MedicineWorld.Org
Your gateway to the world of medicine
Home
News
Cancer News
About Us
Cancer
Health Professionals
Patients and public
Contact Us
Disclaimer

Medicineworld.org: HOXB7 gene promotes tamoxifen resistance

Back to breast cancer blog Blogs list Cancer blog  


Subscribe To Breast Cancer Blog RSS Feed  RSS content feed What is RSS feed?

HOXB7 gene promotes tamoxifen resistance




A gene target for drug resistance, a triple-drug cocktail for triple negative breast cancer, and patients' risk for carpal tunnel syndrome are among study highlights scheduled to be presented by Johns Hopkins Kimmel Cancer Center researchers during the 33rd Annual CTRC-AACR San Antonio Breast Cancer Symposium, held Dec. 8-12. The information is embargoed for the time of presentation at the symposium.

A number of postmenopausal women with early-stage breast cancers who initially respond well to tamoxifen become resistant to the drug over time and develop recurrent tumors. Johns Hopkins Kimmel Cancer Center scientists have observed that a gene called HOXB7 appears to be the culprit in tamoxifen resistance.



HOXB7 gene promotes tamoxifen resistance

Taken by mouth, tamoxifen is used at every stage of breast cancer to treat existing tumors and prevent new ones from developing. The drug works only in women whose tumor cells have a protein, called the estrogen receptor, which binds to the estrogen hormone. Tamoxifen binds to this estrogen receptor and blocks estrogen's effect on fueling cancer cells.

In experiments on cancer cells, the researchers observed that when the HOXB7 gene is overexpressed, as occurs in a number of breast cancers, tumors cells became resistant to tamoxifen. Overexpression of HOXB7 results in proteins that interact with a series of other estrogen-activated genes and proteins, including the HER2 gene, known to make breast cancers aggressive. When the researchers knocked out the HOXB7 gene in one group of breast cancer cells, HER2 activation decreased and the cells became more responsive to tamoxifen. The researchers then showed how the HOXB7-HER2 interaction works.

"HOXB7 appears crucial in orchestrating estrogen receptors, HER2 and other receptors that promote aggressive tumor growth in breast cancer cells," says senior author Saraswati Sukumar, PhD, professor of oncology and co-director of the Breast Cancer Program at Johns Hopkins. "Dialing down expression of the HOXB7 gene could stave off tamoxifen resistance".

Though it's still not evident how to shut down HOXB7, Sukumar says that oncologists could potentially use the drug Herceptin to kill tumors in patients whose HER2 expression increases.


Posted by: Janet    Source




Did you know?
A gene target for drug resistance, a triple-drug cocktail for triple negative breast cancer, and patients' risk for carpal tunnel syndrome are among study highlights scheduled to be presented by Johns Hopkins Kimmel Cancer Center researchers during the 33rd Annual CTRC-AACR San Antonio Breast Cancer Symposium, held Dec. 8-12. The information is embargoed for the time of presentation at the symposium.

Medicineworld.org: HOXB7 gene promotes tamoxifen resistance

BREAST CANCER MAIN| Home| Breast cancer news| Common terms| Breast cancer treatment| Breast cancer treatment by stage| Mammogram and breast cancer screening| Surgical treatment of breast cancer| Chemotherapy of breast cancer| Chemo drugs used in breast cancer| Doxorubicin| Cyclophosphamide| Methotrexate| Hormonal therapy of breast cancer| Radiation therapy of breast cancer| Monoclonal therapy| High dose chemotherapy for breast cancer| Recurrent breast cancer| Bisphosphonates and breast cancer| Pregnancy and breast cancer| Risk factors for breast cancer| Risk details| My risk| Comprehensive breast cancer information| Breast cancer statistics| African Americans and breast cancer| Ashkenazi and breast cancer| Asians| Hispanic| Men| Native Americans| Older women and breast cancer| Younger women| Pregnant women and breast cancer| BRCA|

Copyright statement
The contents of this web page are protected. Legal action may follow for reproduction of materials without permission.