Herceptin

This drug, Herceptin, is one that I received while getting my chemo therapy, because my cancer was the more aggressive HER2+ specific.

Breast Cancer Update

American Cancer Society Breast Cancer Update

March 2012

Finding Cures: What's New in Breast Cancer Research and Treatment?

Herceptin: One of the Greatest Advances in Breast Cancer Treatment in the Past 20 Years

When Dennis Slamon, MD, PhD, began his work identifying unique molecular changes in tumors, none of the federal funding agencies would give him money. “People didn’t think our approach would work,” he says. Slamon was hoping to find genetic alterations that could be targets for new drugs.

The American Cancer Society, however, saw the potential in Slamon’s research, and gave him a grant to pursue his idea. That research resulted in the 1998 US Food and Drug Administration’s (FDA) approval of the drug Herceptin (trastuzumab) for breast cancer that has spread to other parts of the body, turning one of the deadliest forms of the disease into one of the most treatable. Herceptin goes to work in those breast tumors with an overabundance of the protein HER2, which affects 15% to 25% of women diagnosed with breast cancer.

Slamon led the research to identify HER2 as a cancer target while at the University of California, Los Angeles Jonsson Comprehensive Cancer Center, where he today is director of clinical/translational research. He answered some of our questions about his groundbreaking research.

Q: What does the HER2 protein do in the cell?
A: HER2 sits on the outside of the cell like an antenna, detecting growth signals from the cell’s surroundings. In normal quantities, HER2 plays an important role in maintaining the breast cell’s growth.

But breast cancer cells in about one-third of all women make extra copies of the HER2 gene. Those extra copies result in excess HER2 protein on the surface of the cell. Cells with an overabundance of HER2 protein amplify the growth signals from the environment and, as a result, divide more rapidly than normal and propagate the tumor. It’s that extra protein that doctors look for when deciding whether women will respond to Herceptin.

Q: Are tumors with the HER2 mutation different from other tumors?
A: When we began our work, women with HER2 alterations had among the worst survival rates. Their tumors were more likely to spread and less likely to respond to treatment. With the advent of Herceptin, things have reversed. Patients with HER2 now have among the best survival rates. This is an example of how a pretty aggressive cancer can become quite treatable.

Q: How does Herceptin work?
A: Herceptin binds to the HER2 protein and prevents it from relaying a signal that stimulates the cancer cell to divide. It has far fewer side effects than standard chemotherapy because it only disrupts cancerous cells containing HER2.

Q: Herceptin is often considered to be among the first forms of personalized medicine for cancer treatment. Is this a glimpse at the future of cancer treatment?
A: There’s no question that personalization is where cancer treatment is going. The “one size fits all” approach is starting to ebb. In the past, all people with a particular type of tumor would receive the same treatment. In the future, a person will receive the treatment that is most appropriate for the genetic changes present in his or her tumor.

Q: So not all tumors in a particular tissue are the same.
A: No. Breast cancer is not one disease. It’s a multiplicity of diseases, depending on how the cell became altered. There are many roads that can lead to cancer, which results in many subclasses of cancers.

Q: When you began this work, did you know that tumors would break down into these genetic subclasses?
A: We didn’t know, but we suspected. When HER2 was identified, it looked like it might be a receptor that detects growth signals from the cell’s environment. We thought we’d look in the major cancers to see if any carried alterations in that gene. We didn’t see anything until we got to a group of breast cancer specimens that contained too many copies of the gene. We found that the tumors containing the HER2 alteration were much more aggressive than normal tumors, making that protein an excellent drug target.

Q: That’s the work that was funded by your first American Cancer Society grant.
A: That’s right. That kick-off grant was very small but also very timely. It was Society money that allowed us to do the first work to convince the major federal funders that our approach could work to identify genetic alterations in tumors that could be drug targets. I now have an American Cancer Society Clinical Research Professorship, which is more of a career award to fund ongoing research.

The American Cancer Society is currently funding hundreds of breast cancer research grants worth $115.2 million.

©Excerpted from Triumph magazine, with permission of the American Cancer Society and Pace Communications, Inc.

For more information on the American Cancer Society, visit us at www.cancer.org.

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Copyright 2000-2012 © American Cancer Society

A movie was made about the trials and tribulations Dr. Slamon went through in trying to get approvals and money for this miracle drug - Living Proof. Very enlightening regarding what researchers must endure. Certainly explains why the cost of many drugs is so high.