{"id":{"repo_id":"buffalo","oai_identifier":"oai:ubir.buffalo.edu:10477/79845"},"canonical_url":"https://search.dev.ndltd.org/etd/buffalo/oai:ubir.buffalo.edu:10477/79845","repository":{"repo_id":"buffalo","name":"Buffalo","base_url":"https://ubir.buffalo.edu/oai/request"},"display":{"title":"Hsp60 Promotes Aggressive Prostate Cancer by Modulating Mitochondrial Function","abstract":"Ph.D.","abstract_html":"Ph.D.","abstract_has_math":false,"creators":["O'Malley, Jordan; 0000-0002-1276-947X"],"institution":"State University of New York at Buffalo","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":["Chandra, Dhyan","Roswell Park"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2019,"date_issued":"2019-07-29T20:35:17Z","date_published":"2019-07-29T20:35:17Z","updated_at":"2026-07-27T19:05:19Z","subjects":["pharmacology"],"languages":["eng"],"rights":["Users of works found in University at Buffalo Institutional Repository (UBIR) are responsible for identifying and contacting the copyright owner for permission to reuse. University at Buffalo Libraries do not manage rights for copyright-protected works and cannot assist with permissions.","Copyright retained by author."],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/10477/79845","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Chandra, Dhyan","Roswell Park"]},{"key":"dc:creator","label":"Author","values":["O'Malley, Jordan; 0000-0002-1276-947X"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2019-07-29T20:35:17Z","2019","2019-05-02 16:05:51"]},{"key":"dc:publisher","label":"Institution","values":["State University of New York at Buffalo"]},{"key":"dc:type","label":"Dc Type","values":["Text","Dissertation"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["pharmacology"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["eng"]},{"key":"dc:rights","label":"Dc Rights","values":["Users of works found in University at Buffalo Institutional Repository (UBIR) are responsible for identifying and contacting the copyright owner for permission to reuse. University at Buffalo Libraries do not manage rights for copyright-protected works and cannot assist with permissions.","Copyright retained by author."]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["http://hdl.handle.net/10477/79845"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Ph.D.","Prostate cancer is the second most diagnosed cancer in American men and the third leading cause of cancer-related death in American men. Although the five-year survival rate for patients with androgen-sensitive prostate cancer is ~100%, the five-year survival rate for recurrent or metastatic prostate cancer dramatically decreases to ~30%. The current therapeutic approach for prostate cancer involves chemical castration, also known as androgen deprivation therapy (ADT), which inhibits androgen receptor signaling. ADT provides initial benefit in terms of prostate cancer remission. However, in the majority of metastatic disease, prostate cancer develops resistance to ADT and becomes castrate resistant (CRPC). The most aggressive subset of CRPC appears with altered or deleted tumor suppressors Rb1/p53, and as a result has low/no AR expression. This aggressive phenotype readily metastasizes, displays resistance to chemotherapeutic agents and absence of the AR renders them inherently resistant to ADT. Thus, alternative therapeutic approaches to combat aggressive metastatic CRPC that do not involve targeting traditional AR signaling must be identified. We hypothesized that Hsp60 is a viable target in aggressive CRPC, and its inhibition suppresses phenotypes characteristic of aggressive CRPC. Specifically, we hypothesized that Hsp60 inhibition reduces oncogenic burden, metastatic potential, cisplatin resistance, and mediates these phenotypes in part through β-catenin.","**To request an accessible version of the file(s) associated with this item, contact library@buffalo.edu. Please include the item's persistent URL [http://hdl.handle.net/. . .] in your request.**"]},{"key":"dc:format","label":"Dc Format","values":["application/pdf"]},{"key":"dc:title","label":"Title","values":["Hsp60 Promotes Aggressive Prostate Cancer by Modulating Mitochondrial Function"]}]}],"canonical_facts":{"dc:contributor":["Chandra, Dhyan","Roswell Park"],"dc:creator":["O'Malley, Jordan; 0000-0002-1276-947X"],"dc:date":["2019-07-29T20:35:17Z","2019","2019-05-02 16:05:51"],"dc:description":["Ph.D.","Prostate cancer is the second most diagnosed cancer in American men and the third leading cause of cancer-related death in American men. Although the five-year survival rate for patients with androgen-sensitive prostate cancer is ~100%, the five-year survival rate for recurrent or metastatic prostate cancer dramatically decreases to ~30%. The current therapeutic approach for prostate cancer involves chemical castration, also known as androgen deprivation therapy (ADT), which inhibits androgen receptor signaling. ADT provides initial benefit in terms of prostate cancer remission. However, in the majority of metastatic disease, prostate cancer develops resistance to ADT and becomes castrate resistant (CRPC). The most aggressive subset of CRPC appears with altered or deleted tumor suppressors Rb1/p53, and as a result has low/no AR expression. This aggressive phenotype readily metastasizes, displays resistance to chemotherapeutic agents and absence of the AR renders them inherently resistant to ADT. Thus, alternative therapeutic approaches to combat aggressive metastatic CRPC that do not involve targeting traditional AR signaling must be identified. We hypothesized that Hsp60 is a viable target in aggressive CRPC, and its inhibition suppresses phenotypes characteristic of aggressive CRPC. Specifically, we hypothesized that Hsp60 inhibition reduces oncogenic burden, metastatic potential, cisplatin resistance, and mediates these phenotypes in part through β-catenin.","**To request an accessible version of the file(s) associated with this item, contact library@buffalo.edu. Please include the item's persistent URL [http://hdl.handle.net/. . .] in your request.**"],"dc:format":["application/pdf"],"dc:identifier":["http://hdl.handle.net/10477/79845"],"dc:language":["eng"],"dc:publisher":["State University of New York at Buffalo"],"dc:rights":["Users of works found in University at Buffalo Institutional Repository (UBIR) are responsible for identifying and contacting the copyright owner for permission to reuse. University at Buffalo Libraries do not manage rights for copyright-protected works and cannot assist with permissions.","Copyright retained by author."],"dc:subject":["pharmacology"],"dc:title":["Hsp60 Promotes Aggressive Prostate Cancer by Modulating Mitochondrial Function"],"dc:type":["Text","Dissertation"]},"updated_at":"2026-07-27T19:05:19Z"}