You may not know that there are different kinds of breast cancer. Researchers call these “pathways.” There’s the well-known estrogenic (estrogen positive) breast cancer, caused by an overabundance of estrogen (much of which is from the environment). There’s also progestin positive breast cancer, and the highly publicized BRCA1 and BRCA2 genetic forms of the disease.  My cancer is HER2+, meaning that some of my cells make too much of the HER2 protein (this is termed “overexpression”).  HER2 overexpression is the culprit in about 25% of breast cancers and has been linked to nearly 10% of ovarian cancers as well.

We breast cancer patients who overexpress HER2 proteins sometimes do not respond as well as other patients to traditional treatments such as certain chemotherapy drugs.  Thankfully, the discovery of this cancer pathway allows better chemotherapy drugs to be developed and there are targeted treatments too, including Tykerb (generic name: lapatanib) and Herceptin (generic name: trastuzumab).

HER2 proteins are what is called receptor proteins, which the cells use to communicate with one another, and between the inside of the cell and the “outside.” These proteins are found on the surface of every cell and are usually exclusive; that is, if the protein doesn’t “match” the receptor it cannot bind to it. These receptors come from different “families” and work in different ways, and interact with different molecules.

This really is too intricate to get into here, so we’ll leave it at this: HER2 (also called HER2/neu) receptor molecules are signal transductors, meaning they take signals from inside the cell to the outside (or vice versa), so nearby cells can communicate with one another.

It works like this: signal—reception—transduction—response.

The reception is on the surface of the cell membrane, the transduction occurs through the cell membrane and within the cells, and the response occurs in the nucleus of the cell, in the DNA and the proteins it is told to produce. In this case, the cell is told to produce too many HER2 receptors and may not send proper signals to the cell to grow, mature and die (a process called apoptosis, which happens to of my all-time favorite words).

Finding out about these pathways is important to the increased survival in breast cancer patients, as well as to my own treatment. There are chemotherapies, called non-targeted therapy, and targeted biological therapies such as those I will be getting both in the next round of chemo and after surgery for about a year.

The latter types of therapies work in two ways. First, by binding to the HER2 receptors it “flags” them for destruction by the patient’s immune system. Next, it signals to HER2 receptors “downstream” from the one flagged that it needs to stop producing so many. Lapatanib works from inside the cell out, and herceptin from outside in, and both shrink the tumor (or so we hope!).

As I begin round two of my chemotherapy (weekly infusions of the drug Taxol) I’m also preparing to take one of the targeted therapies, lapatinib. This is part of a clinical trial, as the drug is only FDA approved for metastatic breast cancer at this point and they are researching if it works on in situ breast cancers as well. Both types of treatment provide the patient with all sorts of interesting side effects, from the really scary to the simply annoying. You’ll hear more about these soon.