000009954 001__ 9954
000009954 005__ 20240124114331.0
000009954 0247_ $$2DOI$$a10.6083/4t64gn939
000009954 037__ $$aETD
000009954 245__ $$aIdentification of TLK/ASF1 as a novel pathway for mediating IL-1B-driven acute myeloid leukemia
000009954 260__ $$bOregon Health and Science University
000009954 269__ $$a2022
000009954 336__ $$aDissertation
000009954 502__ $$bPh.D.
000009954 520__ $$aGenetic heterogeneity makes clinical interventions challenging for patients with acute myeloid leukemia (AML). Identifying and targeting common microenvironment-driven pathways should allow the development of effective therapies across AML genetic subtypes. Our laboratory has previously shown that the AML microenvironment is rich in proinflammatory cytokine interleukin-1B (IL-1B) and promotes the growth of AML progenitors. To elucidate the molecular underpinnings of IL-1B-driven AML progression, transcriptome analysis was performed and identified that ASF1B (anti-silencing function-1B) is one of the most differentially expressed genes in AML compared to healthy progenitors. This dissertation focuses on how ASF1B, and its regulator tousled-like kinase 2 (TLK2) contribute to AML cell growth and IL-1B-driven AML progression.
000009954 542__ $$fIn copyright - single owner
000009954 650__ $$aInterleukin-1$$020917
000009954 650__ $$aDNA Damage$$017979
000009954 650__ $$aHistone Chaperones$$038612
000009954 6531_ $$atousled like kinase 2
000009954 6531_ $$amouse
000009954 6531_ $$aacute myeloid leukemia
000009954 6531_ $$aasf1b protein
000009954 691__ $$aSchool of Medicine$$041369
000009954 692__ $$aDepartment of Cell, Developmental and Cancer Biology$$041399
000009954 7001_ $$aLin, Hsin-Yun
000009954 8564_ $$9b7db1a56-0833-4b51-8a76-a409df4fb168$$s3014468$$uhttps://digitalcollections.ohsu.edu/record/9954/files/Lin.HsinYun.2022.pdf
000009954 905__ $$a/rest/prod/4t/64/gn/93/4t64gn939
000009954 909CO $$ooai:digitalcollections.ohsu.edu:9954$$pstudent-work
000009954 980__ $$aTheses and Dissertations