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The protein NOS2 isn't good for ER-negative breast cancer patients

10.18.10 | JCI Journals

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Breast cancers can be divided into different subtypes based on several criteria, including whether or not they express the protein to which the female hormone estrogen binds; that is, the estrogen receptor (ER). Patients with ER-negative breast tumors have a worse outlook than those with ER-positive breast tumors. However, even among ER-negative breast tumors, those characterized as basal-like are the most aggressive and difficult to treat. New therapeutic targets for this subtype of breast cancer are urgently needed. Now, a team of researchers, led by Stefan Ambs, at the National Cancer Institute, Bethesda, report data that suggest that the protein NOS2 could be a good drug target in this context. The data, generated by analysis of human breast cancer samples and cell lines, lead the authors to conclude that high levels of NOS2 are a predictor of survival in patients with ER-negative breast tumors and to suggest that selective NOS2 inhibitors might be of benefit to these individuals.

TITLE: Increased NOS2 predicts poor survival in estrogen receptor–negative breast cancer patients

AUTHOR CONTACT:
Stefan Ambs
National Cancer Institute, Bethesda, Maryland, USA.
Phone: 301.496.4668; Fax: 301.480.4676; E-mail: ambss@mail.nih.gov .

View this article at: http://www.jci.org/articles/view/42059?key=e19810fc296c1ecf1474

Journal of Clinical Investigation

Keywords

Article Information

Contact Information

Karen Honey
JCI Journals
press_releases@the-jci.org

How to Cite This Article

APA:
JCI Journals. (2010, October 18). The protein NOS2 isn't good for ER-negative breast cancer patients. Brightsurf News. https://www.brightsurf.com/news/12VW70Y1/the-protein-nos2-isnt-good-for-er-negative-breast-cancer-patients.html
MLA:
"The protein NOS2 isn't good for ER-negative breast cancer patients." Brightsurf News, Oct. 18 2010, https://www.brightsurf.com/news/12VW70Y1/the-protein-nos2-isnt-good-for-er-negative-breast-cancer-patients.html.