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There is no known cure for Alzheimer’s disease, a brain disorder that severely affects memory, thinking, learning, and organizing skills. It eventually decreases a person’s ability to carry out simple, daily activities. It is predicted that over 14 million Americans will develop Alzheimer’s without effective treatment options. Mild cognitive impairment (MCI) is a stage prior to Alzheimer’s when memory problems become noticeable. A patient’s ability to function and live independently remain intact as the brain compensates for disease-related changes.

Advanced colorectal carcinoma is currently incurable, and new therapies are urgently needed. Ephrin (Eph) receptors are a clinically relevant class of receptor tyrosine kinases. Related signaling pathways are associated with oncogenesis of a number of cancers. NCI investigators found that phosphotyrosine-dependent Eph receptor signaling sustains colorectal carcinoma cell survival, thereby uncovering a survival pathway active in colorectal carcinoma cells.

The Transforming Growth Factor Beta (TGF-ß) ligands (i.e., TGF-ß1, -ß2, -ß3) are key regulatory proteins in animal physiology. Disruption of normal TGF-ß signaling is associated with many diseases from cancer to fibrosis. In mice and humans, TGF-ß activates TGF-ß receptors (e.g., TGFBR1), which activates SMAD proteins that alter gene expression and contribute to tumorigenesis.  Reliable animal models are essential for the study of TGF-ß signaling.

Cytokines are a broad category of intercellular signaling proteins that are critical for intercellular communication in human health and disease. However, systematic profiling of cytokine signaling activities has remained challenging due to the short half-lives of cytokines, and the pleiotropic functions and redundancy of cytokine activities within specific cellular contexts.

The use of tumor transcriptomics for precision oncology has made significant advances, mainly by identifying cancer driver genes or actionable mutations for treatment with targeted therapies.  However, this strategy misses out on broader genetic interactions that could reveal additional biologically testable biomarkers for therapy response prediction and inform the selection of more effective drugs for targeted treatment.

The Corona virus disease, 2019 (COVID-19) pandemic is a worldwide public health crisis with over 153 million confirmed cases and 3.2 million deaths as of April 2021. COVID-19 is caused by a novel coronavirus called SARS-CoV-2. SARS-COV-2 infects hosts via its spike (S) protein, which has two portions, S1 that binds the cell and S2 that is involved in viral entry via fusion with the cell membrane. There are several vaccines available for COVID-19 patients that directly target SARS-CoV-2 by systemic immunization.

Tumor cell lines are important tools for the study of cancer. However, most tumor cell lines available today do not mimic physiological tumor development, progression, and host immune responses. Autochthonous tumors include spontaneously occurring tumors and chemical, viral, or physical carcinogen-induced tumors. They are considered to model human tumors more closely than transplanted tumors. Autochthonous tumors can be generated de novo in a model organism of interest and are thought to resemble physiological human tumor conditions.

Bioluminescence imaging with luciferin-luciferase pairs is a well-established technique for tracking cells and other biological features in animal models. Bioluminescent is a chemical process which does not require an external input for excitation. Bioluminescent imaging is often limited to monitoring single processes in vivo due to the lack of distinguishable probes. Additionally, existing probes typically operate with light in the visible range, which is highly scattered and exhibits poor tissue penetration. 

Immune checkpoint inhibitors (ICIs) vastly improved the outcome of various advanced cancers; however, many are less likely to respond to single-agent ICI. Tumors with low T-cell infiltration are "immunologically cold" and less likely to respond to single-agent ICI therapy. This diminished response is presumably due to the lack of neoantigens necessary to activate an adaptive immune response. On the other hand, an "immunologically hot" tumor with high T-cell infiltration has an active anti-tumor immune response following ICI treatment.

Nonalcoholic fatty liver disease is caused by several factors including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), an environmental contaminant. TCDD causes lipid accumulation in humans by inducing the Solute Carrier Family 46 Member 3 (SLC46A3) gene expression. To effectively study TCDD-mediated lipid accumulation, research tools such as SLC46A3 knockout cells and animal models are required.