
ABNORMAL BLOOD VESSELS add to the havoc inside a tumor and prevent treatments from reaching cancer cells.
Image: KEITH KASNOT
In Brief
- Abnormal and dysfunctional blood vessels are a hallmark of solid tumors, one that contributes directly to malignant properties of a cancer as well as preventing treatments from reaching and attacking tumor cells.
- Normalizing tumor vessels allows cancer therapies to penetrate the mass and to function more effectively.
- Unexpectedly, drugs originally designed to destroy tumor blood vessels act to repair them for a time, opening a new avenue for cancer treatment as well as restoration of abnormal vasculature in other diseases.
—The Editors
While still a graduate student in 1974, I had a chance to see malignant tumors from a most unusual perspective. I was working at the National Cancer Institute in the laboratory of the late Pietro M. Gullino, who had developed an innovative experimental setup for studying cancer biology—a tumor mass that was connected to the circulatory system of a rat by just a single artery and a single vein. As a chemical engineer, I decided to use this opportunity to measure how much of a drug injected into the animal would flow to the tumor and back out again. Amazingly, most of the substance injected into the rat never entered the tumor. To make matters worse, the small amount that did reach the mass was distributed unevenly, with some areas accumulating hardly any drug at all.
My immediate concern was that even if a small fraction of the cancer cells in a human tumor did not receive an adequate dose of whatever anticancer drug was being applied, those cells could survive—causing the tumor to grow back sooner or later. Perhaps the engineer in me was also drawn to trying to understand and solve the apparent infrastructure problem inside tumors that posed a major obstacle to the delivery of cancer therapies.
This article was originally published with the title Taming Vessels to Treat Cancer.
Already a Digital subscriber? Sign-in Now
If your institution has site license access, enter here.



See what we're tweeting about





Comments
Add Comment