Abstract Rationale: In the United States, there are currently about 100,000 people diagnosed with pulmonary fibrosis, with an estimated additional 50,000 cases every year. Pulmonary Fibrosis (PF) is a detrimental disease since it has a 50% survival rate over two years, according to BMC Pulmonary Medicine. Previously, Jak1 has been identified as playing a major role in the pathogenesis of PF through experiments that involve Jak/STAT inhibitors. However, the role of Jak1 in causing inflammation, recruiting dendritic cells, and inducing fibrosis is poorly understood. Objective: We aimed to explore the role of Janus Kinase 1(Jak1) by using the Jak1 overexpression mouse model during bleomycin‐induced pulmonary fibrosis in mice. Methods: We used the c57/bl6-SPADE mouse model resulting from inducing a heterozygous missense mutation in the Jak1 gene. These mice were initially obtained from Japan, and the colony is currently maintained in our facility, with breeding scaled up according to the requirements of my project. Bleomycin is used to induce pulmonary fibrosis in my experiment. We then assessed lung injury using histopathology methods, mainly through the modified Ashcroft scoring system.

Breast cancer is the most commonly diagnosed cancer in women globally, with subtypes including estrogen receptor–positive (ER⁺) tumors (~80% of invasive cases) and Triple Negative Breast Cancer (TNBC), which lacks targeted therapies. Many ER⁺ tumors are inherently resistant or acquire resistance to endocrine therapy, making endocrine resistance a critical barrier to improved patient outcomes. ATAD2 (ATPase family AAA domain–containing protein 2) regulates gene expression by recognizing acetylated histones and initiating transcription, and elevated levels of ATAD2 have been found in various types of cancers with indications that it promotes tumor proliferation, survival, and metastasis. However, its functional contribution to hormone therapy resistance and its therapeutic potential in advanced breast cancer remains unclear. This project hypothesizes that ATAD2 is overexpressed in advanced breast cancer subtypes and functions as a key driver of endocrine therapy resistance; consequently, pharmacological inhibition of ATAD2 will sensitize tumor cells to standard-of-care treatments such as doxorubicin and suppress tumor proliferation. ATAD2 expression has been verified via western blot of cell lines HCC1806, HCC1395, and MCF-7. Functional impact of single and combination therapy has been assessed through cell viability and colony formation assays. This work addresses a critical need by identifying ATAD2 as a novel therapeutic target for breast cancer, with the potential to inform more effective treatment strategies for patients.

Struggles with fertility and reproductive health are a major concern for many men and women in America. Diagnoses such as endometriosis and adenomyosis are understudied and not much is known about the genetic causes and potential treatments. Previous research has shown that SUV39H1, a histone methyltransferase, is downregulated in endometriosis​. SUV420H2 is a similar regulator that has shown to play key roles in the cell cycle. However the role SUV420H2 may play in reproductive development and regulation remains unclear. Here we show that mice with SUV420H2 knocked out display abnormal uterine phenotypes. Certain SUV KO mice displayed hydrometra, an abnormal accumulation of fluid within the uterine horns. All SUV KO mice tested also displayed uterine cysts when sliced and imaged. Preliminary data tracking the time spent in estrous cycles found that SUV KO mice spent more time in metestrus and estrus stages, which are known to rely heavily on estrogen signaling. They also tend to display abnormal cycling trends. RT-PCR found that levels of Wnt4, Muc1, and Ctnnb1 are significantly increased in the uteri of SUV KO mice. Preliminary fertility trials suggest the SUV KO mice take longer between litters compared to control mice. The combined results seen in the uterine tissue and cycling suggests a possible link to endometriosis or adenomyosis. Few models of endometriosis or adenomyosis exist and this could potentially answer questions about the underlying genetic causes.

The dysregulation of oxidative phosphorylation and amyloid beta misfolding are observed early in Alzheimer’s disease (AD). Protein misfolding has been shown to disrupt mitochondrial function and lead to neurodegeneration. Oxidative phosphorylation is a key component of energy homeostasis that maintains neuronal integrity, which limits the progression of neurodegenerative diseases. As Aβ42 plaques are a hallmark of AD, it is important to investigate genes that can prevent Aβ42 plaque accumulation and inhibit disease progression. Our lab identified the Drosophila gene Atossa (Atos)—a key regulator of oxidative phosphorylation and ATP production—and determined that the human homolog AtosA is linked to AD-associated cognitive decline. This study shows that manipulation of Atos can help regulate Aβ42 plaque accumulation and cognitive function in a Drosophila model. There is evidence that loss of Atos increases neuronal death in the presence of pathogenic Aβ42 as demonstrated by increased necrosis of the eyes when examined across varying genotypes. The experiments conducted in this study will serve as a starting point for a more advanced understanding of the causes of Alzheimer’s disease, as well as the development of potential therapeutic approaches to reverse or prevent its pathogenesis.

The primary challenge in canine genomics is accurately attributing phenotypic traits like body size, ear shape, or behavioral tendencies to their ancestral breed origins within individual dogs, especially in those of mixed breeds. Breeds were established from small founding populations, so genetic markers could be the result of genetic drift rather than from them controlling a certain gene. Selective breeding has also resulted in many traits becoming fixed amongst the population, so studies within members of only a specific breed can be impossible to conduct. To address this issue, phenotype data for 60+ breeds was catalogued from the American Kennel Club and compared against previously collected genomic data via GWAS analysis through PLINK and GEMMA. We were able to identify significant mutant regions that correlated to phenotypic expression in certain breeds. Mapping out verified genomic regions with their expressed phenotype will allow for more specific breed distinction and aid in genotyping a mixed-breed dog.