Researchers at the NCI have developed a method of improving the immune response in cancer immunotherapy by exploiting in the role of the Linker Adapted for T-Cell Signaling (LAT) molecule. The LAT molecular can enhance signaling through TCRs, thus, improving a patient’s own immune response to cancer or infectious diseases.
Researchers at the NCI have developed a vaccine technology that stimulates the immune system to selectively destroy metastasizing cells. Stimulation of T cells with the Brachyury peptide promote a robust immune response and lead to targeted lysis of invasive tumor cells. NCI seeks licensing or co-development of this invention.
The Surgery Branch of the National Cancer Institute is seeking statements of capability or interest from parties interested in collaborative research to carry out genotypic as well as phenotypic analysis of the 888 mel cell line in order to better understand the nature of tumor cells that respond to therapy.
The National Cancer Institute seeks parties interested in collaborative research to co-develop or license methods of treating disorders related to polyomavirus, as well as vaccines for patients undergoing immunosuppressive treatment such as multiple sclerosis, rheumatoid arthritis, B cell cancers, and Crohn’s disease.
The Eunice Kennedy Shriver National Institute of Child Health and Human Development, Section on Molecular Neurobiology seeks parties interested in licensing or collaborative research to further evaluate or commercialize specific rabbit monoclonal antibodies generated against the ErbB4 receptor (also known as HER4) that have been validated for specificity using tissue sections and extracts from ErbB4 knockout mice.
Pulmonary surfactant plays a critical role in preventing alveolar collapse by decreasing surface tension at the alveolar air-liquid interface. Surfactant deficiency contributes to the pathogenesis of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), common disorders that can afflict patients of all ages and carry a mortality rate greater than 25%. Excess surfactant leads to pulmonary alveolar proteinosis. NCI investigators created a G-protein coupled receptor GPR116 mutant mouse model and showed that GPR116 plays a previously unexpected, essential role in maintaining normal surfactant levels in the lung. The National Cancer Institute seeks partners interested in collaborative research to license surfactant modulating agents for the treatment of surfactant related lung disorders.
Researchers at the National Cancer Institute (NCI) have developed an engineered storage unit for frozen tissue, that provides a permanent base on which to mount tissue frozen in OCT and an enclosure for storage. The unit provides for chain-of-custody labeling and acts as an insulating container to protect the specimen. Other elements include devices for freezing the tissue to the base, as well as a holder for the base to facilitate cryosectioning. Application of the storage system allows a frozen tissue specimen to be moved between storage and cryosectioning without loss of label, deformation of tissue, or thermal alterations.
The invention is a novel methodology for predicting a mantle cell lymphoma (MCL) cancer patient’s survival prognosis. This information is important in helping determine the best course of treatment for the patient.
Available for licensing from the National Cancer Institute are fully human monoclonal antibodies that were selected from the first human post-alloHSCT antibody library. The library was generated from a time point after transplantation at which antibodies to B-CLL cell surface antigens peaked, thus indicating its therapeutic value.
Researchers at the National Cancer Institute (NCI) developed a genetic assay for detecting transcription errors in RNA synthesis. This new assay extends the familiar concept of an Ames test which monitors DNA damage and synthesis errors to the previously inaccessible issue of RNA synthesis fidelity. The FDA requires genetic DNA focused tests for all drug approval as it assesses the in vivo mutagenic and carcinogenic potential of a drug. The new assay will open an approach to monitoring the impact of treatments on the accuracy of RNA synthesis. Errors in transcription have been hypothesized to be a component of aging and age-related diseases. The National Cancer Institute (NCI) seeks licensing partners for the genetic assay.
The National Cancer Institute's Cancer and Inflammation Program is seeking statements of capability or interest from parties interested in licensing monoclonal antibodies to IGF-1 and IGF-II for the treatment of cancer.
The National Cancer Institute seeks licensees and/or co-development partners for methods that provide significant improvements in examining clinically relevant tissue samples, by improving spatial resolution and tissue depth using optical trapping.
T cell receptors (TCRs) are proteins that recognize antigens in the context of infected or transformed cells and activate T cells to mediate an immune response and destroy abnormal cells. The National Cancer Institute's Surgery Branch seeks interested parties to license or co-develop the use of T cell receptors (TCRs) cloned against the SSX-2 antigen for the treatment of cancer.
The National Institute of Child Health & Human Development (NICHD), Program in Genomics of Differentiation, seeks interested parties to further co-develop small molecule inhibitors of RNase H1, especially in regards to genome instability, transcription, and translation.
The National Cancer Institute (NCI) seeks licensees for a monoclonal antibody specific to the GalNAc1-3Gal antigen that is present in human carcinomas. The antibody can be used as a research tool for a variety of purposes, including immunohistochemical staining of various human carcinomas. The antibody may also be useful as a prognostic marker for cervical cancer.
Researchers at the National Cancer Institute (NCI) have developed peptidomimetic inhibitors that disrupt Polo-like kinase 1 (Plk1)-mediated protein interactions by targeting polo-box domain (PBD). These compounds are designed to selectively cause mitotic arrest in cancer cells with abnormal Plk1 expression. Researchers seek licensing and/or co-development research collaborations to further develop the inhibitors.