Michael J. Thirman, M.D.


  • Associate Professor, Department of Medicine - Section of Hematology/Oncology, Cancer Research Center, Committee on Cancer Biology


M.D., University of Michigan, 1986
B.A., University of Michigan, 1982


The University of Chicago
NB007J (MC 2115)
5841 South Maryland Avenue
Chicago, Illinois 60637


Phone:  (773) 702-4133

Webpage (Medical Center)

Webpage (Dept. of Medicine)


Characterization of 11q23 translocations in acute myeloid and acute lymphoblastic leukemia

The research in my laboratory focuses on the characterization of 11q23 translocations, frequent chromosomal aberrations in both acute myeloid and acute lymphoblastic leukemia. We have found that the critical consequence of these 11q23 chromosomal breaks is the disruption of the MLL gene and its subsequent in-frame fusion to a gene on other chromosomes. In previous work, we developed a molecular diagnostic technique for identifying MLL gene rearrangements in all patients with 11q23 translocations. Subsequently, we cloned the gene, ELL, that fuses to MLL in the (11;19)(q23;p13.1) translocation. Recently, we have characterized the spatial and temporal pattern of expression of ELL in murine development. By immunofluorescence, we have determined that ELL is expressed diffusely in the nucleus but excludes nucleoli. Recently, ELL was found to function as an RNA Polymerase II transcription elongation factor. The elucidation of the aberrant functions of ELL when fused to MLL is our major area of investigation at this time. Experiments in progress in the laboratory include identification of proteins that interact with MLL and ELL, development of a mouse model of MLL-ELL leukemia, cloning of (11;19) chromosomal breakpoint junctions, and characterization of potential targets of transcriptional elongation by ELL.

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