December 4, 2018
The actual San Antonio Breast Cancer Symposium kicks off tomorrow, but there were several education sessions held on Tuesday afternoon to get us warmed up.
The first session was on the Molecular Biology of Breast Cancer. The first talk was by Lori Friedman, the senior director of Translational Oncology at Genentech. She described how scientists at Genentech investigate which mutations in a tumor are “druggable” and then figure out how to drug them. Basically, they focus on identifying critical points in the tumor’s development. The problem is that a tumor is typically able to figure out an escape mechanism to get around the barrier the drug puts up. This means you have to block both the critical point and the escape mechanism. And then you have to hope that you haven’t also caused some collateral damage somewhere else. It is clearly complicated.
San Antonio Breast Cancer Symposium 2018 kicks off tomorrow
Nicholas Turner, a medical oncologist at the Institute of Cancer Research in the U.K., explained how scientists are using circulating DNA analysis to develop new drugs. (This was one of several talks I heard today on this topic.) As I’ve discussed before, we now have the ability to detect isolated tumor cells in the blood, and even DNA from these cells. The million-dollar question is: What clinical values do these cells—and their DNA—have? Not every tumor cell or piece of tumor DNA represents a metastatic lesion, just as not everyone who heads out in a boat to cross the Atlantic makes it to the New Land. However, the more cells or DNA you find, the more likely they are significant. But getting to the new land is not enough. Once the cells arrive, they have to dodge the dangers that await them and figure out how to sustain themselves. Whether they are successful depends on the conditions that surround them—the microenvironment. In short: we have a long way to go before this work will be ready for prime time.
Kornelia Polyak, a medical oncologist at the Dana-Farber Cancer Institute in Boston, talked about the tumor microenvironment that affects the circulating cancer cells. This is one of my favorite topics. Those circulating or should we say migrating tumor cells have to land somewhere and be able to thrive—but not all our organs are hospitable to these cancer cells. So, what it is about the places the cells go? Again, this is still a work in progress, but it is very interesting.
Sessions included presentations on breast cancer tumor treatments and potential new drugs
The final talk addressed triple negative tumor cells. This designation always has bothered me because it implies that these types of cancer cells are triply bad when, in fact, they just don’t have the three markers—HER2, ER and PR—that we see in other types of breast cancer cells. It turns out that these triple negative tumors contain a sort of a grab bag of all tumor cells that don’t have hormone receptors or overexpress Her 2. In fact, it may turn out that there are actually several subgroups of triple negative tumors. In general, we think of these tumors as aggressive, but that may just be because we don’t yet have a targeted therapy to treat them with
My closing thoughts of the day: When I started in this field, we believed all cancers were alike and the question was only whether they had spread and, if so, how far. Now, we know that there are many different types of cancer, and we’re looking at a future where we hope to match the right treatment to any cancer, just as we can determine the right antibiotic for a specific infection. It’s pretty amazing!