Lukas D. Wartman, M.D.

Assistant Professor
Internal Medicine
Oncology

Molecular Cell Biology Program
Molecular Genetics and Genomics Program

  • 362-9669

  • 314-273-1308

  • 8007

  • 6th floor of the Southwest Tower

  • lwartman@dom.wustl.edu

  • The role of loss of function mutations in Kdm6a in the role of AML and cancer pathogenesis

Research Abstract:

The current focus of my research is to define the role of KDM6A in normal and leukemic hematopoiesis. KDM6A encodes a H3K27 histone demethylase on the X chromosome that is mutated in a wide range of human cancers, including acute myeloid leukemia. Inactivating mutations of Kdm6a are the most common acquired progression events in our mouse model of acute promyelocytic leukemia (APL), occurring in approximately 50% of mouse APL samples studied to date. To define the functional consequences of Kdm6a inactivation, we are analyzing a Kdm6a conditional knockout mouse to define the role of Kdm6a in normal and leukemic hematopoiesis.

Selected Publications:

Grieselhuber NR, Klco JM, Verdoni AM, Lamprecht T, Sarkaria SM, Wartman LD, Ley TJ. Notch signaling in acute promyelocytic leukemia. Leukemia, 2013. 27(7):1548-57. PMID:23455394.

Wartman LD, Welch JS, Uy GL, Klco JM, Lamprecht T, Varghese N, Nagarajan R, Ley TJ. Expression and function of PML-RARA in the hematopoietic progenitor cells of Ctsg-PML-RARA mice. PLoS ONE, 2012. 7(10): e46529. PMID: 23056333.

Wartman LD. Larson DE. Xiang Z. Ding L. Chen K. Lin L. Cahan P. Klco JM. Welch JS. Li C. Payton JE. Uy GL. Varghese N. Reis RE. Hoock M. Kobodlt DC. McLellan MD. Schmidt H. Fulton RS. Abbott RM. Cook L. McGrath SD. Fan X. Dukes AF. Lamprecht TL. Graubert TA. Tomasson MH. Mardis ER. Wilson RK. Ley TJ. Conserved progression mutations revealed by sequencing a mouse acute promyelocytic leukemia genome. Journal of Clinical Investigation, 2011. 121(4):1445–1455. PMCID: PMC3069786.

Last Updated: 12/16/2013 11:25:10 AM

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