by Kim Tankersley, Patient Advocate Back to Advocacy main 2008 31st Annual San Antonio Breast Cancer Symposium Download Event Info Chapter One: San Antonio Breast Cancer Symposium, December, 2007 Chapter Two: San Antonio Breast Cancer Symposium, December, 2008 Last year I was your typical “first-timer” at the San Antonio Breast Cancer Symposium (SABCS); I was simultaneously confused and enthralled, and it was then that I first realized how little I knew about the disease that affects so many of us so deeply. I reflect back upon that momentous event through the eyes of a woman who has since run the gamut of life experiences, from the pain of losing dear friends to breast cancer, to the joy of discovering new, meaningful friendships through breast cancer advocacy. This year, as a second-year recipient of a Breast Cancer Care and Research Fund (BCCRF) scholarship, I arrived in San Antonio, along with an amalgamation of 9,000 clinical oncologists, surgeons, researchers, and breast cancer advocates from around the world. I was enthusiastic, and wielding a veritable surplus of breast cancer knowledge. You see, during the summer, I had the honor of attending the National Breast Cancer Coalition Fund (NBCCF) Project LEAD Institute in Denver, CO. To quote the NBCCF, “The Project LEAD Institute is a five-day science course that covers the basics of cancer biology, genetics, epidemiology, research design, and advocacy.” The course “provides a foundation of scientific knowledge upon which participants can strengthen and empower themselves as activists.” For me, as a breast cancer survivor and advocate, I found that attending Project LEAD enabled me not only the ability to interpret scientific research, but also broadened my scope regarding cancer research in action by participating in a visit to the University of Colorado cancer laboratory; additionally, I was able to meet and network with likeminded people from around the country who were eager and willing to have an impact in the elimination of breast cancer whether it be through education, legislative change, or research advocacy. Alongside Dr. James Waisman, breast medical oncologist, Michele Rakoff, Executive Director of Breast Cancer Care and Research Fund and patient-advocate/ first-time attendee, Christine LaBriola, I set out to tackle the challenges of the 2008 SABCS. One important piece that I brought to San Antonio from Project LEAD was The Hallmarks of Cancer, a landmark article by Drs. Douglas Hanahan and Robert A. Weinberg in which they describe the six essential cell changes that define most cancers. According to Hanahan and Weinberg, these “hallmarks” of cancer cells consist of the following: Self-sufficiency in growth signals—The cancer cell can propagate without needing any other outside growth factors. Insensitivity to antigrowth signals—Normal cells are regulated by signals and factors which tell those cells specifically not to take over, mutate, and conquer. Cancer cells avoid these signals. Tissue invasion and metastasis—Cancer cells have the ability to separate from the primary tumor, travel to distant sites in the body, and make themselves “at home.” The metastases are invaders. Limitless potential for replication –Cancer cells do not generally have the mechanism to censor their own replication, therefore they will reproduce limitlessly. Sustained angiogenesis—To grow and metastasize, cancer cells must have the ability to grow blood vessels, and retain a sustained vascular property. Evading apoptosis—Cancer cells have the ability to avoid “cell-death” which is inherently programmed into all normal cells. This resistance helps the cancer tumor cells to survive and reproduce. What I realized was that to understand these “hallmarks,” or to understand how these “pathways to cancer” work is to understand how and why treatments work. It was armed with this basic science knowledge that I set out to understand the research to be presented. The pathways of cancer have been understood for some time, however, what has arisen from new breast cancer research are breakthroughs leading to a paradigm shift—that is, looking at what we already know in new and different ways, therefore changing the way that we have previously looked at treating breast cancers. The “one-size fits most” treatment regimen seems to be on its way out, at the level of cancer staging, type, and hormone receptor status; looking at the individual through genomic profiling is making its way to the forefront in treatment decisions. What that means to us, the patients, is that researchers have been examining the clinical relevance of gene profiling—namely, through many different types of gene expression assays such as Oncotype DX and MammaPrint, two of the more widely utilized genetic typing analyses. Through an examination of the genomic profile of one’s tumor, it can sometimes be determined how a patient will respond to a particular treatment, rather than “waiting to see” whether the patient will have a response to treatments previously utilized for a particular type of breast cancer. Essentially, an individual tumor’s genomic study will help guide the oncologist in personalizing each patients’ therapy regimen. One of the standout presentations at this year’s Symposium addressed the idea of “differences.” Dr. Patricia Steeg, a renowned molecular biologist from the National Cancer Institute, and whose accomplishments include having identified the first metastasis suppressor gene, gave a talk entitled “Molecular insights into Breast Cancer Metastasis.” In the not-so-distant-past, many viewed metastasis as a certain death sentence. In more recent years, with the advent of new chemotherapy drugs, targeted treatments, and hormonal therapies, metastatic patients have been “living with cancer,” many continuing on to lead long and productive lives. In the past, doctors have examined the pathology of the patient’s primary tumor and used that information to determine how to treat that patient’s metastatic disease. What Dr. Steeg has brought to light through her research is that primary tumors and metastatic tumors are not, in her words, “hardwired identically.” Her discovery of Nm23-HI, a gene that suppresses metastatic growth and has no effect on a primary tumor leads us to the next phase of research. Essentially, there are molecular differences between a woman’s primary breast cancer tumor and that of her metastatic disease, and if we can identify and target these differences, we will be following the most efficient path for treating that woman’s individual cancer. What this means to the patient is that even though women with metastatic disease have been living longer than ever, the potential for increased survival could be exponential. Since Dr. Steeg uncovered the first metastasis suppressor gene, many more have been revealed through diligent research, however, only a small fraction of funding continues to be funneled toward metastasis investigations. With the identification of multiple suppressor genes, the opportunity is now available for researchers to focus on specific targets which have been revealed. According to the American Cancer Society, breast cancer (primarily metastatic disease) killed nearly 41,000 people in 2008. Given the newer genetic profiling assays available, the potential for successful prognoses is immeasurable, and with the current rate of discoveries in the laboratory setting, we should find these numbers dwindling. In addition to Dr. Steeg’s extraordinary work, Baylor College of Medicine’s esteemed Dr. Jenny Chang presented a significant study focusing on recognizing the needs of an individualized treatment based on the genetic makeup of the tumor. In her talk, “PI3-kinase activation and response to trastuzumab or lapatinib in HER-2 overexpressing locally advanced breast cancer (LABC),” Dr. Chang proposes that there is a biomarker (low PTEN gene expression) that may help an oncologist determine which HER-2+ tumors will respond to lapatinib (Tykerb); additionally, she reports two biomarkers (low PTEN expression and mutations in PI3-k) that could help predict which HER-2+ tumors will be resistant to trastuzumab (Herceptin). This is extremely meaningful for patients because again, looking at a tumor based on genes will help with individualization and personalization of treatment for not only that specific patient’s HER-2+ breast cancer, but for that specific tumor. Recognizing these biomarkers could theoretically be a determiner of whether a patient receives Herceptin or Tykerb by differentiating to which therapy a patient’s tumor is sensitive; in this way, the treatment can be tailored to the patient rather than to the standard of tailoring to the disease. If we were to identify an overall theme in this year’s Symposium, it would have to be not only a “paradigm shift,” but a more “widely accepted paradigm shift.” Knowing the hallmarks of cancer, and what is required for cancers to develop and grow, researchers have, in the last several decades, developed therapies to directly address those properties. In recent years, however, with the identification of specific genes, scientists are able to consider the possibilities of treating individual tumors at the molecular level. What we can take away from the 2008 San Antonio Breast Cancer Symposium is that the more specific the research, the more specific the treatment—the better the treatment, the better the cure. We can also take away that though Project LEAD did not make me a clinical oncologist, all told, I learned enough to know that we are headed in the right direction, which is ultimately to eradicate breast cancer. Hanahan, D. and Weinberg, R. 2000. The Hallmarks of Cancer. Cell 100: 57-70.

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