Objective The purpose of this systematic review is to summarize the best available evidence on interventions that could be implemented in the college environment to increase HPV vaccination uptake in college students who were not previously vaccinated. Methods Pubmed, CINAHL, PsycINFO, Cochrane, and EBSCO were searched in December 2017 to identify all literature meeting the following criteria: human subjects, English language, HPV, HPV vaccination, and college. PRISMA recommendations were followed. We focused only on manuscripts that reported vaccine uptake, excluding studies that only reported vaccine intentions. We identified 2989 articles; 101 relevant after screening; nine eligible for final qualitative review. Results Vaccine uptake rates ranged from 5% to 53%. Theory-based variables (e.g., perceived susceptibility and self-efficacy) were associated with vaccine uptake in most studies. A study exposing participants to a narrative video about HPV vaccination led by a combination of peers and medical experts produced the greatest difference in HPV vaccination initiation compared to a control group (21.8% vs 11.8%) of all the studies reviewed. Conclusions Few interventions resulted in substantial HPV vaccine uptake. A combination of peer and provider encouragement may be the most effective method to increase vaccine uptake in this population.

Pediatric patients with high-risk neuroblastoma often relapse with chemotherapy-resistant, incurable disease. Relapsed neuroblastomas harbor chemo-resistant mesenchymal tumor cells and increased expression/activity of the transcriptional co-regulator, the Yes-Associated Protein (YAP). Patients with relapsed neuroblastoma are often treated with immunotherapy such as the anti-GD2 antibody, dinutuximab, in combination with chemotherapy. We have previously shown that YAP mediates both chemotherapy and MEK inhibitor resistance in relapsed RAS mutated neuroblastoma and so posited that YAP might also be involved in anti-GD2 antibody resistance. We now show that YAP genetic inhibition significantly enhances sensitivity of mesenchymal neuroblastomas to dinutuximab and gamma delta (γδ) T cells both in vitro and in vivo . Mechanistically, YAP inhibition induces increased GD2 cell surface expression through upregulation of ST8SIA1 , the gene encoding GD3 synthase and the rate-limiting enzyme in GD2 biosynthesis. The mechanism of ST8SIA1 suppression by YAP is independent of PRRX1 expression, a mesenchymal master transcription factor, suggesting YAP may be the downstream effector of mesenchymal GD2 resistance. These results therefore identify YAP as a therapeutic target to augment GD2 immunotherapy responses in patients with neuroblastoma.