First-Generation College Students & Campus Resources

The purpose of this research was to analyze how campus resources at Valparaiso University affect first-generation college students. Specifically, this study looked at the effect campus resources have on feelings of belonging on campus and academic success. First generation college students are defined as students whose parents have not obtained a four-year degree. This study used a questionnaire that was emailed to every known first-generation college student at Valparaiso University. This consisted of five sections: demographics, campus resource use, the campus community, academic preparedness, and experience. The use of campus resources section used a Likert scale to see how often students used different campus resources. The campus community and academic preparedness sections also used a Likert scale to see how much students related to questions such as, “I feel like I fit in at Valpo”. Finally, the experience section allowed for students to write in specific challenges they have faced on Valparaiso University\u27s campus. These results can help further develop the Persistence and Success Program (PSP), a first-generation college student program on campus

Combined AURKA and H3K9 Methyltransferase Targeting Inhibits Cell Growth By Inducing Mitotic Catastrophe

International audienceThe current integrative pathobiologic hypothesis states that pancreatic cancer (PDAC) develops and progresses in response to an interaction between known oncogenes and downstream epigenomic regulators. Congruently, this study tests a new com-binatorial therapy based on the inhibition of the Aurora kinase A (AURKA) oncogene and one of its targets, the H3K9 methylation– based epigenetic pathway. This therapeutic combination is effective at inhibiting the in vitro growth of PDAC cells both, in monolayer culture systems, and in three-dimensional spheroids and organoids. The combination also reduces the growth of PDAC xenografts in vivo. Mechanistically, it was found that inhibiting methyltransferases of the H3K9 pathway in cells, which are arrested in G 2 –M after targeting AURKA, decreases H3K9 meth-ylation at centromeres, induces mitotic aberrations, triggers an aberrant mitotic check point response, and ultimately leads to mitotic catastrophe. Combined, these data describe for the first time a hypothesis-driven design of an efficient combinatorial treatment that targets a dual oncogenic–epigenomic pathway to inhibit PDAC cell growth via a cytotoxic mechanism that involves perturbation of normal mitotic progression to end in mitotic catastrophe. Therefore, this new knowledge has significant mech-anistic value as it relates to the development of new therapies as well as biomedical relevance. Implications: These results outline a model for the combined inhibition of a genetic-to-epigenetic pathway to inhibit cell growth and suggest an important and provocative consideration for harnessing the capacity of cell-cycle inhibitors to enhance the future use of epigenetic inhibitors