Associate Professor of Medicine, University of Chicago Medicine
Hematology
Dr. Michael J. Thirman, MD
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Dr. Michael J. Thirman works in the field of Hematology. He went to University of Michigan Medical School. He received awards:"Regional Top Doctor" and "CMS Meaningful Use Stage 1 Certification". Michael Thirman is a published MD as well. He has 54 publications published. The latest was: Developmental analysis and subcellular localization of the murine homologue of ELL. Michael Thirman accepts Medicare payments and is listed with Medicare.gov.
Publications
- A novel clofarabine bridge strategy facilitates allogeneic transplantation in patients with relapsed/refractory Leukemia and high-risk myelodysplastic syndromes.
- Regulation of MEIS1 by distal enhancer elements in Acute leukemia.
- GFI1B, EVI5, MYB-Additional genes that cooperate with the human BCL6 gene to promote the development of Lymphomas.
- A Manganese Superoxide Dismutase (SOD2)-Mediated Adaptive Response.
- Unexplained Anemia Predominates Despite an Intensive Evaluation in a Racially Diverse Cohort of Older Adults From a Referral Anemia Clinic.
- MLL fusion proteins preferentially regulate a subset of wild type MLL target genes in the leukemic genome.
- Gene mutations, epigenetic dysregulation, and personalized therapy in Myeloid neoplasia: are we there yet?
- PDCD2, a protein whose expression is repressed by BCL6, induces apoptosis in human Cells by activation of the caspase cascade.
- Aberrant overexpression and function of the miR-17-92 cluster in MLL-rearranged Acute leukemia.
- Dynamic bookmarking of primary response genes by p300 and RNA polymerase II complexes.
- Consistent deregulation of gene expression between human and murine MLL rearrangement Leukemias.
- Distinct microRNA expression profiles in Acute myeloid leukemia with common translocations.
- Loss of MLL PHD finger 3 is necessary for MLL-ENL-induced hematopoietic stem Cell immortalization.
- Repression of the PDCD2 gene by BCL6 and the implications for the pathogenesis of human B and T Cell lymphomas.
- Methylation-independent silencing of the tumor suppressor INK4b (p15) by CBFbeta-SMMHC in Acute myelogenous leukemia with inv(16).
- Apoptosis induction and growth suppression by U19/Eaf2 is mediated through its ELL-binding domain.
- The elongation factor ELL (eleven-nineteen lysine-rich Leukemia) is a selective coregulator for steroid receptor functions.
- The human BCL6 transgene promotes the development of Lymphomas in the mouse.
- ELL and EAF1 are Cajal body components that are disrupted in MLL-ELL Leukemia.
- ELL-associated factor 2 (EAF2), a functional homolog of EAF1 with alternative ELL binding properties.
- 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.
- Successful autologous stem cell collection in patients with chronic myeloid Leukemia in complete cytogenetic response, with quantitative measurement of BCR-ABL express...
- High Dose Cytarabine and Mitoxantrone: An Effective Induction Regimen for High-Risk Acute Myeloid Leukemia (AML).
- Fludarabine, melphalan, and alemtuzumab conditioning in adults with standard-risk advanced Acute myeloid leukemia and myelodysplastic syndrome.
- Distinct and separable roles of the complement system in factor H-deficient bone marrow chimeric mice with immune complex Disease.
- Performance status and comorbidity predict transplant-related mortality after allogeneic hematopoietic Cell transplantation.
- Irreversible myelosuppression after fludarabine-melphalan conditioning: observations in patients with graft rejection.
- Bronchiolitis obliterans organizing pneumonia as a complication of allogeneic bone marrow transplantation.
- Cloning of cDNAs of the MLL gene that detect DNA rearrangements and altered RNA transcripts in human leukemic Cells with 11q23 translocations.
- Neurotoxicity of meperidine.
- DNA rearrangements and altered transcripts of the MLL gene in a human T-ALL Cell line Karpas 45 with a t(X;11) (q13;q23) translocation.
- Abnormalities of chromosome band 11q23 and the MLL gene in pediatric myelomonocytic and monoblastic Leukemias. Identification of the t(9;11) as an indicator of long su...
- The human MLL gene: nucleotide sequence, homology to the Drosophila trx zinc-finger domain, and alternative splicing.
- Detection of 11q23/MLL rearrangements in infant Leukemias with fluorescence in situ hybridization and molecular analysis.
- U937 Cell line has a t(10;11)(p13-14;q14-21) rather than a deletion of 11q.
- A t(11;12) 11q23 leukemic breakpoint that disrupts the MLL gene.
- Do terminal deletions of 11q23 exist? Identification of undetected translocations with fluorescence in situ hybridization.
- Detection of MLL gene rearrangements in adult Acute lymphoblastic leukemia. A Cancer and Leukemia Group B study.
- Cloning of ELL, a gene that fuses to MLL in a t(11;19)(q23;p13.1) in Acute myeloid leukemia.
- Molecular analysis of the T-cell Acute lymphoblastic leukemia-associated t(1;7)(p34;q34) that fuses LCK and TCRB.
- Induction of cytochrome CYPIA1 and formation of toxic metabolites of benzo[a]pyrene by rat aorta: a possible role in atherogenesis.
- Rearrangements of the MLL gene in therapy-related Acute myeloid leukemia in patients previously treated with agents targeting DNA-topoisomerase II.
- Heterogeneity of breakpoints of 11q23 rearrangements in hematologic Malignancies identified with fluorescence in situ hybridization.
- Rearrangement of the MLL gene in Acute lymphoblastic and Acute myeloid leukemias with 11q23 chromosomal translocations.
- Variability of 11q23 rearrangements in hematopoietic Cell lines identified with fluorescence in situ hybridization.
- Distribution of 11q23 breakpoints within the MLL breakpoint cluster region in de novo Acute leukemia and in treatment-related Acute myeloid leukemia: correlation with ...
- Analysis of the t(6;11)(q27;q23) in Leukemia shows a consistent breakpoint in AF6 in three patients and in the ML-2 cell line.
- Therapy-related myeloid Leukemia.
- Developmental analysis and subCellular localization of the murine homologue of ELL.
- Chromatin-related properties of CBP fused to MLL generate a myelodysplastic-like syndrome that evolves into myeloid Leukemia.
- 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.
Schools
Univ Of Mi Med Sch
University Of Chicago Hosps
University Of Mn Affil Hosps
Procedures Preformed
- HPC Transplantation (Stem Cell Transplant)
- Thoracentesis
Conditions Treated
- Acute Leukemia
- Anemia
- Basal Cell Carcinoma
- Chronic Myeloid Leukemia (CML)
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Doctors Specialties
- Medical Oncology
- Oncology
- Hematology
Accepted Insurances
Awards
- Regional Top Doctor
- CMS Meaningful Use Stage 1 Certification
Education
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University of Chicago -
University of Michigan Medical School
Hospital
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University of Chicago Medical Center
Drug Facts
| NPI NUMBER | 1356522460 | |
| NPPES Provider LastName | THIRMAN | |
| NPPES Provider FirstName | MICHAEL | |
| NPPES Provider ZIPCode | 606371447 | |
| NPPES Provider State | IL | |
| Specialty Description | Hematology/Oncology | |
| Total Claim Count | 161.0 | |
| Distinct Opioid Count | 0.0 | |
| Opioid Claim Count | 0.0 | |
| Percent Opioid Claims | 0.0 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1356522460 |
| Last Name Of The Provider | THIRMAN |
| First Name Of The Provider | MICHAEL |
| View All |
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