Filtering by
- All Subjects: Cancer
- All Subjects: Social Media
- Creators: School of Life Sciences
- Creators: School of International Letters and Cultures
Glioblastoma (GB) is one of the deadliest cancers and the most common form of adult primary brain tumors. SGEF (ARHGEF26) has been previously shown to be overexpressed in GB tumors, play a role in cell invasion/migration, and increase temozolomide (TMZ) resistance.[3] It was hypothesized parental LN229 cell lines with SGEF knockdown (LN229-SGEFi) will show decreased metabolism in the MTS assay and decreased colony formation in a colony formation assay compared to parental LN229 cells after challenging the two cell lines with TMZ. For WB and co-immunoprecipitation (co-IP), parental LN229 cells with endogenous SGEF and BRCA were expected to interact and stain in the BRCA1:IP WB. LN229-SGEFi cells were expected to show very little SGEF precipitated due to shRNA targeted knockdown of SGEF. In conditions with mutations in the BRCA1 binding site (LN229-SGEFi + AdBRCAm/AdDM), SGEF expression was expected to decrease compared to parental LN229 or LN229-SGEFi cells reconstituted with WT SGEF (LN229-SGEFi + AdWT). LN229 infected with AdSGEF with a mutated nuclear localization signal (LN229-SGEFi + AdNLS12m) were expected to show BRCA and SGEF interaction since whole cell lysates were used for the co-IP. MTS data showed no significant differences in metabolism between the two cell lines at all three time points (3, 5, and 7 days). Western blot analysis was successful at imaging both SGEF and BRCA1 protein bands from whole cell lysate. The CFA showed no significant difference between cell lines after being challenged with 500uM TMZ. The co-IP immunoblot showed staining for BRCA1 and SGEF for all lysate samples, including unexpected lysates such as LN229-SGEFi, LN229-SGEFi + AdBRCAm, and LN229-SGEFi + AdDM. These results suggested either an indirect protein interaction between BRCA1 and SGEF, an additional BRCA binding site not included in the consensus, or possible detection of the translocated SGEF in knockdown cells lines since shRNA cannot enter the nucleus. Further optimization of CO-IP protocol, MTS assay, and CFA will be needed to characterize the SGEF/BRCA1 interaction and its role in cell survival.
Cancer rates vary between people, between cultures, and between tissue types, driven by clinically relevant distinctions in the risk factors that lead to different cancer types. Despite the importance of cancer location in human health, little is known about tissue-specific cancers in non-human animals. We can gain significant insight into how evolutionary history has shaped mechanisms of cancer suppression by examining how life history traits impact cancer susceptibility across species. Here, we perform multi-level analysis to test how species-level life history strategies are associated with differences in neoplasia prevalence, and apply this to mammary neoplasia within mammals. We propose that the same patterns of cancer prevalence that have been reported across species will be maintained at the tissue-specific level. We used a combination of factor analysis and phylogenetic regression on 13 life history traits across 90 mammalian species to determine the correlation between a life history trait and how it relates to mammary neoplasia prevalence. The factor analysis presented ways to calculate quantifiable underlying factors that contribute to covariance of entangled life history variables. A greater risk of mammary neoplasia was found to be correlated most significantly with shorter gestation length. With this analysis, a framework is provided for how different life history modalities can influence cancer vulnerability. Additionally, statistical methods developed for this project present a framework for future comparative oncology studies and have the potential for many diverse applications.
The Charlie Hebdo attacks fueled an online debate over freedom of expression and religion, whereas the purpose of social media evolved into a humanitarian one following the November 13 attacks in Paris. This research looks into the individual evolutions of the related hashtags that surfaced in 2015, including #JeSuisCharlie (and its opposites, such as #JeNeSuisPasCharlie), #DonDuSang, #PorteOuverte and #RechercheParis, among others. Another research point was with the September 11 attacks—with the 9/11 attacks against the United States, few to no channels were available for the kind of immediate discussions and support seen after the Paris attacks. After spending time in Paris during the spring 2015 semester and researching the aftermath of the Charlie Hebdo attacks and the history of the publication, the conclusion rests on the idea that the online discussions perpetuated by both supporters and dissenters of the magazine contribute to a more robust, open democracy supported by these social media platforms.
A portion of this thesis also delves into the parallels and differences between the American First Amendment and the French free speech laws—all of which pertain to the Charlie Hebdo content and the online responses to the 2015 Paris attacks.
The interviews conducted include a French art history professor at the Sorbonne University in Paris, two creators of the “Je Suis Charlie” Facebook page, an American journalist living in Paris who covered the Charlie Hebdo attack and who was present during the November attacks, and a Muslim-American doctor in Phoenix who founded the American Islamic Forum for Democracy. The ideas surrounding free speech, the value of art such as that found within the pages of Charlie Hebdo, the media’s treatment of religion, traditional democratic freedoms and ties to social media revolutions are all components of this research thesis.