Benjamin Z. Stanton
Biochemistry, Genetics and Molecular Biology · The Ohio State University
Publications
89
Citations
3,225
Est. group size
~3
Recurring co-author estimate
Active years
23
Publishing since 2004
Benjamin Z. Stanton's lab studies the molecular and genetic drivers of pediatric cancers, especially fusion-positive rhabdomyosarcoma, a childhood muscle cancer driven by an abnormal fusion protein (PAX3::FOXO1). The work focuses on how this fusion protein and related factors (like MYCN and SNAI2) rewire gene activity and chromatin (the packaging of DNA) to promote tumor growth, and explores potential drug targets such as chromatin-modifying enzymes and immune-based therapies like NK cell and CAR T-cell treatments. Overall, the research bridges cancer genetics, epigenetics (chemical modifications that control gene activity without changing DNA sequence), and translational efforts toward new sarcoma and leukemia therapies.
Publication output has grown from a handful of papers in 2017 to a steadier, higher rate of about 7-13 per year since 2021, indicating a generally increasing and now stable level of research activity over the past decade.
Generated by claude-sonnet-5 from public bibliographic data · Jul 20, 2026
- Abstract B029: Oncogenic MIR17HG Expression Is Transcriptionally Regulated by PAX3::FOXO1 and MYCN in Fusion-Positive Rhabdomyosarcoma
Cancer Research · 2026
- Abstract B015: PAX3::FOXO1 establishes dosage-dependent transcriptional states in rhabdomyosarcoma
Cancer Research · 2026
- Abstract B010: Immunoediting of fusion-positive rhabdomyosarcoma after NK cell-based immunotherapy
Cancer Research · 2026
- Fusion transcription factor dosage controls cell state in rhabdomyosarcoma
bioRxiv (Cold Spring Harbor Laboratory) · 2025
- Discovery and Characterization of a Cellular Potent Positive Allosteric Modulator of the Polycomb Repressive Complex 1 Chromodomain, CBX7
UNC Libraries · 2025
- MIR17HG Expression Is Transcriptionally Regulated by PAX3::FOXO1 and MYCN and is Necessary for Oncogenic Activity in Fusion-Positive Rhabdomyosarcoma
bioRxiv (Cold Spring Harbor Laboratory) · 2025
- Role of Myc family proteins in transcriptional regulation of growth and oncogenic transformation in fusion-positive rhabdomyosarcoma
bioRxiv (Cold Spring Harbor Laboratory) · 2025
- KDM3B inhibitors disrupt the oncogenic activity of PAX3-FOXO1 in fusion-positive rhabdomyosarcoma
Nature Communications · 2024
- Epigenetic determinants of fusion-driven sarcomas: paradigms and challenges
Frontiers in Cell and Developmental Biology · 2024
- A stem cell epigenome is associated with primary nonresponse to CD19 CAR T cells in pediatric acute lymphoblastic leukemia
Blood Advances · 2023
- The 3D chromatin landscape of rhabdomyosarcoma
NAR Cancer · 2023
- High-throughput approaches to uncover synergistic drug combinations in leukemia
SLAS DISCOVERY · 2023
- A SNAI2/CTCF Interaction is Required for <i>NOTCH1</i> Expression in Rhabdomyosarcoma
Molecular and Cellular Biology · 2023
- Data from SNAI2-Mediated Repression of <i>BIM</i> Protects Rhabdomyosarcoma from Ionizing Radiation
2023
- Supplementary Tables 1-5 from SNAI2-Mediated Repression of <i>BIM</i> Protects Rhabdomyosarcoma from Ionizing Radiation
2023
- Cancer Research×15
- bioRxiv (Cold Spring Harbor Laboratory)×14
- Nature Communications×4
- iScience×3
- Nature Genetics×2
- Benjamin D. Sunkel
Biochemistry, Genetics and Molecular Biology · The Ohio State University
- Alexi Tallan
Biochemistry, Genetics and Molecular Biology · The Ohio State University
- Chongli Yuan
Biochemistry, Genetics and Molecular Biology · Purdue University West Lafayette
- Brian R. Calvi
Biochemistry, Genetics and Molecular Biology · Indiana University
- Jonathan W. Picking
Biochemistry, Genetics and Molecular Biology · The Ohio State University
This profile was generated automatically from public scholarly data (OpenAlex). Group size and activity levels are estimates derived from co-authorship patterns.
Last updated Jul 19, 2026.
Claim or correct this profile