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Angiotensin Peptide Slows Cancer by Blocking New Blood Vessel Formation

By LabMedica International staff writers
Posted on 07 Sep 2009
Cancer researchers reported identifying a small peptide that slows cancer growth by inhibiting the process that leads to the formation new blood vessels.

Investigators from Wake Forest University School of Medicine (Winston-Salem, NC, USA) had shown previously that the seven amino acid peptide angiotensin-(1-7) [Ang-(1-7)] slowed the growth of human lung cancer cells growing in culture and reduced the size of human lung tumor xenografts in immunocompromised mice.

In the current study, which was published in June 9, 2009, online edition of the journal Molecular Cancer Therapeutics, the investigators extended their work by injecting Ang-(1-7) or a saline control into mice human carrying human lung cancer tumors. More...
After six weeks they found that the tumors in the animals treated with Ang-(1-7) were reduced in size, while the tumors in the saline-treated animals continued to grow. Ultimately, the tumors in the treated mice weighed nearly 60% less than the tumors in the control animals.

Other experiments carried out in tissue culture and in chick embryos revealed that Ang-(1-7) inhibited growth of new vascular tissue. This effect could be completely blocked by the specific Ang-(1-7) receptor antagonist [d-proline7]-Ang-(1-7), suggesting that these biological actions were mediated by an Ang-(1-7) receptor.

"Because it is a peptide, it is very small and can be made very easily,” said contributing author Dr. Patricia E. Gallagher, professor of molecular genetics at Wake Forest University School of Medicine. "We sometimes like to say we are the aspirin of cancer therapy. If you are diagnosed with lung cancer today, you have got a 15% chance of surviving five years--and that is just devastating. Those other 85 people--85%--they are not going to see their kids graduate. They are not going to see their children get married.”

Related Links:
Wake Forest University School of Medicine


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