About

Michael W Drazer is an Assistant Professor in the Section of Hematology/Oncology at the University of Chicago. He was raised on a family farm and graduated from Indiana University with degrees in Biochemistry, Biology, and English. He earned both an MD and a PhD in Human Genetics from the University of Chicago. His clinical care focuses on hereditary blood disorders and hereditary cancer syndromes, and he is involved in programs related to Hematology, Leukemia, Stem Cell Transplant/Cellular Therapy, Mesothelioma, Myeloma, and Cancer Risk at UChicago. Drazer also serves as a trainer in the Human Genetics PhD program and is the Associate Program Director of the Physician Scientist Development Program in the Department of Medicine, where he directs the development of physician scientists pursuing accelerated residency and fellowship training.

Research topics

• Genetics
• Biology
• Computer Science
• Medicine
• Oncology
• Database
• Immunology
• Internal medicine

Selected publications

• Hematologic complications in patients exposed to poly-ADP ribose polymerase inhibitors

  Haematologica · 2026-01-29

  articleOpen accessSenior author

  Not available.

  PublisherDOI

• The International Association for the Study of Lung Cancer Pleural Mesothelioma Staging Project: Impact of Common Molecular Alterations and Programmed Death-Ligand 1 Expression on Overall Survival in a Select Cohort From the International Association for the Study of Lung Cancer Ninth Edition Staging Database

  Journal of Thoracic Oncology · 2026-03-01

  articleOpen access
  PublisherOA PDFDOI

• Targeting Menin in T-lineage Acute Lymphoblastic Leukemia

  Molecular Cancer Therapeutics · 2026-03-04

  articleOpen access

  T-lineage acute lymphoblastic leukemia (T-ALL) lacks effective targeted therapies, with poor outcomes in relapsed/refractory disease. HOXA-high T-ALL is biologically aggressive and often resistant to standard therapy. Menin inhibitors, recently approved for KMT2A-rearranged leukemias, may be effective in T-ALL, but biomarkers of response remain undefined. This study aims to evaluate the efficacy of menin inhibition in T-ALL and identify molecular predictors of sensitivity. We tested menin inhibitors (ziftomenib, revumenib, VTP-50469) in 14 primary T-ALL samples and 8 cell lines, representing HOXA-high and HOXA-low genotypes. In vitro sensitivity assays, xenograft mouse models, transcriptomics, proteomics, and phosphoproteomics were used to characterize drug response. MEF2C modulation experiments and combination studies with CDK1/2 and ERK1/2 inhibitors were performed in vitro and in vivo. Menin inhibitors suppressed leukemic growth in a subset of HOXA-high and HOXA-low primary human T-ALL samples. Similarly, ziftomenib was effective in reducing tumor burden in xenografts without major toxicity. Upon treatment, we observed down-regulation of canonical menin targets (HOXA, MEIS1, MEF2C) and upregulation of T-cell differentiation programs. Phosphoproteomic studies identified MEF2C S222 phosphorylation-mediated by CDK1/2 and ERK1/2-as a predictor of ziftomenib sensitivity in T-ALL. MEF2C overexpression promoted proliferation and ziftomenib resistance, while knockdown impaired growth. Ziftomenib synergized with CDK1/2 and ERK1/2 inhibitors in vitro and improved survival in xenografted mice. In conclusion, a subset of T-ALL, defined by high p-MEF2C S222, is sensitive to menin inhibition. Combining ziftomenib with CDK or ERK inhibition offers synergistic efficacy, supporting biomarker-driven clinical trials of this strategy in relapsed/refractory T-ALL.

  PublisherDOI

• Germline genetic testing and privacy concerns in patients with mesothelioma

  Genetics in Medicine · 2026-03-04

  articleSenior author
  PublisherDOI

• Generation of an induced pluripotent stem cell line CGOi001-A from a patient with hereditary thrombocytopenia and a germline ANKRD26 mutation

  Stem Cell Research · 2026-01-31

  articleOpen accessSenior authorCorresponding

  Thrombocytopenia 2 (OMIM 610855) is a hereditary thrombocytopenia and blood cancer syndrome caused by germline mutations in the 5' untranslated region of ANKRD26. We generated an induced pluripotent stem cell (iPSC) line (CGOi001-A) from a donor with a germline ANKRD26 mutation and hereditary thrombocytopenia. This line is a valuable resource for studying the ANKRD26-mutant cellular phenotype.

  PublisherDOI

• Inherited bone marrow failure syndromes

  2025-06-20

  book-chapter1st authorCorresponding
  PublisherDOI

• Spiritual wellness and quality-of-life in adult patients with newly diagnosed acute leukemia receiving initial therapy: Patient-reported outcomes (PROs) from a prospective observational study

  Blood · 2025-11-03

  articleOpen access

  Abstract Introduction Acute leukemia (AL) is a life-threatening hematologic malignancy that often necessitates urgent hospitalization and rapid initiation of intensive, frequently toxic, therapies within hours to days of diagnosis. AL carries a markedly higher acuity than most cancers and presents with great variability in illness trajectories, treatment paradigms, and potentials for cure – even in the relapsed and refractory settings. The unique clinical dynamics of AL care often disrupt multiple domains of quality-of-life (QOL), including psychosocial, physical, emotional, and spiritual well-being. Patients with newly diagnosed AL are often confronted with multiple time-sensitive, complex decisions which can lead to profound spiritual distress as they navigate the emotional and existential impact of their illness. While increased spiritual wellness (SW) has been associated with improved physical functionality and QOL in patients with advanced cancers, particularly at the end-of-life, its role remains poorly understood in the distinct context of newly diagnosed AL. To address this gap, we conducted a prospective observational multi-methods study at the University of Chicago using patient-reported outcome measures (PROMs) to evaluate SW and QOL among adults with newly diagnosed AL receiving initial therapy. We evaluated early changes in PROMs and investigated the relationship between SW and QOL in this population. Methods Adult patients with newly diagnosed AL were prospectively enrolled and completed validated PROMs assessing SW (FACIT-Sp12) and QOL (FACT-Leu) within 7 days of AL diagnosis and again 30 days later. Five additional free-response questions exploring areas of spiritual practices, coping mechanisms, community support, and changes in outlook were asked at both time points and coded thematically using an open, double-coded approach. PROM changes over time were assessed via paired t-tests. The relationship between PROMs were assessed with Pearson correlation coefficients. Patients' SW scores were then stratified categorically into low, average, or high spirituality levels based on established national data (Munoz et al., Cancer, 2015). Chi-square tests examined associations between patients' spirituality levels and selected sociodemographic or biologic factors at both time points. Results Thirty patients were enrolled and completed all assessments. The median age was 52 years (range 21-93), 60% were female, and 53% had acute myeloid leukemia. All patients received disease-specific therapy during hospitalization. Qualitative analysis revealed 3 core themes: personal practice, community support, and perceived growth. Personal practices most commonly included prayer, meditation, and positive thinking. Community support ranged from spouses and family members to friends and religious/spiritual groups. Finally, 53% (16/30) reported a positive change in outlook, comfort, or hope between baseline and day 30. While the mean SW score did not significantly increase from enrollment to day 30 (36.5 vs 37.8, p = 0.31), QOL scores did significantly improve over the same period (111.3 vs 129, p = 0.022). SW had moderate, significant positive correlations with QOL at both enrollment (r = 0.47, p = 0.012) and day 30 (r = 0.43, p = 0.022). The distribution of patients' spirituality levels was 13.3% low, 76.7% average, and 10% high at enrollment; and 13.3%, 73.3%, and 13.3%, respectively, at day 30. Four patients (13%) demonstrated an increase in spirituality level between enrollment and day 30 (2 from low to average and 2 from average to high). Patients in the low spirituality level at enrollment were significantly more likely to have higher household income (50% with $100,000 or more, p = 0.044). No other sociodemographic or biologic factor differed significantly by spirituality level at either time point. Conclusions While SW is significantly correlated with QOL, only QOL significantly improved in the first 30 days following AL diagnosis and treatment initiation. This finding suggests that QOL in this population could improve further through a multidisciplinary care model that actively supports SW. During hospitalization for AL, many personal and community-based sources of encouragement, hope, and strength are often disrupted, which can contribute to spiritual distress. Integrating spiritual care into AL treatment paradigms has the potential to enhance patient-centered care and improve patient-reported outcomes.

  PublisherOA PDFDOI

• Genomics of Acute Myeloid Leukemia at Diagnosis and Remission

  medRxiv · 2025-12-07

  articleOpen access

  Abstract Accurate and comprehensive genetic characterization of acute myeloid leukemia (AML) is essential for diagnosis, prognostication, and treatment selection. We report here, in 255 adults with AML enrolled in a prospective clinical protocol at 18 major cancer centers across the USA, the results of whole genome DNA-sequencing (WGS) at diagnosis and post-treatment remission. WGS effectively recapitulated, and frequently identified genetic alterations missed by, conventional standard of care clinical testing. These new findings included important prognostic and predictive biomarkers, copy number alterations, regulatory element, splicing, and structural variants including partial tandem duplications within KMT2A. All patients had a pathogenic variant detected at diagnosis, and approximately ten percent also had evidence of a potential inherited myeloid malignancy predisposition. This comprehensive atlas of adult AML genomics provides novel insights into disease biology, creates an evidentiary basis to support clinical testing improvements, and is a resource for both diagnostics and drug development. <This work is embargoed, with agreement of medRxiv, until 7th December 2025> . Statement of Significance Acute myeloid leukemia is a diagnostic category encompassing multiple rare hematological malignances. We show, in this nationwide multicenter study, that standardized unbiased whole genome DNA-sequencing and disease-optimized bioinformatics can replicate conventional “standard of care” AML clinical testing results, while also revealing currently underdiagnosed AML disease biology and potential genetic predisposition.

  PublisherOA PDFDOI

• 1830P Leveraging family history to refine high-risk stratification in lung cancer

  Annals of Oncology · 2025-09-01

  article
  PublisherDOI

• ANKRD26-related thrombocytopenia: Hematologic malignancy characteristics, clinical outcomes, and precursor states

  Blood · 2025-11-03

  articleOpen access

  Abstract Introduction Heterozygous germline pathogenic variants (PVs) in the 5' untranslated region of ANKRD26 cause inherited thrombocytopenia and predisposition to hematologic malignancy (HM). The estimated lifetime HM risk is ~10% based on families ascertained from an inherited thrombocytopenia cohort. However, the malignancy spectrum, molecular features, precursor states, and overall clinical outcomes remain poorly defined. Methods We established an international, multicenter cohort of individuals with ANKRD26-related thrombocytopenia diagnosed after undergoing genetic evaluation due to a personal and/or family history of thrombocytopenia and/or HM. Clinical, pathologic, and molecular data were collected for 27 individuals with germline ANKRD26 PVs from 21 unrelated families treated at 11 institutions across 5 countries. Statistical analyses were performed using R (v4.4.2). Results Patients were predominantly male (18/27) and white (25/27). Thrombocytopenia was typically identified in childhood (median age 10 years, range 0-48) with a genetic diagnosis made later (median age 53 years, range 2-80). The mean (+/- SD) pre-malignancy platelet count was 45 +/- 24 K/uL (range 5-87). ANKRD26 PVs observed in each family included: c.-126T>C (n=9), c.-128G>A (n=3), c.-134G>A (n=3), c.-116C>T (n=3), c.-118C>T (n=2), and c.-118C>A (n=1). Thirteen HMs were diagnosed in 11 of 27 (41%) patients, including myelodysplastic neoplasm/syndrome (MDS, n=5), acute myeloid leukemia (AML, n=3), chronic myeloid leukemia (CML, n=2), MDS/myeloproliferative neoplasm (MPN) overlap (n=2), and Langerhans cell histiocytosis (n=1). The median age at first HM diagnosis was 63 years (range 49-80). Recurrent somatic features in myeloid malignancies included complex karyotype (4/11, 36%) and TP53 mutations (5/10, 50%). Of the 3 patients with AML, 1 achieved a partial remission (PR) with venetoclax combined with cladribine, idarubicin, and cytarabine but relapsed, 1 achieved a PR with azacitidine but relapsed <100 days after haploidentical allogeneic stem cell transplantation (alloSCT), and 1 had primary refractory disease. Among 5 patients with MDS, 1 was refractory to decitabine, 1 underwent alloSCT but relapsed 2 years post-transplant, 1 remains in remission post-alloSCT with 1 year of follow-up, 1 is undergoing alloSCT evaluation, and 1 was lost to follow-up. Both patients with CML achieved durable major molecular remissions with imatinib. To better estimate HM risk, we assumed 100% penetrance of thrombocytopenia for ANKRD26 PV carriers and included family members with chronic thrombocytopenia who had not had germline genetic testing. In this expanded series (n=62), 16 individuals developed a HM (26%). Additional diagnoses included MDS with progression to AML (n=1), AML (n=1), CML (n=1), and leukemia of unknown type (n=2). Cumulative incidence of HM was 0% by age 40 years, 17% by age 60 years, and 60% by age 80 years. Somatic sequencing of peripheral blood was performed in 5 HM-unaffected ANKRD26 PV carriers. One individual was found to have clonal hematopoiesis driven by TET2 (c.1648C>T, p.Arg550*) with a variant allele frequency (VAF) of 9% at age 55. Bone marrow biopsy showed mild megakaryocytic atypia and 4% blasts without overt evidence of malignancy. To assess the prevalence of ANKRD26-related HM, we assessed the frequency of ANKRD26 PVs in 2 large MDS/AML cohorts. In the ARUP database (9662 AML, 6397 MDS), 2 individuals (0.01%) had an ANKRD26 PV with a VAF consistent with germline origin. In the MSK-IMPACT Heme Germline MDS/AML cohort (n = 284), no ANKRD26 P/LP variants were identified. Conclusions Germline ANKRD26 PVs underlie <1% of MDS/AML diagnoses but may represent a high-risk subtype characterized by complex karyotype, TP53 mutations, and high risk of relapse. Among our series, the incidence of HM was low early in life but increased substantially with age, reaching 60% by 80 years. This exceeds prior estimates, which were derived from individuals ascertained from thrombocytopenia-based registries. Together, our findings suggest that ANKRD26-associated HM may represent a high-risk clinical entity, and that age and family history should inform surveillance strategies. More studies are needed to define genetic and environmental modifiers of HM risk as well as precursor states to enable early detection and disease interception.

  PublisherOA PDFDOI

Frequent coauthors

• Hamish S. Scott

  Centre for Cancer Biology

  36 shared

• Lucy A. Godley

  Robert H. Lurie Comprehensive Cancer Center of Northwestern University

  35 shared

• Anna Brown

  University of South Australia

  34 shared

• Christopher N Hahn

  University of South Australia

  33 shared

• Claire C. Homan

  South Australia Pathology

  28 shared

• Andreas Schreiber

  27 shared

• Peer Arts

  South Australia Pathology

  22 shared

• David Lawrence

  Centre for Cancer Biology

  22 shared

Labs

• The Drazer GroupPI

Education

• B.S., Biochemistry; Biology; English

  Indiana University

• Ph.D., Human Genetics

  University of Chicago

• M.D.

  University of Chicago

• Other, Internal Medicine

  University of Chicago

• Other, Hematology/Oncology

  University of Chicago