Hybridomas Producing Antibodies to Neuraminidase for Influenza A (H3N2) Diagnostics, Vaccine, and Therapeutic Development

Influenza A and B viruses can cause seasonal flu epidemics ― commonly known as the “flu season” ― and infect the nose, throat, eyes, and lungs in humans. Typically, flu seasons that are dominated by influenza A (H3N2) virus activity have higher associated hospitalizations and deaths in at-risk groups, such as people ages 65 and older and young children. Influenza A (H3N2) virus can also cause respiratory disease in animals, such as canines and swine.

Treatment of the beta-globinopathies through inhibition of RIOK3 activity

Disorders of adult beta-globin synthesis, which include sickle cell disease (SCD) and beta-thalassemia, are the most common monogenic disorders in the world. While the curative potential of bone marrow transplantation has been demonstrated, this approach is limited to a small fraction of affected patients due to the requirement for an HLA-matched donor, the highly specialized approach that requires critical infrastructure, and the high cost.

TSLP Induces Neutrophil-mediated Killing of Methicillin-resistant Staphylococcus Aureus (MRSA)

This technology includes the use of thymic stromal lymphopoetin (TSLP) for the treatment of MRSA. Our studies show that mouse neutrophils express the TSLP receptor, TSLPR, and that TSLP protein is increased during cutaneous MRSA infection. Using in vitro MRSA whole blood killing assays, we show that TSLP acts on mouse neutrophils to enhance MRSA killing. In an in vivo MRSA intradermal ear infection, TSLPR-deficient mice exhibit increased MRSA burden compared to wild-type mice.

Epstein-Barr Virus (EBV)-feeder Cell Line

This technology includes irradiated Epstein-Barr virus-transformed lymphoblastoid cell lines (EBV-LCL) as feeder cells for the ex vivo expansion of natural killer (NK) cells. EBV-LCL feeder cells, altered by radiation to prevent uncontrolled growth, provide a supportive environment for NK cells to multiply effectively. This method addresses the challenge of obtaining sufficient quantities of functionally active NK cells, which are crucial components of the immune system known for their ability to target and destroy tumor cells and virally infected cells.

Highly Efficient Gene Transfer into Primary and Expanded Human Natural Killer Cells by Lentiviral Transduction for Cancer Therapy

This technology includes an efficient lentiviral vector-based method for gene transfer into NK cells and demonstrates a stable and long-term robust expression of transgenes for the treatment of cancer. High gene transfer rates into primary cells being transduced and the ability to produce high titers of virus particles for large-scale transduction of patient cells are prerequisites for clinical trials. Lentiviral vectors can be produced in high titer and concentrated without compromising their transduction efficiency.

A Highly Efficient Differentiation Protocol for Placental Cells Derived from Human Pluripotent Stem Cells for Diagnostic and Therapeutic Applications

This technology includes in vitro-generated trophectoderm (TE) cells, which are ideal for modeling diseases of the placenta, drug screening, and cell-based therapies. The TE lineage which gives rise to placental cells during early human development. Derivation of definitive placental cells from human pluripotent stem cells in culture remains controversial and so far, placental cells can only be derived directly from primary placental tissue, which largely limits their access and study in the laboratory.

LZK and DLK Inhibitors to Target LZK and Suppress MYC Expression, Inhibit AKT Activation, and Promote Cancer Cell Death and Tumor Regression

This technology includes the use of LZK and DLK inhibitors to be used for the treatment of head and neck squamous cell carcinoma (HNSCC) or lung squamous cell carcinoma (LSCC). Specifically, we demonstrate that inhibitors that can be repurposed to target LZK suppresses LZK kinase-dependent stabilization of MYC and activation of the PI3K/AKT pathway. In vivo preclinical cell line xenograft mouse model demonstrates that targeting LZK will suppress tumor growth. We also demonstrate that several additional compounds potently inhibit LZK and could serve as new therapeutic modalities.

A Mouse Model of Multiple Endocrine Neoplasia, Type I

The current invention embodies a mouse model which is heterozygous for a null allele at the Men1 locus of murine chromosome 19. Men1 has similar exon-intron organization and amino acid identity compared with its human analog MEN1, which has been implicated in the pathogenesis of multiple endocrine neoplasia, type I (MENI). This mouse model has been shown to develop features remarkably similar to those of MEN1, which include tumors of the endocrine pancreas, pituitary, and parathyroids.