Our annual fall conference features three tracks because breast cancer is not just one disease. Clifford A. Hudis, MD, chief of the breast medicine service and attending physician at Memorial Sloan Kettering Cancer Center in New York City, wrote this blog post about the reasons for these tracks and how breast cancer treatment became more individualized. A member of LBBC’s medical advisory board, Dr. Hudis will lead our morning plenary session on metastatic breast cancer.
Given LBBC’s recognition that not all breast cancer is the same and not all patients need the same information, it is natural to see that the annual fall conference, Breast Cancer Today: Individual Treatments, Shared Experiences, is organized in tracks that enable participants to most efficiently focus on what they find to be most relevant.
Not Just One Disease
Starting with oncology pioneer George Beatson’s 1896 report that some, but not all, women with advanced breast cancer responded to treatment that reduces estrogen in the body, it was clear that we confront more than one, uniform disease. The subsequent description of the estrogen receptor by cancer researcher Elwood Vernon Jensen in 1958 simply allowed us to test for what we already knew – that some cancers are more or less likely to respond to hormone therapies.
The more recent description of the human epidermal growth factor receptor–2 (HER2) and the development of effective treatments that target it added another dimension to “binning” breast cancers. With effective hormone and anti-HER2 therapies we can no longer pretend that cancer is cancer is cancer. One size does not fit all, and one disease is not the same as another.
Using two types of markers, the estrogen and progesterone receptors to define potential hormone sensitivity, and HER2 to sensitivity to anti-HER2 agents, we end up with four potential subtypes of breast cancer:
But this is not done simply to make things orderly. It is done because these subtypes of breast cancer are truly different. They are driven by HER2, driven by hormones, or independent of these two factors. (We don’t consider the so-called “triple-positives” to be more than a subtype of HER2 positive disease, at least for now.) Most importantly, each of these three now-conventional subtypes (HER2, hormone-receptor positive, or triple-negative) has a different typical natural history and response to therapies. In many ways, this is similar to the way we talk about metastatic breast cancer as distinct from early-stage disease. To those unfamiliar with the disease, they are both “breast cancer,” but as you know well, they are leagues apart in meaning.
A Program That Reflects Your Experience
The tracks of the annual fall conference represent a mixture of the new biology of breast cancer (receptor-expression defining disease) and older, anatomic staging (metastatic as opposed to early-stage) disease distribution. This yields these three tracks for this conference:
- triple-negative breast cancer
- hormone receptor-positive breast cancer and HER2-positive breast cancer
- metastatic breast cancer
Within each track, participants will find customized sessions, morning plenaries and, of course, opportunities to connect with peers. In reflecting on our shared communal goals and the commonality that everyone dealing with breast cancer faces, all three tracks will come together at the end of the day for a single concluding plenary session.
I hope you find this structure more useful, informative, and engaging. I look forward to seeing you Sept. 27.