000009487 001__ 9487
000009487 005__ 20240124114323.0
000009487 0247_ $$2DOI$$a10.6083/z890rt88b
000009487 037__ $$aETD
000009487 245__ $$aTargeting epigenetic dysregulation in acute myeloid leukemia via BET protein inhibition: mechanisms of resistance and contributions towards the anti-tumor response
000009487 260__ $$bOregon Health and Science University
000009487 269__ $$a2022
000009487 336__ $$aDissertation
000009487 502__ $$bPh.D.
000009487 520__ $$aAcute Myeloid Leukemia (AML) is a genetically and phenotypically heterogeneous white blood cell cancer with a poor prognosis and limited therapeutic options. For many decades the current standard of care has been an intensive chemotherapy regimen, to which only a fraction of patients respond and are physically able to withstand. However, the advent of deep genetic sequencing has led to the discovery of a number of mutational lesions targetable by small-molecule inhibitors, which more patients can tolerate. This dissertation demonstrates that AML drives in vivo T cell exhaustion, which is coordinated by multiple T cell receptor (TCR) activated transcription factors and BET proteins.
000009487 542__ $$fIn copyright - single owner
000009487 650__ $$aStandard of Care$$039491
000009487 650__ $$aT-Lymphocytes$$026731
000009487 650__ $$aT-Cell Exhaustion$$013992
000009487 6531_ $$aacute myeloid leukemia
000009487 6531_ $$abrd4
000009487 6531_ $$aepigenetics
000009487 691__ $$aSchool of Medicine$$041369
000009487 692__ $$aDepartment of Cell, Developmental and Cancer Biology$$041399
000009487 7001_ $$aRomine, Kyle
000009487 8564_ $$9ccbe2f57-fde4-463e-bca6-10368af1feb5$$s24924111$$uhttps://digitalcollections.ohsu.edu/record/9487/files/Romine.Kyle.2022.pdf
000009487 905__ $$a/rest/prod/z8/90/rt/88/z890rt88b
000009487 909CO $$ooai:digitalcollections.ohsu.edu:9487$$pstudent-work
000009487 980__ $$aTheses and Dissertations