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Related Concept Videos

Tumor Immunotherapy01:27

Tumor Immunotherapy

Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...

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Related Experiment Video

Updated: Jun 13, 2026

Bone Marrow Transplantation Platform to Investigate the Role of Dendritic Cells in Graft-versus-Host Disease
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Published on: March 17, 2020

Inhibition of neovascularization to simultaneously ameliorate graft-vs-host disease and decrease tumor growth.

Olaf Penack1, Erik Henke, David Suh

  • 1Department of Hematology and Oncology, Charité, Campus Benjamin Franklin, 12200 Berlin, Germany. olaf.penack@charite.de

Journal of the National Cancer Institute
|May 14, 2010
PubMed
Summary

Targeting blood vessel formation (neovascularization) using E4G10 antibody effectively treats graft-vs-host disease (GVHD) and inhibits tumor growth after allogeneic bone marrow transplantation (allo-BMT). This dual action improves survival rates in mice.

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Area of Science:

  • * Hematology and Immunology
  • * Oncology
  • * Vascular Biology

Background:

  • * Neovascularization, through angiogenesis or vasculogenesis, is crucial for tissue repair and disease progression.
  • * The roles of neovascularization in graft-vs-host disease (GVHD) and post-transplant tumors following allogeneic bone marrow transplantation (allo-BMT) were previously unknown.
  • * Bone marrow (BM)-derived endothelial progenitor cells (EPCs) contribute to vasculogenesis, a process distinct from angiogenesis.

Purpose of the Study:

  • * To investigate the mechanisms of neovascularization in GVHD and post-allo-BMT tumors.
  • * To evaluate the efficacy of an anti-vascular endothelial-cadherin antibody (E4G10) in inhibiting neovascularization, GVHD, and tumor growth.
  • * To assess the impact of E4G10 treatment on survival rates in mice undergoing allo-BMT.

Main Methods:

  • * Immunofluorescence microscopy and flow cytometry were used to analyze neovascularization and EPC contribution in mice with GVHD after allo-BMT.
  • * E4G10 antibody treatment efficacy was assessed through survival studies, clinical and histopathologic GVHD evaluation, and tumor growth monitoring.
  • * Histopathology, bioluminescence imaging, and cytokine immunoassay were employed to evaluate treatment effects on tumor vasculature and systemic inflammation.

Main Results:

  • * Increased neovascularization via vasculogenesis, not angiogenesis, was observed in GVHD target tissues (liver, intestines).
  • * E4G10 treatment inhibited neovascularization by donor BM-derived cells, suppressed GVHD, reduced tumor growth, and significantly improved survival rates (0.29 vs 0.7 probability at 60 days, P < .001).
  • * E4G10 selectively targeted donor-derived neovascularization without affecting host vasculature.

Conclusions:

  • * Targeting neovascularization presents a novel therapeutic strategy for allo-BMT recipients.
  • * E4G10 antibody demonstrates potential for simultaneously ameliorating GVHD and inhibiting post-transplant tumor development.
  • * This approach offers a promising new avenue for improving outcomes in allogeneic hematopoietic stem cell transplantation.