New Hope for HER2 Positive Breast Cancer Patients

HER2 Breast cancer treatment enhancement on the horizon

/ Author:  / Reviewed by: Joseph V. Madia, MD

(RxWiki News) New research may offer new hope for treating HER2 positive breast cancer, one of the most aggressive forms of this cancer, affecting 20-30 percent of patients. Researchers have found out how the standard drug therapy - Herceptin - works.

They have also discovered that adding medications which increase lymphocyles (a form of infection-fighting white blood cells) improves the effectiveness of treating HER2 positive breast cancer.

"Improving treatment for HER2 positive breast cancer is being studied."

HER2 is caused when the body makes too much of a particular protein called human epidermal growth factor-2 (HER2). HER2 promotes the growth of cancer cells. 

The drug Herceptin (trastuzumab) is used to treat this form of breast cancer because it blocks HER2 from encouraging cancer growth. However, exactly how Herceptin works has remained a mystery until now.

In animal studies, Professor John Stagg, a CRCHUM researcher, Professor Mark J. Smyth, with the Peter MacCallum Cancer Centre in Australia and their colleagues have found that Herceptin also helps in the production of interferons, proteins that defend the body against viruses, bacteria, parasites and cancers. These interferons in turn activate lymphocytes, immune cells that protect against infections.

"These findings open another avenue for breast cancer treatment for nearly a third of all women who are affected," notes Stagg.

Scientists have believed that lymphocytes in tumors improve treatment success. These findings support that view. In addition to revealing the precise workings of Herceptin, this study also showed that combining Herceptin with a therapy that stimulates lymphocytes greatly increases its efficacy in animals.

The authors add that clinical trials could start in the near future and that could pave the way for more targeted therapies.

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Review Date: 
May 24, 2011
Last Updated:
July 5, 2013