{"id":{"repo_id":"buffalo","oai_identifier":"oai:ubir.buffalo.edu:10477/79321"},"canonical_url":"https://search.dev.ndltd.org/etd/buffalo/oai:ubir.buffalo.edu:10477/79321","repository":{"repo_id":"buffalo","name":"Buffalo","base_url":"https://ubir.buffalo.edu/oai/request"},"display":{"title":"Systemic DNA Damage in Cooperation with High-Fat Diet as a Model of Accelerated Aging","abstract":"Ph.D.","abstract_html":"Ph.D.","abstract_has_math":false,"creators":["Gitlin, Ilya"],"institution":"State University of New York at Buffalo","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":["Gudkov, Andrei","Roswell Park"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2019,"date_issued":"2019-04-04T18:55:20Z","date_published":"2019-04-04T18:55:20Z","updated_at":"2026-07-27T19:05:14Z","subjects":["biophysics","cellular","molecular"],"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/10477/79321","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Gudkov, Andrei","Roswell Park"]},{"key":"dc:creator","label":"Author","values":["Gitlin, Ilya"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2019-04-04T18:55:20Z","2019","2019-01-16 12:56:30"]},{"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":["biophysics","cellular","molecular"]}]},{"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/10477/79321"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Ph.D.","Models of accelerated aging are primarily driven by genetic modification to DNA damage response (DDR) factors. Accumulation of DNA damage is thought to contribute to accumulation of senescent cells (SCs), which are believed to contribute to systemic sterile inflammation (a contributing factor in mammalian aging). This work reveals a nuance, that DNA damage in mesenchymal cells of young mice rescued by bone marrow transplantation from lethal dose of total body irradiation (TBIBMT mice) can be unrecognized in vivo throughout animals’ lifespan without deleterious effects (conversion into SCs or accelerated aging). Regardless of the duration of time that passed from systemic DNA damage it is possible to illicit DDR and senescence programs in TBIBMT mice to convert mesenchymal cells into senescent by forcing the cells to proliferate. A phenomenon we named Dormant Senescence-Prone Cells (DSPC). A depleted pool of proliferation capable mesenchymal precursors leads to impaired wound healing and tumor growth due to inefficient formation of stroma. Additionally, TBIBMT can be used as a model of accelerated aging on obesity-inducing diet, providing a model for obesity-associate health decline of cancer survivors who underwent genotoxic treatment."]},{"key":"dc:format","label":"Dc Format","values":["application/pdf"]},{"key":"dc:title","label":"Title","values":["Systemic DNA Damage in Cooperation with High-Fat Diet as a Model of Accelerated Aging"]}]}],"canonical_facts":{"dc:contributor":["Gudkov, Andrei","Roswell Park"],"dc:creator":["Gitlin, Ilya"],"dc:date":["2019-04-04T18:55:20Z","2019","2019-01-16 12:56:30"],"dc:description":["Ph.D.","Models of accelerated aging are primarily driven by genetic modification to DNA damage response (DDR) factors. Accumulation of DNA damage is thought to contribute to accumulation of senescent cells (SCs), which are believed to contribute to systemic sterile inflammation (a contributing factor in mammalian aging). This work reveals a nuance, that DNA damage in mesenchymal cells of young mice rescued by bone marrow transplantation from lethal dose of total body irradiation (TBIBMT mice) can be unrecognized in vivo throughout animals’ lifespan without deleterious effects (conversion into SCs or accelerated aging). Regardless of the duration of time that passed from systemic DNA damage it is possible to illicit DDR and senescence programs in TBIBMT mice to convert mesenchymal cells into senescent by forcing the cells to proliferate. A phenomenon we named Dormant Senescence-Prone Cells (DSPC). A depleted pool of proliferation capable mesenchymal precursors leads to impaired wound healing and tumor growth due to inefficient formation of stroma. Additionally, TBIBMT can be used as a model of accelerated aging on obesity-inducing diet, providing a model for obesity-associate health decline of cancer survivors who underwent genotoxic treatment."],"dc:format":["application/pdf"],"dc:identifier":["http://hdl.handle.net/10477/79321"],"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":["biophysics","cellular","molecular"],"dc:title":["Systemic DNA Damage in Cooperation with High-Fat Diet as a Model of Accelerated Aging"],"dc:type":["Text","Dissertation"]},"updated_at":"2026-07-27T19:05:14Z"}