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"Antimyeloangiogenic" therapy for cancer by inhibiting PlGF

Sonja Loges1, Thomas Schmidt, Peter Carmeliet

  • 1Vesalius Research Center (VRC), VIB, Katholieke Universiteit Leuven, Leuven, Belgium.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|May 28, 2009
PubMed

Insights

Targeting placental growth factor (PlGF) with an antibody may overcome cancer resistance to anti-VEGF therapies by reducing myeloid cell infiltration. This approach is being evaluated in clinical trials.

Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Tumor angiogenesis inhibition is a key cancer treatment, but resistance limits efficacy.
  • Vascular Endothelial Growth Factor (VEGF) inhibitors are common, yet tumors develop resistance.
  • Myeloid cell infiltration into tumors contributes to resistance against anti-VEGF therapies.

Purpose of the Study:

  • To review the role of Placental Growth Factor (PlGF) and its receptor VEGFR-1 in angiogenesis and inflammation.
  • To discuss the potential of an anti-PlGF antibody (alphaPlGF) to overcome resistance to VEGF(R) inhibitors.
  • To highlight the clinical evaluation of a humanized alphaPlGF antibody (TB403) in cancer patients.

Main Methods:

  • Review of preclinical and clinical data on PlGF/VEGFR-1 signaling.
  • Analysis of the antimyeloangiogenic activity of alphaPlGF.
  • Summary of ongoing Phase I clinical trials for TB403.

Main Results:

  • PlGF and VEGFR-1 play roles in promoting tumor angiogenesis and inflammation.
  • alphaPlGF demonstrates antimyeloangiogenic activity, potentially overcoming resistance.
  • TB403, a humanized alphaPlGF antibody, is under investigation in cancer patients.

Conclusions:

  • Targeting PlGF offers a novel strategy to enhance antiangiogenic therapy efficacy.
  • alphaPlGF may overcome resistance mediated by myeloid cell infiltration.
  • TB403 shows promise for improving cancer treatment outcomes by targeting PlGF.

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