A3 Adenosine Receptor Agonists to Treat Chemotherapy-induced Peripheral Neuropathy

This invention claims species-independent agonists of A3AR, specifically (N)-methanocarba adenine nucleosides and related pharmaceutical compositions. The A3 adenosine receptor (A3AR) subtype has been linked with helping protect the heart from ischemia, controlling inflammation, and regulating cell proliferation. Agonists of the human A3AR subtype have been developed that are also selective for the mouse A3AR while retaining selectivity for the human receptor.

Probe Set Global Optimization

Available for licensing and commercial development are methods to optimize sequence-based assays such as microarrays, multiplexed PCR or multiplexed antibody methods. This computational method uses numerical optimization to identify an optimal probe set to be used in an assay for the measurement of a specified set of targets. The method incorporates the sequence information of the target (protein, DNA, RNA or other polymer), the assay characteristics, limits on probe set size and assay probe length in its optimization.

Methods of Screening for Risk of Cancer Using Human Lactoferrin DNA Probe or Primer

While normal breast ductal epithelium and neutrophilic granulocytes contain lactoferrin, their malignant counterparts frequently do not. The NIH announces primers or probes corresponding to the human lactoferrin gene, its promoter region, and its protein product, obtained from human breast tissue. The lactoferrin primer or probes can be used to screen for malignancy arising from tissues that normally secrete lactoferrin, or as a test to check the recovery of a patient from a malignancy.

Heterocyclic P2Y14 Antagonists for the Treatment of Various Conditions

The technology discloses composition of compounds that are highly selective P2Y14 receptor antagonists,
with moderate affinity with insignificant antagonism of other P2Y receptors. These compounds might provide a
treatment for patients for various disease conditions, including lung inflammation, kidney inflammation,
asthma, diabetes, obesity, and neuropathic pain of diverse states. In vivo data using mouse lines with the
receptor knocked out in specific tissues showed that P2Y14 receptor antagonists act on adipocytes to improve

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.

Blocking CD38 using Protein G Complexed Daratumumab Antibodies (PGDARA) to Protect Natural Killer Cells from Daratumumab-induced Apoptosis and Cell Death for the Treatment of Multiple Myeloma

This technology includes the method of blocking CD38 in expanded natural killer (NK) cell therapy in combination with daratumumab in patients with multiple myeloma. Our in vitro studies have already confirmed the addition of NK cells to myeloma cells that have been exposed to daratumumab enhances myeloma killing compared to single agent treatment.

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.
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