Benjamin (BJ) Purow

About

Benjamin (BJ) Purow is a research faculty member with a primary appointment as a Professor of Neurology at the University of Virginia School of Medicine. He holds a BA in Chemistry and Physics from Harvard University and an MD from Johns Hopkins University. His research focuses on developing innovative approaches to treating brain tumors and other cancers, with particular emphasis on neuroimmunology, cancer biology, and translational science. Dr. Purow's laboratory is dedicated to exploring novel therapeutic strategies, including targeting the Notch pathway, microRNAs, and proteins such as DGKalpha, to improve treatment outcomes for brain cancers like gliomas and glioblastoma. His work involves investigating the role of microRNAs in cancer survival and exploring the potential of existing drugs for new anti-cancer applications. Notably, his research has demonstrated that inhibiting DGKalpha can enhance the efficacy of other therapies such as radiation and immunotherapy, with some compounds already identified as safe in clinical trials. His team also investigates the anti-cancer properties of medications approved for other indications, aiming to facilitate rapid translation of findings into clinical practice.

Research topics

• Biology
• Cancer research
• Cell biology
• Genetics
• Biochemistry
• Chemistry
• Internal medicine
• Medicine

Selected publications

• Tissue factor is a critical regulator of radiation therapy-induced glioblastoma remodeling

  Cancer Cell · 2023 · 79 citations

  GBM cells and orchestrates oncogenic TME remodeling by activating both tumor-autonomous signaling and extrinsic coagulation pathways. Intratumoral F3 signaling induces a mesenchymal-like cell state transition and elevated chemokine secretion. Simultaneously, F3-mediated focal hypercoagulation states lead to activation of tumor-associated macrophages (TAMs) and extracellular matrix (ECM) remodeling. A newly developed F3-targeting agent potently inhibits the aforementioned oncogenic events and imp…

  PublisherDOI

• The nuclear DICER–circular RNA complex drives the deregulation of the glioblastoma cell microRNAome

  Science Advances · 2020 · 49 citations

  results in the restoration of cytosolic localization of DICER and widespread derepression of the microRNAome, leading to transcriptome-wide rearrangements that mitigate the tumorigenicity of glioblastoma cells in vitro and in vivo with correlation to favorable outcomes in patients with glioblastoma. These findings uncover the mechanistic foundation of microRNAome deregulation in malignant cells.

  DOI

• Glioblastoma Cell Resistance to EGFR and MET Inhibition Can Be Overcome via Blockade of FGFR-SPRY2 Bypass Signaling

  Cell Reports · 2020 · 39 citations

  SPRY2 is a purported tumor suppressor in certain cancers that promotes tumor growth and resistance to receptor tyrosine kinase inhibitors in glioblastoma. Here, we identify a SPRY2-dependent bypass signaling mechanism in glioblastoma that drives resistance to EGFR and MET inhibition. In glioblastoma cells treated with EGFR and MET inhibitors, SPRY2 expression is initially suppressed but eventually rebounds due to NF-κB pathway activation, resultant autocrine FGFR activation, and reactivation of…

  DOI

• Understanding current experimental models of glioblastoma-brain microenvironment interactions

  Journal of Neuro-Oncology · 2024-01-01 · 16 citations

  reviewOpen accessSenior author
  PublisherOA PDFDOI

• The semaphorin 3A/neuropilin-1 pathway promotes clonogenic growth of glioblastoma via activation of TGF-β signaling

  JCI Insight · 2023-10-03 · 16 citations

  articleOpen access

  Glioblastoma (GBM) is the most lethal brain cancer with a dismal prognosis. Stem-like GBM cells (GSCs) are a major driver of GBM propagation and recurrence; thus, understanding the molecular mechanisms that promote GSCs may lead to effective therapeutic approaches. Through in vitro clonogenic growth-based assays, we determined mitogenic activities of the ligand molecules that are implicated in neural development. We have identified that semaphorin 3A (Sema3A), originally known as an axon guidanc…

  PublisherOA PDFDOI

Recent grants

• NIH Grant R01CA136803

  NIH · $1.5M · 2014

• NIH Grant R01CA134768

  NIH · $1.3M · 2013

• Targeting diacylglycerol kinases in glioblastoma

  NIH · $1.6M · 2014–2018

Frequent coauthors

• David Schiff

  University of Virginia

  113 shared

• Roger Abounader

  University of Maryland, Baltimore

  83 shared

• Patrick Y. Wen

  77 shared

• Tracy T. Batchelor

  Dana-Farber Brigham Cancer Center

  70 shared

• Howard A. Fine

  New York Hospital Queens

  64 shared

• Keith L. Ligon

  50 shared

• Andrew D. Norden

  50 shared

• Andrew B. Lassman

  Columbia University

  49 shared

Similar researchers at University of Virginia

• Todd Bauerh-61
• Gustavo Rohdeh-41
• Dave Kashatush-34