Learn more about UC TechAlerts – Subscribe to categories and get notified of new UC technologies

Browse Category: Medical > Disease: Cancer

Categories

[Search within category]

Bioengineered Wnt5a Therapeutics For Advanced Cancers

Researchers at the University of California, Davis have developed RNA-based therapeutics to treat Wnt5A-expressing cancers, including treatment-resistant prostate cancer.

Steroid Sulfatase Inhibitors For Hormone Related Cancers

Researchers at the University of California, Davis have developed several steroid sulfatase inhibitors (STSi) that can be used as a potential treatment for hormone related cancers, specifically castration resistant prostate cancer (CRPC) and breast cancer.

T cell Receptor cDNAs to Treat Gliomas

Brief description not available

Natural Killer Cells with Enhanced Activity (SD 2021-141)

NK cells possess a native ability to kill tumors and virally infected cells without prior antigen priming. Furthermore, NK cells can be administered to patients across HLA allotypes, unlike T cells which require HLA matching to avoid graft-versus-host disease. Many trials utilizing adoptive transfer of allogeneic NK cells demonstrated complete remissions in patients with acute myelogenous leukemia (AML) who are refractory to standard chemotherapy. Another recent clinical study demonstrated effective treatment of lymphoid malignancies using allogeneic CAR-expressing NK cells, with minimal side effects. Thus, NK cells possess a number of advantages over T cells that enables them to be used as safe, effective, “off-the-shelf” adoptive cell therapy product to treat diverse malignancies. Antibody-dependent cellular cytotoxicity (ADCC) is a key pathway that mediates natural killer (NK) cell cytotoxicity against antibody-opsonized target cells. This process helps mediate the therapeutic efficacy of anti-tumor antibodies. On NK cells, ADCC occurs via engagement of antibody-coated target cells with activating receptor leading to proinflammatory cytokine upregulation, degranulation, and target cell death. Upon cellular activation, the     is cleaved from the NK cell surface. Cleavage of the ectodomain prevents further antibody binding and signaling, which dampens NK cell activity. Blocking activation-induced cleavage has been previously demonstrated to augment ADCC activity and provides a novel strategy to improve efficacy of therapeutic antibodies in combination with adoptive transfer of engineered NK cells. 

T Cell Receptor cDNAs to Treat Gliomas

Brief description not available

Broad spectrum anti-cancer agents

One of the main problems in using immune checkpoint inhibitors (e.g. PD-L1/PD-1/PD-L2/CTLA4) as a cancer treatment is that there is a large percentage of patients (~60-70%) who do not respond to the treatment or become resistant to it. Researchers all over the world are looking for ways to increase response to immunotherapy in this large population of patients, such as identifying new signaling pathways and/or new targets involved in this process as well as identifying synthetic molecules that can modulate the functions of those pathways and targets.

AKR1C3 and Androgen Receptor-Inhibiting Compounds for Treatment of Advanced Cancers

Researchers at the University of California, Davis have developed compounds with the potential to be dual inhibitor therapies to target AKR1C3 and the androgen receptors that promote malignant cell growth.

Lys-Covalent Pan-Inhibitors of Apoptosis Proteins (IAP) as Innovative Cancer Therapeutics

Prof. Maurizio Pellecchia and his colleagues at the University of California, Riverside (UCR) have developed novel Lys-covalent IAP inhibitors (Fig. 1) with low nanomolar activity and favorable PK (Fig. 2). When compared to Debio1143 (aka AT-406) and LCL 161, the UCR compounds have improved activity being irreversible.  Recently, new irreversible therapeutics in oncology have been developed as potential therapies for a variety of cancer. These irreversible agents present improved pharmacodynamics/ pharmacokinetics (PD/PK) properties over reversible agents, but their design is limited to targets that present a Cys residue within their binding site. UCR deployed a technology consisting of introducing a stable aryl-fluorosulfate electrophile that selectively interacts with Lys residues. UCR Compound 1 (Fig 1) is a potent, pan-IAP, Lys-covalent agent with favorable cell permeability and PK properties and that is likely superior to Debio1143 and LCL161 (Fig. 3). Fig. 1 Chemical composition and covalent docking of compound 1 in the binding pocket of the BIR3 domain of XIAP. Fig. 2 PK studies in mice with compound 1. Fig. 3 TNF sensitization of resistant melanoma cells by AT-406 (aka Debio 1143), LCL161 and the UCR compounds.  

Method And Device For Patterning Cells At Defined Interface

The present invention features a method and device that addresses the need for a low-cost and easy-to-use method and device to pattern a sharp interface between two or more cell populations or, more generally, two or more coatings wherein their interfacing properties are of interest. As a result, the present invention enables new types of experiments that analyze cell-cell interactions and the study of tissue biology in general. 

Potent and Effective Anti-Metastatic EphA2 Agonists

Prof. Maurizio Pellecchia and his colleagues at the University of California, Riverside have developed peptide-based EphA2 agonistic agents that have nanomolar activities. These agents, having the same mechanism of action as the natural (ephrinA1-Fc) ligands, effectively degrade EphA2 receptors and  delay cell migration in key cancer cell lines.  These agonistic agents may be effective therapeutics that may result in less unwanted side effects that have been observed in the clinic with ADCs targeting EphA2. Fig. 1 Top, X-ray structure of EphA2 in complex with UCR agent.. Bottom, Treatment with ephrinA1-Fc or UCR agent 135H12 on an orthotopic mouse model of prostate cancer with PC-3-GFP cells (n = 5 mice per treatment group). The mean fluorescence intensity related to metastases detected at day 7 from mice in each group, control (the solvent formulation used for 135H12), ephrinA1-Fc treated, 135H12 treated. Error bars represent standard deviation. ** p < 0.01.

3D-Bioprinted All-Inclusive Bioanalytical Platforms for Cell Studies

Common drug screen models, such as animals and 2D cell cultures, do not properly recapitulate human organ structure and environment. Using 3D bioprinting technology, researchers at UCI have developed all-inclusive customized organ-on-a-chip-like platforms. These platforms produce cell models that properly mimic the microenvironment of cells for drug screening and cell-therapeutic response studies.

Mitochondrial Transplantation to alter energy metabolism

Mitochondrial cardiomyopathy occurs when cardiomyocytes possess defective mitochondrial DNA. There is no cure and current treatment involves providing patients various dietary supplements. A novel biotherapy in which healthy mitochondria are transplanted directly into cells can help pave the way for treating mitochondrial-related diseases.

Polarization-Sensitive Optical Coherence Tomography Using a Polarization-Insensitive Detector

A polarization-sensitive optical coherence tomography (PS-OCT) is a common approach to non-invasively imaging in biomedical applications. The inventors have come up with a new way of creating a PS-OCT that is cheaper and simpler.

Personalized Oncology Drug Efficacy Monitoring Chip

Researchers at UCI have developed a novel microfluidic-based platform that enables personalized drug screening of patient-derived cancer cells. This versatile device features real-time, continuous screening of patient samples without the need for expensive labeling reagents, large sample sizes, or bulky readout equipment.

Novel Prodrug For Anti-Cancer Therapeutic Applications

Inventors at UCI have developed a modified nutrient transporter inhibitor for use as a cancer therapeutic with minimal side effects.

Combination Therapy For Pancreatic Cancer

Pancreatic cancer is an aggressive disease with limited treatment options and a high mortality rate. Pancreatic cancer is the 3rd leading cause of cancer death in the United States; despite some recent advances in systemic therapy, survival remains dismal in large part due to its profound drug resistance and its propensity for early metastasis. Typically, diagnosis of pancreatic cancer occurs only with advanced stages of the disease since there are currently no early markers for detection. Individuals with pancreatic cancer have a poor prognosis due to the late diagnosis, the extent of metastasis, and ineffective treatments. Survival rates are dismal and pancreatic cancer is not typically responsive to radiation and chemotherapy. An alternative approach for the treatment of pancreatic cancer as well as the design of a new class of therapeutics that can be used to treat this devastating disease is an immediate unmet medical need.

Identification of a Novel Target for Inhibition of Leukemia

Rho-family small (~21kDa) GTPases are essential for regulation of numerous cellular functions. There are 20 members of the Rho family in mammals, of which four (Rac1, Rac2, Rac3, RhoG) belong to the Rac subfamily. Each Rac GTPase functions as a molecular switch by cycling between an active GTP-bound form and an inactive GDP-bound form. In addition to their normal cellular functions, Rac GTPases contribute to cancer development as downstream effectors of growth factor receptor signaling and oncogenic mutations in the Ras pathway. Rac GTPases represent attractive targets for therapy in hematologic cancer, however direct targeting of small GTPases has proved difficult and largely ineffective. A thorough understanding of the diverse mechanisms controlling Rac activation in cancer will therefore be essential towards identifying new therapeutic avenues and improving outcomes in patients One insight into the regulation/activation of the Rac GTPases involves examining Ras proteins and their signal transduction pathways since mutations that produce abnormally active Ras proteins are found in 30% of all human cancers. Moreover, after activation, RAS signaling is mediated through interaction with RAS-binding domains or through the domain RAS association (RA), transmitted to downstream effectors. Notably, many downstream effectors are oncogenes or tumor suppressor genes that are mutated or silenced in cancers independently of RAS. Ras proteins are involved in Ras association domain-containing protein 2 (RASSF2) and it has recently been shown that in Acute myeloid leukemia cells with low expression of RASSF2 are more resistant to pharmacological inhibition of Dedicator of cytokinesis protein 2 (DOCK2), a guanine nucleotide exchange factor (GEF). Acute myeloid leukemia cells with high expression of RASSF2 are sensitive to pharmacological inhibition of DOCK2.

Bioengineered RNA Molecules for Cancer Therapy

Researchers at the University of California, Davis have developed a method to use biologic RNA molecules for cancer research and therapy.

Bioengineered Let-7c Therapy for HCC Treatment

Researchers at the University of California, Davis have developed a bioengineered, RNA-based treatment for advanced liver cancer and hepatocellular carcinoma (HCC).

Monoclonal Antibodies Specific to Canine PD-1 and PD-L1

Researchers at the University of California, Davis have developed monoclonal antibodies with multiple applications relevant to canine PD-1 and PD-L1.

Use of UBA7 and its Regulated Genes as Novel Biomarkers in Treating Human Cancers

Human Ubiquitin-like modifier-activating enzyme 7 (UBA7) is a protein is involved in protein modification, specifically involving the pathway for protein ubiquitination. The modification of proteins with ubiquitin is an important cellular mechanism for targeting abnormal or short-lived proteins for degradation. Ubiquitination involves at least three classes of enzymes: ubiquitin-activating enzymes, or E1s, ubiquitin-conjugating enzymes, or E2s, and ubiquitin-protein ligases, or E3s. UBA7  encodes a member of the E1 ubiquitin-activating enzyme family. Moreover, ubiquitination and ubiquitin-like post-translational modifications (PTMs) regulate activity and stability of oncoproteins and tumor suppressors. Biomarkers are very important as companion diagnostic tools to guide clinical practice in treating human cancers, especially for targeted therapies. In the era of precision medicine, it is important for development companion diagnostic tools that can guide clinical practice for treating human cancers using targeted therapies.

  • Go to Page: