Hydrocarbon Stapled Peptides that Inhibit the Linear Ubiquitin Chain Assembly Complex (LUBAC) for the Therapy of the Activated B Cell-like (ABC) Subtype of Diffuse Large B Bell Lymphoma (A Type of Non-Hodgkin’s Lymphoma)

Diffuse large B-cell lymphoma (DLBCL) is the most common type of non-Hodgkin’s lymphoma and consists of three subtypes: activated B-cell (ABC), germinal center B-cell (GBC), and primary mediastinal B-cell (PMB). Despite advances in the front-line therapy for DLBCL, approximately one-third of patients will relapse. Substantially worse outcomes have been reported for patients diagnosed with ABC DLBCL and treated with standard chemoimmunotherapy, suggesting the need for novel strategies that improve treatment outcomes.

Transgenic Mouse Model of Human Basal Triple Negative Breast Cancer

The NCI Laboratory of Cancer Biology and Genetics seeks parties interested in collaborative research to further develop this mouse model of triple-negative breast cancer (TNBC) to study cancer biology and for preclinical testing.  As a Research Tool, patent protection is not being pursued for this technology; more information to access this strain can be found here: https://www.jax.org/strain/030386.

Optical Microscope Software for Breast Cancer Diagnosis

The successful treatment of cancer is correlated with the early detection of the cancerous cells. Conventional cancer diagnosis is largely based on qualitative morphological criteria, but more accurate quantitative tests could greatly increase early detection of malignant cells. It has been observed that the spatial arrangement of DNA in the nucleus is altered in cancer cells in comparison to normal cells. Therefore, it is possible to distinguish malignant cells by mapping the position of labeled marker genes in the nucleus.

Angiogenesis-Based Cancer Therapeutic

Vascular Endothelial Growth Factor-A (VEGF-A) is an angiogenic agent that drives blood vessel formation in solid tumors and other diseases, such as macular degeneration and diabetic retinopathy. Several therapies that target the ability of VEGF to stimulate angiogenesis have been approved. These therapies regulate VEGF-A activity by binding VEGF-A, thereby blocking VEGF-A from binding to its receptor on target cells. This technology utilizes a different approach to regulating VEGF-A activity by providing a VEGF-A protein antagonist that is produced by engineering native VEGF-A protein.