Dr. Michael J. Thirman M.D.
Hematologist-Oncologist | Hematology & Oncology
5841 S Maryland Ave Section Of Hematolog Chicago IL, 60637Rating
1/5
About
Dr. Michael Thirman specializes in the medical management of adults with leukemia, lymphoma, myelodysplastic syndromes, and myeloproliferative disorders. His laboratory focuses on the role of MLL and ...
Education and Training
Univ of Mi Med Sch, Ann Arbor Mi 1986
University of Michigan Medical School 1986
Board Certification
Internal MedicineAmerican Board of Internal MedicineABIM- Medical Oncology
Internal MedicineAmerican Board of Internal MedicineABIM
Provider Details
Expert Publications
Data provided by the National Library of Medicine- Retrovirus-mediated gene transfer of MLL-ELL transforms primary myeloid progenitors and causes acute myeloid leukemias in mice.
- EAF1, a novel ELL-associated factor that is delocalized by expression of the MLL-ELL fusion protein.
- The elongation domain of ELL is dispensable but its ELL-associated factor 1 interaction domain is essential for MLL-ELL-induced leukemogenesis.
- The human programmed cell death-2 (PDCD2) gene is a target of BCL6 repression: implications for a role of BCL6 in the down-regulation of apoptosis.
- ELL-associated factor 2 (EAF2), a functional homolog of EAF1 with alternative ELL binding properties.
- ELL and EAF1 are Cajal body components that are disrupted in MLL-ELL leukemia.
- The elongation factor ELL (eleven-nineteen lysine-rich leukemia) is a selective coregulator for steroid receptor functions.
- Apoptosis induction and growth suppression by U19/Eaf2 is mediated through its ELL-binding domain.
- Methylation-independent silencing of the tumor suppressor INK4b (p15) by CBFbeta-SMMHC in acute myelogenous leukemia with inv(16).
- Successful autologous stem cell collection in patients with chronic myeloid leukemia in complete cytogenetic response, with quantitative measurement of BCR-ABL expression in blood, marrow, and apheresis products.
- Loss of MLL PHD finger 3 is necessary for MLL-ENL-induced hematopoietic stem cell immortalization.
- Consistent deregulation of gene expression between human and murine MLL rearrangement leukemias.
- Dynamic bookmarking of primary response genes by p300 and RNA polymerase II complexes.
- Aberrant overexpression and function of the miR-17-92 cluster in MLL-rearranged acute leukemia.
- MLL fusion proteins preferentially regulate a subset of wild-type MLL target genes in the leukemic genome.
Clinical Trials
Treatments
- Blood Cancers, Leukemia, Lymphoma And More
- Anemia
- Acute Myeloid Leukemia (aml)
- Leukemia
- Dermal Aesthetics
- Oral Surgery Procedures
- Extra Corporeal Shockwave Therapy
Professional Memberships
- Member American Society of Hematology
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PROVIDENT HOSPITAL OF CHICAGOl
500 E 51ST ST CHICAGO IL 60615