Tumours can make their own blood vessels and so, don't have to draw sustenance from their host's blood vessels, reports a new study.
The findings offer an explanation for why a class of drug once heralded as a game-changer in cancer treatment is proving less effective than had been hoped.
In both studies, researchers worked with tumour samples from patients with an aggressive type of brain cancer called glioblastoma. They found that many of the blood-vessel cells within the tumours contained genetic markers characteristic of the cancer cells, suggesting that the blood vessels were of tumour origin.
In a dish, these cells could make blood vessels and, when they were injected into the brains of mice, tumours developed with blood vessels that clearly came from the original human cells. Those stem-like cells, the researchers concluded, could form both tumour and blood vessel.
One of the groups, led by Viviane Tabar, a neurosurgeon and stem-cell researcher at the Memorial Sloan-Kettering Cancer Center in New York City, applied Avastin to cells in a dish to try to block these events.
Although the drug did affect differentiation into blood-vessel cells, "we found that Avastin does not alter that first process whatsoever," said Tabar.
In the second study, Ruggero De Maria from the Italian National Institute of Health in Rome and his colleagues selectively killed the tumour-related blood-vessel cells. This caused the tumours to shrink, showing their reliance on those blood vessels. However, the number of tumour-derived blood-vessel cells in each tumour sample varied from 20 percent to 90 percent, suggesting that blood-vessel formation was more important for some tumour cells than others.
This isn't the first time researchers have suggested that cancer cells can make their own blood vessels. In 1999, Mary Hendrix, a cancer researcher now at Northwestern University in Chicago, Illinois, and her colleagues reported a similar effect in melanoma cells which they called "vascular mimicry".
"There are many more ways to affect the vasculature" than through such drugs. It means we need to identify either more than one drug" to shut down blood vessels of tumour and non-tumour origin, "or a common molecular mechanism affecting both the tumour and the vasculature," said Cheresh, who co-authored two such studies.
The studies have been published in Nature.