Margaret Schwarz

Margaret Schwarz

Mechanisms of Cancer Progression


Adjunct Professor, Department of Chemistry and Biochemistry, University of Notre Dame
Professor, Department of Pediatrics and Integrative Biology Graduate Program, Indiana University School of Medicine, South Bend, IN
Associate Professor, Department of Pediatrics, Division of Critical Care, Division of Pulmonary and Vascular Biology, Integrative Biology Graduate Program, UT Southwest Medical Center, Dallas, TX
Associate Professor, Department of Surgery, Division of Surgical Sciences; Department of Pediatrics, UMDNJ Robert Wood Johnson Medical School
Assistant Professor, Department of Surgery, Division of Surgical Sciences; Department of Pediatrics, UMDNJ Robert Wood Johnson Medical School
Director, Pediatric Critical Care Fellowship, Children's Hospital of Los Angeles
Assistant Professor, Department of Pediatrics, Critical Care Medicine, Division of Cardiothoracic Critical Care, University of Southern California
Assistant Professor, Department of Pediatrics, Division of Critical Care Medicine, Columbia University, New York
Instructor, Department of Anesthesia, Division of Pediatrics Critical Care Medicine, University of Pittsburgh
Fellowship, Pediatric Critical Care, Children's Hospital of Pittsburgh, Pittsburgh, PA
Pediatric Residency, Children's Hospital, Columbus, OH
Pediatric Internship, Children's Hospital, Columbus, OH
M.D., University of Missouri Six-Year Medical School
1986 Biology, University of Missouri

Selected Awards

Member, Society of Pediatric Research
Dr. Edward Livingston Trudeau Scholar, American Lung Association
Finalist for the Louis N. Katz Basic Science Research Prize, American Heart Association
Pediatric Research Award, Society of Critical Care Medicine
Clinician Scientist Award, American Heart Association

Research Interests

The Schwarz lab uses transgenic mice, three dimensional cell culture, in vivo tumor, and lung developmental models to determine mechanisms by which the vasculature regulates cancer progression and alveolar formation.

Our main interests are the role that the anti-angiogenic mediator Endothelial Monocyte Activating Polypeptide II (EMAP II, also known as AIMP-1, Scye-1, and p43) has in lung and tumor development. On the cell surface, EMAP II undergoes proteolytic cleavage to generate an extracellular »22-kDa C-terminal peptide that functions as an anti-angiogenic protein through inhibition of endothelial cell adhesion to fibronectin, blockade of fibronectin matrix assembly via a5b1 integrin, and interference with vascular endothelial growth factor (VEGF) induced pro-angiogenic signaling.

Earlier studies identified a direct interaction between vascular growth factors and the regulation of tissue formation. Using pulmonary developmental models, we have shown that vascular growth factors can also impact epithelial –mesenchymal transdifferentiation, extracellular matrix deposition, and airway simplification resulting in physiologic changes in pulmonary function. Currently, our studies focus on the mechanisms that modulate pulmonary vascular growth and the subsequent impact that the vasculature has on alveolar growth by examining vessel mediation of interstitial lung disease, deposition of the extracellular matrix protein, and epithelial cell proliferation.

By using a pancreatic cancer models (intraperitoneal and subQ), targeted multi-drug therapy strategies are utilized to determine the role that anti-angiogenic factors alone and in combination with chemotherpeutic agents have in regulating tumor cell proliferation and microenvironment including the dense tumor stromal layer, extracellular matrix deposition and vessel formation. Recent studies utilizing this strategy demonstrated that this multi-target approach is effective and superior to current conventional chemotherapeutic strategies.

Recent Papers

  • Legan, S. K.; Lee, D. D.; Schwarz, M. A. "α5ß1 Integrin Mediates Pulmonary Epithelial Cyst Formation." Dev. Dyn. 2017, 246, 475-484.
  • Hassan, M. S.; Awasthi, N.; Li, J.; Schwarz, M. A.; Schwarz, R. E.; von Holzen, U. "A novel intraperitoneal metastatic xenograft mouse model for survival outcome assessment of esophageal adenocarcinoma." PLOS One 2017, 12, e0171824.
  • Lee, D. D.; Lal, C. V.; Persad, E. A.; Lowe, C. W.; Schwarz, A. M.; Awasthi, N.; Schwarz, R. E.; Schwarz, M. A. "Endothelial Monocyte-Activating Polypeptide II Mediates Macrophage Migration in the Development of Hyperoxia-Induced Lung Disease of Prematurity." Am. J. Respir. Cell Mol. Biol. 2016, 55, 602-612.
  • Awasthi, N.; Scire, E.; Monahan, S.; Grojean, M.; Zhang, E.; Schwarz, M. A.; Schwarz, R. E. "Augmentation of response to nab-paclitaxel by inhibition of insulin-like growth factor (IGF) signaling in preclinical pancreatic cancer models." Oncotarget 2016, 7, 46988-47001.
  • Lee, D. D.; Schwarz, M. A. "Adapted approach to profile genes while reconciling Vegf-a mRNA expression in the developing and injured lung." Am. J. Physiol. Lung Cell. Mol. Physiol. 2015, 308, L1202-11.
  • Xu, H.; Malinin, N. L.; Awasthi, N.; Schwarz, R. E.; Schwarz, M. A. "The N terminus of pro-endothelial monocyte-activating polypeptide II (EMAP II) regulates its binding with the C terminus, arginyl-tRNA synthetase, and neurofilament light protein." J. Biol. Chem. 2015, 290, 9753-9766.

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