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Anti-VEGF Wound Healing — SCE Medical Oncology MCQ

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HardImmunotherapy & Targeted TherapyAnti-VEGF Wound HealingSCE Medical Oncology

A 58-year-old woman with advanced gastric cancer is started on ramucirumab (anti-VEGFR2) + paclitaxel second-line. She develops non-healing wound after a minor skin laceration. What class effect of anti-VEGF therapy is responsible?

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Correct answer: A — Inhibition of VEGFR2-dependent angiogenesis required for normal tissue repair

Ramucirumab blocks VEGFR2-dependent neovascularisation, impairing the angiogenic phase of normal tissue repair and wound healing. Inhibition of VEGFR2-dependent platelet production required for primary haemostasis: VEGFR2 blockade affects angiogenesis rather than marrow platelet production as the wound mechanism. Inhibition of VEGFR2-dependent keratin synthesis required for epithelial closure: VEGF principally drives neovascularisation, not keratin synthesis. Inhibition of VEGFR2-dependent collagen cross-linking required for scar maturation: collagen cross-linking is not the direct on-target mechanism. Inhibition of VEGFR2-dependent neutrophil migration required for wound sterilisation: the class effect is impaired angiogenesis rather than selective neutrophil trafficking.

Reference: Cyramza UK summary of product characteristics (Updated March 2026): https://www.medicines.org.uk/emc/product/3640/smpc