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Your search keyword '"Herbert, Katharine J."' showing total 8 results
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8 results on '"Herbert, Katharine J."'

2. Transformative Pedagogy with Innovative Methodology: Using Photovoice to Understand Community College Students' Needs

Author

Herbert, Katharine J., Baize-Ward, Amy, and Latz, Amanda O.

Abstract

Community colleges, as open access institutions, shoulder most of the responsibility in serving marginalized individuals accessing higher education. Therefore, community colleges play a critical role. But what are new and incoming community colleges students' needs, in their own words? In this project, we explored an innovative component of a first-year seminar course wherein we asked students to document their unique needs using photographs and words. After situating our study within the extant literature, we present four findings and concomitant implications from a photovoice project in which we were involved during the spring of 2016.

Published
2018
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5. TOPK modulates tumour-specific radiosensitivity and correlates with recurrence after prostate radiotherapy

Author

Pirovano, Giacomo, Ashton, Thomas M., Herbert, Katharine J., Bryant, Richard J., Verrill, Clare L., Cerundolo, Lucia, Buffa, Francesca M., Prevo, Remko, Harrap, Iona, Ryan, Anderson J., Macaulay, Valentine, McKenna, William G., and Higgins, Geoff S.

Subjects
Cell Nucleus, Chromosome Aberrations, Male, Mitogen-Activated Protein Kinase Kinases, TOPK, Prostatic Neoplasms, Apoptosis, Cell Cycle Checkpoints, Quinolones, HCT116 Cells, Radiation Tolerance, Survival Rate, PBK, radiosensitivity, Cell Line, Tumor, Gene Knockdown Techniques, cancer, Humans, Neoplasm Recurrence, Local, Translational Therapeutics, Protein Kinase Inhibitors, HeLa Cells
Abstract

Background:\ud Tumour-specific radiosensitising treatments may enhance the efficacy of radiotherapy without exacerbating side effects. In this study we determined the radiation response following depletion or inhibition of TOPK, a mitogen-activated protein kinase kinase family Ser/Thr protein kinase that is upregulated in many cancers.\ud \ud Methods:\ud Radiation response was studied in a wide range of cancer cell lines and normal cells using colony formation assays. The effect on cell cycle progression was assessed and the relationship between TOPK expression and therapeutic efficacy was studied in a cohort of 128 prostate cancer patients treated with radical radiotherapy.\ud \ud Results:\ud TOPK knockdown did not alter radiation response in normal tissues, but significantly enhanced radiosensitivity in cancer cells. This result was recapitulated in TOPK knockout cells and with the TOPK inhibitor, OTS964. TOPK depletion altered the G1/S transition and G2/M arrest in response to radiation. Furthermore, TOPK depletion increased chromosomal aberrations, multinucleation and apoptotic cell death after irradiation. These results suggest a possible role for TOPK in the radiation-induced DNA damage checkpoints. These findings have clinical relevance, as elevated TOPK protein expression was associated with poorer clinical outcomes in prostate cancer patients treated with radical radiotherapy.\ud \ud Conclusions:\ud This study demonstrates that TOPK disruption may cause tumour-specific radiosensitisation in multiple different tumour types.

Published
2017

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