The 2009 San Antonio Breast Cancer Symposium is now over, and the more than 8,400 attendees are on their way home to 97 countries around the world. After an evening spent with my advocate friends enjoying some Tex-Mex in San Antonio, I’ll be homeward bound, well fed in body and, even more importantly, well fed in spirit.
Every year, I look to this meeting for the inspiration that will sustain me in my work with women who are living with metastatic breast cancer and their families. Like them, I am looking for hope. “You are our eyes and ears,” one woman wrote me in an e-mail I received during the conference. “What do you think were the biggest revelations at this year’s conference? Any disappointments? Any surprises?”
Responding to her questions fully is something that will take time, as I am still digesting the sheer volume of data, and the complexity of the science. But right now I can say that, this year, beyond a palpable sense of the progress being made in understanding the various forms of breast cancer and determining “druggable” targets for new therapies, there appears to be some real signs of hope in the emergence of truly effective, less toxic treatments.
Caution is in order, as promising new approaches often prove disappointing once they are tested in clinical trials. Just a few years ago, we thought starving a tumor’s blood supply with an angiogenesis inhibitor like bevacizumab (Avastin) was going to revolutionize cancer treatment—not just for breast cancer, but for all solid tumors. Yet, to date, in multiple large trials of Avastin—two of which were reported at this year’s San Antonio meeting—there has been no improvement in overall survival, the length of time that patients live. Equally disappointing were the results of clinical trials that looked at the tyrosine kinase inhibitors—sorafenib (Nexavar) and sunitinib (Sutent)—for treating metastatic breast cancer. (These drugs are currently used to treat other types of cancer.)
In contrast, a multiple blockade of the HER2 pathway that was achieved by combining trastuzumab (Herceptin) and lapatinib (Tykerb) did result in increased survival. In addition, researchers are hoping that combining Herceptin with another drug still in development, called pertuzumab (Omnitarg), will also increase survival.
We also learned that patients with HER2-positive metastatic breast cancer who had exhausted most of their treatment options experienced a dramatic benefit when started on a drug called T-DM1. This drug is a conjugate of Herceptin and a derivative of an effective but very toxic chemotherapy drug known as maytansine. It works by making Herceptin bind to the chemotherapy molecules in such a way that they can only be released into the cancer cell. This means the drug spares the rest of the body and has few side effects. In the study that was presented, investigators had enrolled a group of very treatment-resistant women, and they found that 45 percent of them had their tumors shrink or stop growing for a period of six months or more—a virtually unmatched achievement.
Progress also is being made in the research that is looking at how to reverse resistance to hormonal therapies. When that comes to fruition, it will be critical for women with hormone-sensitive cancer. And although not presented at this meeting, it’s been reported that drugs that inhibit PARP show great promise for women who have triple-negative breast cancer or whose tumors have a BRCA mutations. We eagerly await the results of these trials.
This kind of success in drug development and translational science gives me hope that there is more, and better, to come.
There was something else that set this San Antonio meeting apart for me: I presented a poster (this link opens to a PDF) representing the steering committee for the BRIDGE Metastatic Breast Cancer Patient Survey. Sponsored by Pfizer and fielded by Harris International, this global survey asked 1,342 women with metastatic breast cancer from 13 countries what it was like to live with this disease. Topics included available resources, support networks, attention given to metastatic breast cancer relative to early breast cancer, and the personal impact of the disease. Patients also were asked if they had ever participated in, or searched for information about, clinical trials.
I’ve been working as an advocate for many years to help women with metastatic breast cancer and their families get the support, services and recognition they deserve. So it was deeply gratifying to see this project come to fruition, and to participate equally as an advocate and presenter among scientists and clinicians in a meeting I’ve attended now for 14 years.
Musa Mayer
www.AdvancedBC.org
Tags: breast cancer, San Antonio Breast Cancer Symposium, HER2-positive metastatic breast cancer, BRCA mutations, triple-negative breast cancer
December 15, 2009 at 5:47 am |
Why were you disappointed in the Nexavar + Capecitabine vs Capecitabine results? 6.4 months vs 4.1 months PFS, p = 0.0006. That isn’t impressive??
December 16, 2009 at 3:08 pm |
2.3 months of progression-free survival isn’t much of an improvement, when you consider the added toxicity…I’m am also underwhelmed by the Avastin PFS overall. Although the E2100 study looked good, later trials dragged down PFS to about this level as well… If we’re going to rely on PFS rather than overall survival, I want more for women with MBC!
December 16, 2009 at 3:32 pm |
I feel compelled to respond to ‘micro’ and all who are excited by an increased disease-free survival time (or perhaps it was even overal survival time). First of all, it is two months. Secondly an awful LOT of MONEY was spent to develop a drug that basically does not very much.
If each drug gets a two month advantage (hopefully in actual overall survival – extension of life span), a) it will cost a fortune to live even two more years and b) it will cause greater and greater toxicities as each drug has many.
Why can’t we ask, compel, persuade drug companies to aim HIGHER, TRY HARDER, to create drugs that do more, cost less and are less toxic.
That would be impressive.
December 16, 2009 at 11:42 pm |
As a bcmets patient for almost 7 years, I absolutely support Musa’s and Ann’s assessments that 2+ month longer disease-free survival is NOT the boon, or unqualified blessing, that it may seem at first blush, to patients who are just starting out on their bcmets trajectories.
With each treatment, very often there are side effects that continue well beyond the efficacy of the drug or radiation, and often those noxious side effects are cummulative, and may even pop up long after the treatment has been halted. For me, after varying months-long treatments, sequentially, with Taxotere (with Decadron – another side-effect-causing drug, given to combat side effects of the Taxotere!), Xeloda, craniotomies and CyberKnife (SRS) treatments for brain mets (6x), Tykerb, Gemzar, SBRT to my liver – I am left much more susceptible to digestive upsets from treatments, have chronic severe pain stemming from the SBRT focused radiation to a large liver tumor in July 2008 – which is only buffered by high-powered opiate pain meds, and I am very, very resistant to adding yet another possibly QOL-decreasing treatment for my poor, pounded-to-a-pulp physical and emotional self to endure.
The only really great good fortune I’ve had with treatment has been with Herceptin, which luckily has not, so far, caused any left ventricle wall cardiovascular damage, and has seemed to slow my aggressive bcmets to a treatable crawl. Whether that, plus my third treatment round with Xeloda, will buy me enough time to last with some semblance of sturdy resilience, until the next wonder drug (perhaps TDM-1) is available for my treatment, is really doubtful.