treatments

Researchers at the University of California, Davis have developed methods for creating compositions with the potential to prevent or treat cancer or metabolic diseases. These compositions combine conjugates with covalently linked HDAC inhibitors and retinoids.


While splice modulators have entered clinical trials, limited clinical efficacy in splicing factor mutation-driven malignancies, such as acute myeloid leukemia, has remained a challenge. There is a pressing unmet medical need for developing potent small molecule splice modulators for the treatment of a broad array of malignancies characterized by splicing deregulation.  However, the inability to practically access gram-scale lead molecules with viable pharmacological properties continues to hinder their application.

(SD2020-497) Light-activated tetrazines enable live-cell spatiotemporal control of bioorthogonal reactions

Bioorthogonal ligations encompass coupling chemistries that have considerable utility in living systems. Among the numerous bioorthogonal chemistries described to date, cycloaddition reactions between tetrazines and strained dienophiles are widely used in proteome, lipid, and glycan labeling due to their extremely rapid kinetics. In addition, a variety of functional groups can be released after the cycloaddition reaction, and drug delivery triggered by in vivo tetrazine ligation is in human phase I clinical trials. While applications of tetrazine ligations are growing in academia and industry, it has so far not been possible to control this chemistry to achieve the high degrees of spatial and temporal precision necessary for modifying mammalian cells with single-cell resolution.

Blood Based T Cell Biomarker For Cancer Diagnosis And Treatment

In cancer care, specific characteristics of T cells can be used to measure a patient’s response to immunotherapy. Using single-cell RNA-sequencing coupled with TCR sequencing, scientists at UCSF and Harvard detected CD8+ T cell clones shared between blood and tumor in mice and melanoma patients, characterized these matching clones in blood and tumor, and identified potential biomarkers for their isolation in the blood. Their method reveals specific protein signatures (biomarkers) on the surface of T cells that can be therapeutically targeted to treat melanoma and other forms of cancer. It presents a very attractive alternative to obtaining invasive biopsy samples from the tumor, and can be done much more quickly.  

Fem1b Inhibitors

UC Berkeley researchers have discovered novel, specific Fem1b inhibitors. Fem1b is essential in lymphoma and lung cancer cells.  Fem1b inhibition could be beneficial in cancer, metabolic disease, obesity, diabetes and other diseases. 

Inhibitors of Bromodomain and Extra-Terminal (BET) Family Proteins as Potential Treatments for Drug-Resistant Tumors

Researchers at the University of California, Davis have developed small molecule inhibitors for use in treating drug-resistant tumors – including cancerous tumors.

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