SARS-CoV-2 infection was linked to greater short-term outgrowth of lung cancer cells previously implanted in mice. In infected lungs, the vessel-growth factor VEGF increased; an antibody blocking it suppressed tumour growth. This aggressive implanted-cell model does not represent human tumours dormant for years, and the study establishes neither that cancer developed in people nor that a treatment helps them.
Researchers delivered Lewis lung carcinoma cells intravenously to mice susceptible to SARS-CoV-2. Infection began seven days later; outcomes were assessed two weeks after cell delivery and one week after infection. The infected group developed more visible lung tumour foci and larger average lesions than the uninfected group given an equal cell dose. This setup measured outgrowth over a short experimental interval.[1]
Infected lungs showed oxygen deprivation and inflammation alongside increased measures related to vascular endothelial growth factor, or VEGF, and its receptor VEGFR2. Cancer cells engineered to produce more VEGF formed tumours even at lower implanted cell numbers. Vessel density fell and implanted cancer cells grew less when the mice received an antibody against VEGF. The inhibition was also measured among infected animals carrying tumour cells.[1]
Autopsy tissue from 21 adults who died after severe COVID-19 was evaluated alongside lung samples from 15 people without the infection. The comparison addressed blood-vessel and inflammatory markers, while providing no follow-up of later tumour growth. The researchers state that the mouse model does not represent clinical tumour dormancy. A weeks-long experiment using aggressive implanted cells cannot establish human cancer development or the benefit of VEGF treatment after infection.[1]
