Data Loading...
When estrogen isn’t the culprit | Harvard Gazette Flipbook PDF
When estrogen isn’t the culprit | Harvard Gazette http://news.harvard.edu/gazette/story/2011/07/when-estrogen-isn’t-the-
123 Views
28 Downloads
FLIP PDF 429.35KB
When estrogen isn’t the culprit | Harvard Gazette Harvard.edu
Photo & Multimedia Services
For Journalists
About HPAC
Go Go
Search
Friday, Jul. 22, 2011 Fair, 84° F
Today
Campus & Community
Culture & Society
Print /
Engineering & Technology
Email /
HarvardScience
Arts & Culture
HarvardScience
National & World Affairs
Environments & Sustainability
Health & Medicine
Calendar
Multimedia
Life Sciences
Share
Text size:
A
A
A
Health & Medicine
When estrogen isn’t the culprit Study finds new points of attack on breast cancers not fueled by estrogen
A
Athletics
By Rob Levy Dana-Farber Cancer Institute Communications Monday, July 11, 2011
lthough it sounds like a case of gender confusion on a molecular scale, the male hormone androgen spurs the growth of some breast tumors in women. In a new study, Harvard scientists at Dana-Farber Cancer Institute provide the first details of the
cancer cell machinery that carries out the hormone’s relentless growth orders. The study, to be published in the journal Cancer Cell on July 12, provides scientists with several inviting targets — cell proteins that snap into action in response to androgen — for future therapies. Drugs that block those proteins could slow or stifle tumor growth in many breast cancer patients who are not helped by standard hormone-blocking agents such as tamoxifen. “We identified a novel subtype of breast tumor which grows in response to androgen but not estrogen, and have uncovered the signaling pathways involved in its growth. And we’ve demonstrated that drugs capable of blocking these pathways, including the receptor for androgen itself, can inhibit tumor growth,” says Harvard Medical School Professor Myles Brown, the study’s senior author. “This opens new avenues to the treatment of some women with breast cancer that doesn’t respond to standard endocrine therapies.” About 70 to 75 percent of breast tumors are fueled by the female hormone estrogen. Their cells are loaded with estrogen receptors (ER), traplike structures specially shaped to ensnare estrogen molecules. When estrogen becomes lodged in an estrogen receptor, it sets off a chain of events that prompts the cell to grow and proliferate. Drugs such as tamoxifen block estrogen from entering the receptor, thereby thwarting the growth process.
Photo by Sam Ogden
“We identified a novel subtype of breast tumor which grows in response to androgen but not estrogen, and have uncovered the signaling pathways involved in its growth. …. This opens
http://news.harvard.edu/gazette/story/2011/07/when-estrogen-isn’t-the-culprit/[7/22/2011 7:59:46 AM]
When estrogen isn’t the culprit | Harvard Gazette
The remaining 25 to 30 percent of breast cancers, dubbed ER-negative
new avenues to the treatment of some women
tumors, lack estrogen receptors, and thus do not respond to tamoxifen and
with breast cancer that doesn’t respond to
similar agents. Scientists know that the majority of breast tumors — even those with estrogen receptors — have receptors for androgen, but the
standard endocrine therapies,” says Harvard Medical School Professor Myles Brown, the study’s senior author.
reasons for these receptors’ presence, and how they might influence tumor growth, have been unknown. It might seem odd that some women’s breast cancers carry receptors for a
Recommend Confirm
normal development of secondary sexual characteristics in females, Brown breast cancer cells that have receptors for androgen but not for estrogen. The current study set out to find if that is the case and, if so, why. Using published data on the genomic make-up of breast tumor cells, Brown and his colleagues found a distinctive group — accounting for 5 to 10 percent of all breast cancer patients — that had large numbers of androgen receptors, no ERs, and an oversupply of a protein called HER2. Cells of this type proliferated rapidly when exposed to androgen. To understand the mechanism behind this growth, investigators did a mass
2 Submit
Most Popular in Health & Medicine » First U.S. full face transplant patient » Coffee tied to lower prostate cancer risk » Progress against melanoma » ADHD linked to substance abuse risk » Twin dangers: Malnutrition and obesity
Latest Activity
screening of these tumor cells’ genetic material to see which sections of DNA bind to the androgen receptor — an indication of which genes the receptor directly switches on and off. By combining these findings with a survey of all the genes active within these cells, the researchers found that the androgen receptor governs two “transmission lines” — or pathways —
490
14
hormone associated with males, but androgen is also involved in the remarks. Scientists have theorized that androgen propels the growth of
491
Login
You need to be logged into Facebook to see your friends' activity
No recent activity to display. New territory 53 people recommend this.
for growth signals. The pathways, named for important proteins within
Garden party
them (WNT and HER2), play central roles in cell division and proliferation.
18 people recommend this.
When researchers used drugs to handcuff the androgen receptor or the WNT or HER2 proteins in ER-negative breast cancer cells, tumor growth slowed — both in laboratory cell cultures and in mice grafted with the cells. “These findings are strong evidence that therapies that shut down proteins in the WNT or HER2 pathways, or block the androgen receptor itself, can
Of the bean I sing 648 people recommend this. Editing the genome 657 people recommend this. Predicting cancer’s spread Facebook social plugin
be effective anti-tumor agents for women with this variety of breast cancer,” Brown says. “Combination therapies that target proteins at different points in the pathways are likely to have the greatest success.” The study involved a close collaboration between Brown’s lab and the computation biology group at Dana-Farber headed by X. Shirley Liu, an associate professor of biostatistics at Harvard School of Public Health.
Event Calendar
Full calendar
Attitudes Toward Human Diversity in Children: The Specific Case for Anti-fat Attitudes Tue., July 26, 2011, 4 p.m. RCC conference room
Brown and Liu recently founded the Dana-Farber Center for Functional Cancer Epigenetics in order to make the genomic and computational approaches used in this study more widely available to the scientific community. The co-first authors of the study are Min Ni and Yiwen Chen of DanaFarber. Co-authors include Elgene Lim, Shannon Bailey, and Yuuki Imai of Dana-Farber; and Hallie Wimberly and David Rimm of Yale University School of Medicine.
http://news.harvard.edu/gazette/story/2011/07/when-estrogen-isn’t-the-culprit/[7/22/2011 7:59:46 AM]
Multimedia Features
More
When estrogen isn’t the culprit | Harvard Gazette
The study was supported by grants from the National Cancer Institute, National Institutes of Health, and Department of Defense Recommend Confirm
491
490
2
14
Submit
Harvard Medical School researchers crawl a neural network Scientists can finally look at circuits in the brain in all of their complexity. How the mind works is one of the greatest mysteries in nature, and this research presents a new and powerful way for us to explore that mystery. Video 2:36 run time July 11, 2011
Stem cells: Mending a broken heart? Video / Oct 15, '09
Harvard Stem Cell Institute - First 5 years Video / Nov 13, '09
Related Articles What's behind aggressive breast cancer Harvard scientists at Dana-Farber Cancer Institute have identified an overactive network of growth-spurring genes that drive stem-like breast cancer cells enriched in triple-negative breast tumors, a typically aggressive cancer that is highly resistant to current therapies.
New hope for the cure For the 20 percent of patients with socalled triple-negative breast cancer, the outcome is bleak. Now, however, researchers from Harvard Medical School (HMS) and Baylor College of Medicine have identified a critical molecular component to the disease, one that suggests potential therapies involving combinations of FDAapproved, readily available drugs.
The debate over mammograms The debate over whether routine mammogram screenings are useful
http://news.harvard.edu/gazette/story/2011/07/when-estrogen-isn’t-the-culprit/[7/22/2011 7:59:46 AM]
When estrogen isn’t the culprit | Harvard Gazette
diagnostic tools or potentially ineffective and wasteful was the issue of a Harvard School of Public Health forum on March 8.
Editing the genome Treating the chromosome as both an editable and an evolvable template, researchers have demonstrated methods to rewrite a cell’s genome through powerful new tools for biotechnology, energy, and agriculture.
Explore Article Tags Androgen / Breast Cancer / Breast tumor / DanaFarber Cancer Institute / Dana-Farber Center for Functional Cancer Epigenetics / Estrogen / Estrogen receptors / Harvard Medical School / Harvard School of Public Health / HER2. / Myles Brown / Tamoxifen / X. Shirley Liu
Current Issue
Archives
Harvard University Gazette
May 26-September 1, 2011
Subscribe to the Gazette
RSS Feed
Sign up for daily emails with the latest Harvard news.
Subscribe to real-time updates from the Gazette. What's RSS?
Your email address Subscribe Subscribe
View sample email
Harvard Gazette RSS feed More Gazette RSS feeds
Requires Adobe PDF Reader
© 2011 The President and Fellows of Harvard College.
http://news.harvard.edu/gazette/story/2011/07/when-estrogen-isn’t-the-culprit/[7/22/2011 7:59:46 AM]
Privacy Trademark Contact us