About

Dr. Daniel R. Matson is an Assistant Professor of Pathology and Laboratory Medicine at the University of Wisconsin–Madison. His role involves leading research within the Department of Pathology and Laboratory Medicine, contributing to the academic and scientific community through his expertise. The page provides information about his lab members and former trainees, indicating his active involvement in mentoring students and postdoctoral researchers, but does not include specific details about his research focus, background, or key contributions.

Research topics

• Genetics
• Biology
• Cancer research
• Cell biology
• Internal medicine
• Oncology
• Medicine

Selected publications

• Abstract 3467: SUMOylation regulates GATA2 stability to control uterine serous carcinoma invasion

  Cancer Research · 2026-04-03

  articleSenior author

  Abstract Background: Uterine serous carcinoma (USC) is an aggressive uterine cancer subtype that is responsible for 40% of uterine cancer deaths. We recently demonstrated that USCs lose expression of the zinc-finger transcription factor GATA2 which drives USC invasion, predicts USC recurrence, and is closely correlated with poor cancer-related and overall survival. However, the mechanistic basis of GATA2 downregulation in USC remains unknown. Methods: GATA2 RNA transcripts were correlated to patient outcomes derived from The Cancer Genome Atlas (TCGA). GATA2 gene methylation was assessed in isolated genomic DNA from patient USC tumors by bisulfite sequencing. Ark1 and Ark2 USC cell lines were utilized for in vitro studies. GATA2 half-life was measured using cycloheximide chase experiments paired with inhibitors of phosphorylation (staurosporine), acetylation (C646), SUMOylation (ML792), cysteine peptidase activity (N-Ethylmaleimide/NEM), and proteasome-dependent degradation (MG132). Anti-GATA2 immunoprecipitations were performed with custom anti-GATA2 antibodies ( Im et al, 2005). Depletion of PIAS2, SENP1, and SUMO2/3 was performed using commercially available siRNAs. Levels of GAPDH, GATA2, PIAS2, SENP1, and SUMO2/3 were measured by western blotting. USC invasion was assessed using Matrigel-coated membrane transwell inserts. Results: GATA2 IHC protein levels showed no correlation with GATA2 gene body or proximal promoter DNA methylation, and GATA2 transcript levels did not predict patient outcome across TCGA USC cases. Post-translationally, USC GATA2 protein half-life was approximately 60 minutes after cycloheximide treatment. Co-treatment with the SUMOylation inhibitor ML792 or the proteasome inhibitor MG132 prolonged GATA2 half-life compared with vehicle, whereas NEM treatment, which inhibits de-SUMOylation and de-ubiquitination, shortened GATA2 half-life. Direct GATA2 SUMOylation was confirmed by anti-GATA2 immunoprecipitation and SUMO2/3 western blot. A candidate siRNA-based approach found that depletion of the E3 SUMO ligase PIAS2 elevated GATA2 levels, while depletion of the SUMO peptidase SENP1 reduced GATA2 levels. siRNA-mediated SUMO2/3 depletion significantly increased GATA2 levels in USC cells and suppressed USC invasion in vitro compared to siScramble controls. Conclusion: USC GATA2 levels are determined by post-translational mechanisms. GATA2 protein has a rapid 60-minute half-life determined by SUMOylation and proteasome-mediated degradation. Depletion experiments support PIAS2 as the GATA2-targeting E3 SUMO ligase and SENP1 as the GATA2-targeting SUMO peptidase. SUMO inhibition increased USC GATA2 levels and suppressed USC invasion, suggesting that SUMO-targeting agents may suppress USC spread through upregulation of GATA2 levels. Citation Format: Anuoluwapo A. Mattix, Peng Liu, Molly A. Accola, William M. Rehrauer, Daniel R. Matson. SUMOylation regulates GATA2 stability to control uterine serous carcinoma invasion [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 3467.

  PublisherDOI

• Abstract 3349: Loss of GATA2 promotes invasion and predicts cancer recurrence and survival in FIGO stage I uterine serous carcinoma

  Cancer Research · 2025-04-21

  articleSenior author

  Background: Uterine cancer is the 4th most common cancer in women. Its incidence is increasing and its mortality rate also is rising. Uterine serous carcinoma (USC) is an aggressive uterine cancer subtype that is responsible for 40% of uterine cancer deaths. Although 50% of USC patients present with cancer localized to the uterine body (FIGO stage I) and should be cured by staging hysterectomy, 30% of these patients later recur in the absence of adjuvant combination paclitaxel-carboplatin chemotherapy. There is no reliable method to identify which USC patients are at risk of USC recurrence, so most patients receive risk-reducing adjuvant chemotherapy associated with significant morbidity. A priori knowledge of recurrence risk would enable a risk-stratified approach to adjuvant therapy to reduce morbidity and optimize survival. GATA Binding Protein 2 (GATA2) is a transcription factor that supports progesterone receptor signaling in the uterus. We recently generated anti-GATA2 monoclonal antibodies that can routinely detect GATA2 by standard immunohistochemistry (IHC). Methods: We assembled a retrospective multi-institutional cohort of 81 patients with primary FIGO stage I USCs. Associations between GATA2 levels and clinicopathologic metrics were evaluated using Student’s t-test, Fisher’s exact test, Kaplan-Meier method, and Cox proportional hazards ratio. Gene targets including GATA2 were depleted from Ark1 and Ark2 patient-derived USC cell lines using siRNA or shRNA, and cell invasion evaluated using Matrigel-coated membranes and organoid-based natural hydrogel. RNA-seq, anti-GATA2 ChIP-seq, and western blotting enabled identification of GATA2 gene targets. Results: GATA2 expression in USC tumors ranged from 0-100% GATA2+ tumor nuclei. USCs with >15% GATA2+ nuclei were defined as GATA2-high based on an initial inflection point in the data that optimally delineated patients by outcome. The 39% of patients with GATA2-high USCs had 100% recurrence-free, 100% disease-specific, and 87% overall survival. These outcomes were significantly better than patients with GATA2-low USCs. Depletion of GATA2 in USC cell lines increased invasion in vitro. In patients who received no adjuvant chemotherapy (n=18), those with GATA2-high USCs had 100% recurrence-free survival compared to 50% recurrence-free survival in GATA2-low USC patients. A multi-omic approach identified SIN3 Transcription Regulator Family Member B as a GATA2 target gene that suppressed USC invasion in vitro. Conclusions: GATA2 IHC identifies FIGO stage I USC patients with a greatly reduced risk of USC recurrence. A GATA2 guided personalized medicine approach using standard IHC methods could be rapidly implemented in most hospital settings, would reduce treatment-related morbidity, and may optimize survival for USC patients. Citation Format: Usha S. Polaki, Trey E. Gilpin, Apoorva T. Patil, Emily Chiu, Paula M. Manan Mejias, Pei Hui, Maria Virumbrales-Muñoz, Lisa Barroilhet, Stephanie M. McGregor, Emery H. Bresnick, Daniel R. Matson. Loss of GATA2 promotes invasion and predicts cancer recurrence and survival in FIGO stage I uterine serous carcinoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 3349.

  PublisherDOI

• Abstract 2658: GATA2 loss promotes Piezo1 expression and stiffness-dependent invasion in uterine serous carcinoma

  Cancer Research · 2025-04-21

  articleSenior author

  Abstract Background: Piezo1 is a mechanosensitive ion channel that couples extracellular matrix (ECM) properties to intracellular signaling cascades that can modulate cell phenotypes. Piezo1 was recently shown to regulate metastasis in high-grade ovarian serous carcinoma (HGSOC) by promoting tumor budding in an ECM stiffness-dependent manner. Uterine serous carcinoma (USC) is an aggressive gynecologic malignancy that is increasing in incidence and responsible for 40% of uterine cancer deaths. USC rapidly invades and metastasizes via mechanisms that remain incompletely understood. Whether Piezo1 may have a similar function in USC, which shares many molecular and clinical features of HGSOC, is not known. We recently showed that expression of the transcription factor GATA2 is lost in USCs that locally invade into the wall of the uterus versus non-invasive USCs. However, the transcriptional targets of GATA2 that mediate this activity are not known. Methods: We performed RNAseq in patient-derived USC cells lines after GATA2 depletion to identify differentially expressed genes. We performed anti-GATA2 ChIPseq in patient derived USC cells to identify genome wide sites of GATA2 occupancy. Western blots were performed for GATA2, Piezo1, and Tubulin after GATA2 depletion in patient-derived USC cells modified to express doxycycline-inducible anti-GATA2 shRNAs or shScramble control. In vitro models of ECM with different stiffnesses (3.7 and 14 kPa) were generated using an interpenetrating network of collagen I and methacrylated gelatin (GelMA), crosslinked within transwell inserts. USC cells were seeded on top of the gels and monitored over 24 hours for invasion in response to GATA2 depletion. Results: GATA2 depletion led to an increase in Piezo1 transcripts in patient-derived USC cells (log2fold change = 0.28, FDR<0.005), while western blot revealed a significant increase in Piezo1 protein expression after GATA2 depletion in two unique patient-derived USC cell lines. Anti-GATA2 ChIPseq identified two significant peaks of GATA2 occupancy within intron 1 of the Piezo1 gene, each harboring conserved canonical GATA motifs. Depletion of GATA2 in patient-derived USC cells led to increased tumor cell invasion, but only on the stiffer substrates. Conclusions: GATA2 binds two putative GATA enhancers within intron 1 of the Piezo1 gene in USC. GATA2 depletion leads to increased Piezo1 RNA and protein expression, which is accompanied by increased tumor cell invasion in a stiffness-dependent manner. Our findings support a model where loss of GATA2-mediated Piezo1 suppression facilitates increased Piezo1 expression, and Piezo1-driven ECM stiffness-dependent USC tumor invasion. They justify further studies to evaluate whether a GATA2-Piezo1 axis is a critical driver of USC invasion in vivo. Citation Format: Brittany Baikie, Mayuri Dutta, Pamela K. Kreeger, Daniel R. Matson. GATA2 loss promotes Piezo1 expression and stiffness-dependent invasion in uterine serous carcinoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 2658.

  PublisherDOI

• Loss of GATA2 promotes invasion and predicts cancer recurrence and survival in uterine serous carcinoma

  JCI Insight · 2025-04-01

  articleOpen accessSenior author

  BACKGROUNDA priori knowledge of recurrence risk in patients with nonmetastatic (International Federation of Gynecology and Obstetrics [FIGO] stage I) uterine serous carcinoma (USC) would enable a risk-stratified approach to the use of adjuvant chemotherapy. This would greatly reduce treatment-related morbidity and be predicted to improve survival.METHODSGATA2 expression was scored by IHC across a retrospective multiinstitutional cohort of 195 primary USCs. Associations between GATA2 levels and clinicopathologic metrics were evaluated using Student's t test, Fisher's exact test, Kaplan-Meier method, and Cox proportional hazard ratio. Invasion in patient-derived USC cells was assessed by Student's t test. RNA-Seq, anti-GATA2 ChIP-Seq, and confirmatory Western blotting enabled identification of GATA2 targets.RESULTSPatients with FIGO stage I GATA2hi USCs had 100% recurrence-free and 100% cancer-related survival, which was significantly better than patients with GATA2lo USCs. In patients for whom adjuvant chemotherapy was omitted, patients with GATA2hi USC had 100% recurrence-free 5-year survival compared with 60% recurrence-free survival in patients with GATA2lo USC. Depletion of GATA2 in patient-derived USC cells increased invasion in vitro.CONCLUSIONRoutine GATA2 IHC identifies 33% of patients with FIGO stage I USC who have a greatly reduced risk of posthysterectomy USC recurrence. Our results suggest that a GATA2-guided personalized medicine approach could be rapidly implemented in most hospital settings, would reduce treatment-related morbidity, and would likely improve outcomes in patients with USC.FUNDINGNIH grants R01 DK068634, P30 CA014520, S10 OD023526, K08 DK127244, T32 HL007899, the UW-Madison Department of Pathology and Laboratory Medicine, the UW-Madison Centennial Scholars Program, the Diane Lindstrom Foundation, the American Cancer Society, the V Foundation, The Hartwell Foundation, and the UMN Department of Obstetrics, Gynecology, and Women's Health.

  PublisherOA PDFDOI

• 1267 GATA2 Expression in Acute Myeloid Leukemia with Myelodysplasia-Related Change (AML-MRC) Correlates with Reduced Bone Marrow Blast Percentage and Mutations in CEBPA, NPM1, NSD1, and IDH2

  Laboratory Investigation · 2025-03-01

  articleOpen accessSenior author
  PublisherOA PDFDOI

• Immunohistochemical Analysis of GATA2 Expression in Endometrium and its Relationship with Hormone Receptor Expression in Benign and Premalignant Endometrial Disorders

  Reproductive Sciences · 2024-10-23 · 4 citations

  articleOpen accessSenior author

  The GATA gene family encodes highly conserved zinc-finger transcription factors that facilitate the development and function of multiple organ systems including the uterus. In the endometrium, GATA2 functions in a positive autoregulatory loop with the progesterone receptor (PGR) and colocalizes with PGR on chromatin to promote PGR transcriptional programs. GATA2 also has PGR-independent functions that maintain endometrial cell identity, and GATA2 transcripts reportedly are down-regulated in endometrial disorders including endometriosis. This event is accompanied by a reciprocal increase in GATA6. Here, we applied custom anti-GATA2 monoclonal antibodies and performed GATA2 immunohistochemistry (IHC) on patient endometrial tissues corresponding to proliferative, secretory, inactive, and hormone-treated endometrium, as well as endometriosis and endometrial atypical hyperplasia/endometrioid intraepithelial neoplasia (EAH/EIN). We also performed IHC for the estrogen receptor, PGR, and GATA6 in relevant groups. The results reveal a tight correlation between GATA2 and PGR expression in the glandular and stromal cells of benign endometrium. GATA2 expression is markedly reduced in stromal but not glandular cells in endometriosis and EAH/EIN. This reduction in GATA2 expression does not lead to a detectable increase in GATA6 expression in endometriosis. Although average glandular GATA2 expression was preserved in endometriosis and EAH/EIN cases, its expression was decoupled from PGR, implying that alternative pathways regulate GATA2 levels in these disorders. Our findings indicate that GATA2 dysregulation is a feature of endometriosis and EAH/EIN, and support a model whereby loss of stromal GATA2 in these disorders contributes to their progesterone insensitivity.

  PublisherOA PDFDOI

• Intraocular bone marrow formation in end-stage phthisis bulbi

  Journal of Hematopathology · 2024-12-18

  articleOpen accessSenior author
  PublisherOA PDFDOI

• Diffuse Large B-Cell Lymphoma, Not Otherwise Specified (DLBCL NOS) Presenting as Multiple Subcutaneous Nodules: An Unusual Cutaneous Presentation of Systemic Disease

  Case Reports in Pathology · 2023-10-03

  articleOpen accessSenior authorCorresponding

  Diffuse large B-cell lymphoma, not otherwise specified (DLBCL NOS) is the most common lymphoid malignancy in the Western world and classically presents as a rapidly enlarging nodal or extranodal mass. Cutaneous involvement by systemic DLBCL NOS is an infrequent clinical presentation, encountered in only 1.5-3.5% of cases, while disseminated cutaneous disease with multiple subcutaneous nodules at the time of diagnosis is unusual and can present a diagnostic challenge. The differential diagnosis when encountering a high-grade B-cell malignancy at a cutaneous site is broad and includes primary cutaneous follicle center lymphoma (PCFCL), primary cutaneous diffuse large B-cell lymphoma, leg type (PCDLBCL-LT), high-grade B-cell lymphoma with MYC and BCL2 rearrangements (HGBCL-MYC/BCL2), and other potential entities which must all be carefully considered before rendering a final diagnosis. In this report, we describe the case of a 69-year-old man who was seen at our hospital due to generalized weakness and was found to have multiple subcutaneous nodules representing disseminated DLBCL NOS. The case was complicated by concurrent monoclonal B-cell lymphocytosis involving the bone marrow.

  PublisherOA PDFDOI

• Needle in a haystack or elephant in the room? Identifying germline predisposition syndromes in the setting of a new myeloid malignancy diagnosis

  Leukemia · 2023-07-01 · 4 citations

  reviewOpen accessSenior author
  PublisherOA PDFDOI

• A gain-of-function p53 mutant synergizes with oncogenic NRAS to promote acute myeloid leukemia in mice

  Journal of Clinical Investigation · 2023-10-17 · 14 citations

  articleOpen access

  We previously demonstrated that a subset of acute myeloid leukemia (AML) patients with concurrent RAS pathway and TP53 mutations have an extremely poor prognosis and that most of these TP53 mutations are missense mutations. Here, we report that, in contrast to the mixed AML and T cell malignancy that developed in NrasG12D/+ p53-/- (NP-/-) mice, NrasG12D/+ p53R172H/+ (NPmut) mice rapidly developed inflammation-associated AML. Under the inflammatory conditions, NPmut hematopoietic stem and progenitor cells (HSPCs) displayed imbalanced myelopoiesis and lymphopoiesis and mostly normal cell proliferation despite MEK/ERK hyperactivation. RNA-Seq analysis revealed that oncogenic NRAS signaling and mutant p53 synergized to establish an NPmut-AML transcriptome distinct from that of NP-/- cells. The NPmut-AML transcriptome showed GATA2 downregulation and elevated the expression of inflammatory genes, including those linked to NF-κB signaling. NF-κB was also upregulated in human NRAS TP53 AML. Exogenous expression of GATA2 in human NPmut KY821 AML cells downregulated inflammatory gene expression. Mouse and human NPmut AML cells were sensitive to MEK and NF-κB inhibition in vitro. The proteasome inhibitor bortezomib stabilized the NF-κB-inhibitory protein IκBα, reduced inflammatory gene expression, and potentiated the survival benefit of a MEK inhibitor in NPmut mice. Our study demonstrates that a p53 structural mutant synergized with oncogenic NRAS to promote AML through mechanisms distinct from p53 loss.

  PublisherOA PDFDOI

Recent grants

• The Role of the GATA2 Interactome in Erythropoiesis

  NIH · $669k · 2021–2026

Frequent coauthors

• Emery H. Bresnick

  University of Wisconsin Carbone Cancer Center

  40 shared

• Molly A. Accola

  University of Wisconsin–Madison

  15 shared

• William M. Rehrauer

  University of Wisconsin–Madison

  15 shared

• Alexandra A. Soukup

  13 shared

• Kirby D. Johnson

  University of Wisconsin Carbone Cancer Center

  13 shared

• Jerry L. Spivak

  Johns Hopkins Medicine

  12 shared

• Alison R. Moliterno

  Johns Hopkins University

  12 shared

• Leslie Cope

  Johns Hopkins University

  12 shared

Labs

• Daniel R. Matson LaboratoryPI

  Usha Polaki MS Graduate Student (MET)Cady Pagel Undergraduate ResearcherAnu Mattix MS Graduate Student (MCP)Natalie Hanka Undergraduate ResearcherApoorva Patil MS Research SpecialistDr. Daniel R. Matson MD, PhD Assistant Professor of Pathology and Laboratory MedicineFormer Trainees and Where They Are Now Brittany Baikie (Graduate Student 2024-2026) – Exact Sciences Dr. Trey Gilpin (Postdoc 2022-2025) – ThermoFisher Scientific...

Education

• Hematopathology Fellowship, Pathology and Laboratory Medicine

  University of Wisconsin Hospitals and Clinics

  2019

• Anatomic Pathology Residency, Pathology and Laboratory Medicine

  University of Wisconsin Hospitals and Clinics

  2018

• M.D., School of Medicine

  University of Virginia

  2015

• Ph.D., Biochemistry and Molecular Genetics

  University of Virginia

  2013

• B.S.

  University of Wisconsin–Madison

  2007