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Triple negative (progesterone receptor (PR)-, estrogen receptor (ER)-, human epidermal growth receptor 2 (HER2)-) breast cancer (TNBC) is an aggressive subtype that affects 15-20% of the 1.7 million cases of breast cancer occurring annually.  Currently, standard treatments of TNBC include cytotoxic chemotherapies, surgery, and radiation. However, TNBC readily becomes resistant to chemotherapy, and those with TNBC are more likely to have a recurrence or die within five years compared to those with other breast cancer types.

Diverse human cancers like colorectal, pancreatic, ovarian, melanoma, and pre-cancers express NADPH oxidases (NOX) at high levels. Reactive oxygen species (ROS) produced from metabolic reactions catalyzed by NOX in tumors are essential to the tumor’s growth. Though drugs that inhibit ROS production by NOX could be effective against a variety of human cancers, these types of drugs are not widely available.

Researchers at the National Cancer Institute (NCI) have developed orthotopic allograft models for pancreatic cancer that utilize low passage primary pancreatic adenocarcinoma cells or tumor fragments implanted into the cancer-free pancreata of recipient syngeneic immunocompetent mice. Tumor development in these models is more synchronized, latency is substantially shortened, and tumors develop only in one location, as pre-determined by the choice of a site for cells/tumor fragment implantation.

Current therapies for glioblastoma multiforme (GBM), the highest grade malignant brain tumor, are mostly ineffective, and better preclinical model systems are needed to increase the successful translation of drug discovery efforts into the clinic. Scientists at the National Cancer Institute (NCI) have developed and characterized an orthotopic genetically engineered mouse (GEM)-derived model of GBM that closely recapitulates various human GBM subtypes and is useful for preclinical evaluation of candidate therapeutics.

It is well documented in literature that activation of RXFP1 by relaxin induces: 1) up-regulation of the endothelin system which leads to vasodilation; 2) extracellular matrix remodeling through regulation of collagen deposition, cell invasiveness, proliferation, and overall tissue homeostasis; 3) a moderation of inflammation by reducing levels of inflammatory cytokines, such as TNF-a and TGF-b; and 4) angiogenesis by activating transcription of VEGF.

Summary: 
The National Cancer Institute (NCI) seeks co-development partners and/or licensees for a liquid biopsy diagnostic assay capable of detecting loss of heterozygosity (LOH) and somatic mutations in genes important for antigen processing and presentation and interferon-γ response pathways.

Human leukocyte antigen (HLA) LOH (LOH) is a known resistance mechanism by which cancers evade T cell receptor-(TCR-)based immunotherapies. This class of therapies includes immune checkpoint inhibition (ICI, e.g., Pembrolizumab), engineered TCR (T cell receptor)-T cell adoptive transfer, tumor infiltrating lymphocytes (TIL), T-cell engagers, and other modalities. Dozens of therapies in this category were developed with many in clinical trials. The resistance mechanism noted here, HLA LOH, causes these therapies to fail.

Summary: 
The National Cancer Institute (NCI) is actively seeking potential licensees and/or co-development research collaboration partners interested in further developing this family of oxynitidine derivatives as tyrosyl-DNA phosphodiesterase 1 (TDP1) inhibitors and radiosensitizers for the treatment of cancer. 

Summary

The National Cancer Institute (NCI) seeks research co-development partners and licensees for a panel of five fully human antibodies against CD276 for the treatment of solid tumors. The collection also includes human CARs incorporating the antibodies for immunotherapeutic use.

Summary: 
The National Cancer Institute (NCI) seeks co-development partners and/or licensees for a method of identifying and selectively expanding neoantigen-specific T cells.