{"id":{"repo_id":"buffalo","oai_identifier":"oai:ubir.buffalo.edu:10477/79956"},"canonical_url":"https://search.dev.ndltd.org/etd/buffalo/oai:ubir.buffalo.edu:10477/79956","repository":{"repo_id":"buffalo","name":"Buffalo","base_url":"https://ubir.buffalo.edu/oai/request"},"display":{"title":"Targeting Cell Cycle Checkpoints in Triple Negative Breast Cancer and Pancreatic Ductal Adenocarcinoma","abstract":"Ph.D.","abstract_html":"Ph.D.","abstract_has_math":false,"creators":["Chung, Sejin"],"institution":"State University of New York at Buffalo","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":["Smiraglia, Dominic","Roswell Park"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2019,"date_issued":"2019-07-30T15:11:23Z","date_published":"2019-07-30T15:11:23Z","updated_at":"2026-07-27T19:05:21Z","subjects":["biology","cancer sciences"],"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/10477/79956","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Smiraglia, Dominic","Roswell Park"]},{"key":"dc:creator","label":"Author","values":["Chung, Sejin"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2019-07-30T15:11:23Z","2019","2019-05-15 16:11:53"]},{"key":"dc:publisher","label":"Institution","values":["State University of New York at Buffalo"]},{"key":"dc:type","label":"Dc Type","values":["Dissertation","Text"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["biology","cancer sciences"]}]},{"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/10477/79956"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Ph.D.","Historically, cancer treatments such as chemotherapy have targeted the rapidly proliferating characteristic of tumor cells. Chemotherapy is still the standard of care for a multitude of cancers, specifically those that are aggressive and do not have targets to guide drug development. Although substantial efforts have been made to improve current treatments, resistance mechanisms and the heterogeneous nature of cancer cells create a large barrier to successfully eliminating the disease. For instance, targeted therapy in triple negative breast cancer (TNBC) and pancreatic ductal adenocarcinoma (PDAC) such as MEK inhibitors have shown promising results in pre-clinical studies but have yet to yield encouraging developments in the clinic. To address this problem, we wanted to identify better therapies in TNBC and PDAC to improve current treatments (i.e. taxanes or antimetabolites) that have only modestly improved survival rates and cause significant toxicity to the patients. Error- free cell division occurs through a series of regulated steps, termed ‘phases’ of the cell cycle. Progression from one phase to the next depends on molecular checkpoints. If DNA damage is not repaired or mutations not corrected, the mutations will be propagated to daughter cells which can cause genomic instability. Since cancer cells have large mutational burdens, they may be dependent on specific cell cycle checkpoints such as CHK1 to ensure genome stability. As such, utilizing CHK1 inhibitors in combination with DNA damaging agents has been widely investigated in cancers that are aggressive and difficult to target (i.e. pancreatic cancer)."]},{"key":"dc:format","label":"Dc Format","values":["application/pdf"]},{"key":"dc:title","label":"Title","values":["Targeting Cell Cycle Checkpoints in Triple Negative Breast Cancer and Pancreatic Ductal Adenocarcinoma"]}]}],"canonical_facts":{"dc:contributor":["Smiraglia, Dominic","Roswell Park"],"dc:creator":["Chung, Sejin"],"dc:date":["2019-07-30T15:11:23Z","2019","2019-05-15 16:11:53"],"dc:description":["Ph.D.","Historically, cancer treatments such as chemotherapy have targeted the rapidly proliferating characteristic of tumor cells. Chemotherapy is still the standard of care for a multitude of cancers, specifically those that are aggressive and do not have targets to guide drug development. Although substantial efforts have been made to improve current treatments, resistance mechanisms and the heterogeneous nature of cancer cells create a large barrier to successfully eliminating the disease. For instance, targeted therapy in triple negative breast cancer (TNBC) and pancreatic ductal adenocarcinoma (PDAC) such as MEK inhibitors have shown promising results in pre-clinical studies but have yet to yield encouraging developments in the clinic. To address this problem, we wanted to identify better therapies in TNBC and PDAC to improve current treatments (i.e. taxanes or antimetabolites) that have only modestly improved survival rates and cause significant toxicity to the patients. Error- free cell division occurs through a series of regulated steps, termed ‘phases’ of the cell cycle. Progression from one phase to the next depends on molecular checkpoints. If DNA damage is not repaired or mutations not corrected, the mutations will be propagated to daughter cells which can cause genomic instability. Since cancer cells have large mutational burdens, they may be dependent on specific cell cycle checkpoints such as CHK1 to ensure genome stability. As such, utilizing CHK1 inhibitors in combination with DNA damaging agents has been widely investigated in cancers that are aggressive and difficult to target (i.e. pancreatic cancer)."],"dc:format":["application/pdf"],"dc:identifier":["http://hdl.handle.net/10477/79956"],"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":["biology","cancer sciences"],"dc:title":["Targeting Cell Cycle Checkpoints in Triple Negative Breast Cancer and Pancreatic Ductal Adenocarcinoma"],"dc:type":["Dissertation","Text"]},"updated_at":"2026-07-27T19:05:21Z"}