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- All Subjects: Chemotherapy
- Creators: College of Letters and Sciences
Description
Looking into the school community cohesion and how refugee youth integrate into schools is important when addressing refugee resettlement issues at large. It is important that school community identity (SCI) formation for refugee high school youth is understood in order to develop school programs that can better assist integration process of refugee families. Looking at high school refugee youth from Arizona a model was created that better displays the specifics this study found when dealing with this population. Unlike non-refugee high school youth, refugee youth do not develop school community cohesion through voice, resonance, or empowerment like other studies have shown. This study shows that they must first develop a SCI before they can have a strong school community presence. School community identity is an important first step that facilitates sense of school community. Two focus groups were down at the Somali American United Council, and from these two groups four common themes surfaced: faculty support, emotional security, cultural understanding, and partnership/collaboration. Using these themes a refugee school identity model was created to represent the data collected. The participants in the focus group often told stories and used phrases that indicated a lack of identity in their school, and no claims to a need of a voice within their school community was mentioned. This indicates that refugee students need an identity within their school community before they will express a need for voice or influence.
ContributorsReiswig, Clinton Gene (Author) / Klimek, Barbara (Thesis director) / Zayas, Luis (Committee member) / Sambe, Pape (Committee member) / Barrett, The Honors College (Contributor) / College of Letters and Sciences (Contributor) / School of Public Affairs (Contributor) / School of Social Work (Contributor)
Created2015-05
Description
Background: Esophageal adenocarcinoma (EAC) is one of the only malignancies whose incidence is rising in the United States. Current multidrug treatment for EAC has considerable toxic side effects that necessitate the development of less toxic, more specific target drugs. Recent large scale genomic analysis reveals that TP53 is the most frequently inactivated gene in EAC. One of the primary functions of TP53 and its gene product, the tumor suppressor p53, is in regulation of DNA repair in response to DNA damage. Inactivation of TP53 results in loss of the G1/S cell cycle checkpoint, and dependence on the G2/M checkpoint for DNA repair. Activity of cyclin-dependent kinase 1 (CDK1) is necessary for cells to exit the G2/M checkpoint and enter mitosis. Phosphorylation of CDK1 by the wee1 kinase inhibits CDK1 in response to DNA damage, allowing cells to maintain G2 arrest and repair the damaged DNA. Active in normal cells, wee1 kinase is critical in cancer cells to promote DNA repair and cell survival in response to DNA damage, particularly from commonly used DNA damaging therapies. AZD1775 is a small molecule inhibitor of wee1 kinase, currently under investigation in clinical trials. AZD1775 differentially targets cancer cells by blocking wee1 mediated inhibition of CDK1 and consequently preventing G2/M arrest in response to DNA damage. Combination of AZD1775 with DNA damaging agents is thought to push cancer cells with damaged DNA through to mitosis and initiate apoptosis instead of G2/M arrest and DNA repair. Based upon the incidence of TP53 mutation in EAC, we hypothesize that treatment with a DNA damaging agent in combination with AZD1775 will be as effective at eliciting DNA damage and cell death as the more toxic current standard of care, which is comprised of treatment with cisplatin, docetaxel, and radiation. Methods: p53 mutant EAC cell lines were dosed with cisplatin, AZD1775, and the combination of cisplatin and AZD1775, and then assayed for viability. Nude mice were implanted with p53 mutant patient derived xenograft esophageal adenocarcinoma tumors and randomized for treatment with AZD1775 alone, cisplatin and AZD1775, radiation and AZD1775, cisplatin, docetaxel, and radiation or vehicle (control). Tumor volume was measured over the five week treatment course. Results: In vitro and in vivo assays reveal a potent synergistic effect between AZD1775 and DNA damaging agents that is as efficacious as the standard of care therapy. The difference in AZD1775 sensitivity among TP53 mutant EAC cell lines indicates that TP53 alone may not be an adequate biomarker to assess for AZD1775- mediated toxicity.
ContributorsBlomquist, Mylan (Author) / Maley, Carlo (Thesis director) / Inge, Landon (Committee member) / Oberle, Eric (Committee member) / College of Letters and Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2016-05