Web Exclusive: Q&A with Dr. Dennis Slamon

Dennis Slamon, MD, PhD, talks about his involvement in the history of Herceptin.

ELIZABETH WHITTINGTON
PUBLISHED: 10:40 AM, TUE JUNE 9, 2009
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Dennis Slamon, MD, PhD, talked with CURE’s Elizabeth Whittington about his involvement in the history of Herceptin. A full transcript of their conversation follows.

Why was your HER2 research considered non-traditional at the time?

A lot of places were still using traditional approaches to treating cancer, which was to use various chemotherapeutic drugs and radiation—essentially poisons of one type or another—in the hopes of killing more bad cells than good cells. It was a one-size-fits-all approach for a lot of different cancers. All cancers within a classification essentially got the same chemotherapy regimen, but it became clear that the outcome with those regimens was very different. Some patients did very well, but many did very poorly. And once the patient had metastatic disease—meaning the disease traveled outside the primary site and beyond where the surgeon could remove it—then the patient almost always succumbed to the disease. Using chemotherapy really didn’t make an impact on survival at that point. So, a number of groups were frustrated with that and thought about backing up and beginning to study the basic science of the cells to see what converts a normal cell to a malignant cell to see if we could treat that specifically.

Why did you choose to research breast cancer and HER2?

We didn’t specifically choose breast cancer or HER2; what we specifically chose to do was look at all the major cancers. We began to study the DNA from those cancers and ask what gene or genes might be broken in them. We specifically looked at genes that would likely be regulating growth because essentially cancer is an abnormality in growth regulation of cells. In ‘84 and ‘85, the genome hadn’t been sequenced yet, so there were only a handful of genes that were really known to be bonafide genes that played a role in regulating growth control. We had banked away a lot of different types of tumor specimens and extracted the DNA, the genetic blueprint, from all those different tumors. We looked at the genes that were known at that time and looked at the DNA of all these different tumor types to see if we could find anything grossly broken using what is now pretty primitive techniques. When we got to the breast cancer specimens, we found that this gene HER2, which was a growth factor receptor, was broken in about 25 percent of breast cancers.

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