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Journal of the National Cancer Institute Advance Access originally published online on October 30, 2009
JNCI Journal of the National Cancer Institute 2009 101(22):1530-1532; doi:10.1093/jnci/djp425
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© Oxford University Press 2009.

NEWS

Why Do Tumors Become Resistant to Antiangiogenesis Drugs?

Charlie Schmidt

The first 150 words of the full text of this article appear below.

Two independent studies published earlier this year bear out a prediction made 6 years ago about why tumors might become resistant to antiangiogenic therapy. The reports suggest that hypoxia generated by angiogenesis inhibition (AI), or the blockage of new blood vessels, triggers signaling molecules that make tumors more aggressive and metastatic.

Published in Cancer Cell in March, the studies are the latest entries in the effort to discover why the antitumor effects of these drugs don’t seem to last and, in some studies, appear to even accelerate metastasis in a rebound effect. The authors say their findings support one of the most popular of the theories proposed to explain rebound: the idea that by cutting off oxygen to cancer cells, the AIs eventually force those cells to migrate to other, nonhypoxic locations. However, reflecting the challenges of antiangiogenic research, these results—generated in preclinical studies with animals—don’t necessarily mirror what has . . . [Full Text of this Article]

Mounting Frustration

Back to the Future

Confirming Earlier Predictions

Diverging Clinical Evidence


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