Once we got the results of my liver biopsy, confirming that we were dealing with breast cancer, not uterine leiomyosarcoma, the next question was, what type of chemotherapy?
In our initial phone conversation after the biopsy results came in, Dr. M made an important – and apparently prescient – observation: “things that show up quickly tend to respond quickly to treatment.”
This was good news, obviously. All those tumors in my liver had grown sometime since last November, and that’s pretty darn fast.
We made an appointment to meet with Dr. M at Dana Farber the following week, on May 8. I also had a chest CT and an initial measurement of my liver tumor markers during that visit. (They had not measured the tumor markers during my April 26 abdominal/pelvic CT because they hadn’t realized there was any need to do so until we saw the results.) The tumor markers are used to evaluate the cancer’s progression and response to treatment. It’s interesting to note that not everyone has tumor markers, regardless of the severity of their case. Having them makes life easier, though, because they serve as a good indicator.
Dr. M reiterated that HER2+ breast cancer has had major advances in treatment over the past 10-15 years. So let’s take a minute to talk about what HER2 is.
To begin with, the HER2 gene regulates development of the HER2 (human epidermal growth factor receptor 2) protein that exists on the outside of breast cells. The protein acts as a receptor that directs cell growth, division, and repair. When you have a mutation in the HER2 gene (like me!), the genetic instructions go haywire, telling cells to produce far too many HER2 receptors on the cells. This, in turn, makes the cells grow like crazy. And, voila! HER2+ breast cancer.
HER2 status is described on a scale from 0 to 3+, where 0 = HER2 negative and 3+ means >10% of tumor cells overproduce the HER2 protein. On the pathology report from my liver biopsy, >95% of the tumor cells were overproducing. What can I say? I’m an overachiever.
This brings us to treatment options. Specifically, “first line” treatment options. First line treatment refers to the fact that you want to hit the cancer hard with the medicines that are known to have the greatest effect. (Duh.) Second line treatments come down the line, if the first line approaches aren’t effective. Let’s take a moment to hope that I won’t need second line treatment.
There are two standard types of
chemotherapy used in first line treatment for HER2+ breast cancer: Taxol and Taxotere. By the by, both of these drugs are extracts from Pacific Yew tree bark.
While Taxol and Taxotere serve the same purpose, they are delivered quite differently. Taxol is a once/week treatment, while Taxotere is delivered once every 3 weeks. Taxotere is known to be a little more taxing (har har) on the liver, while Taxol takes a greater toll on the heart. For this reason, Dr M also ordered an echocardiogram to be sure my heart is strong enough to withstand the Taxol. (It is! Hallelujah! Part of my body is healthy, at least.)
In addition to the chemo drugs, the standard of care for HER2+ cancer involves the use of two targeted antibodies. Antibodies are Y-shaped proteins that are often described as keys that match a lock. When the antibody key is inserted into the lock (in this case, the HER2 receptor is the lock), the antibody blocks the receptor, rendering it useless. This is where the science gets CRAZY cool.
One antibody, Herceptin, is used to block the HER2 receptor on the outside of the cell, in the standard way I just described. A major clinical trial showed that using Herceptin extended progression-free survival of HER2+ patients significantly, making this a go-to part of treatment since the early 2000s. The second antibody, Perjeta, only came onto the scene very recently, following the “CLEOPATRA study,” published in 2015.* The function of Perjeta was explained brilliantly to us by one of the Dana Farber pharmacists, Dr. A, via this simple drawing.
Here’s how she explained it. Herceptin comes along and blocks the HER2 receptor on the outside of the cell membrane. But researchers discovered that after this blockage, the “tails” of the HER2 receptor positioned within the cell would start wiggling in an effort to connect. Once they connected, the HER2 receptor would pop back up outside of the cell membrane! Damn little tricky bastards! Perjeta was developed to create another blockage in the HER2 receptor, but it targeted the space between the HER2 receptor’s tails within the cell, creating a wedge that prevents the HER2 tails from reconnecting. Wicked!
With all that background, the decision as of May 8 consult with Dr. M was that we would go our separate ways, do some reading, look at the results of the tumor marker test, and then come back to decide which way to proceed. I also told him at this point that I wanted to get a brain scan done, just to be sure there was no cancer there. We have no evidence to indicate the cancer might have spread to my brain, but I want to know for sure. Dr. M also ordered an MRI of my thoracic spine to try to get an explanation for why I had been having some mid-back pain. The plan was that we would use all this information (the tumor markers, echocardiogram, CT scans, and MRI results) to make a final decision about which course of treatment to pursue. We set May 18 for the MRIs and May 22 as the tentative start date for chemo.
That was all well and good until the liver tumor marker results came in later that day. Dr. M once again called us at home. He had expected the markers to be high, given the state of my liver, but high would have been in the 100s. My markers were in the 1000s.
This result removed the option of using Taxotere, because my liver function was already too impaired. Instead, I would have to use Taxol, since my heart is strong enough, and he promised to move heaven and Earth to get the treatments started that week. The reason he wanted to start chemo immediately was to prevent my liver function from getting worse. If it did, this would make it more difficult for my liver to process the chemo, complicating the entire process.
True to his word, Dr. M pounded the pavement at DF to move things around so I could get in for treatment that week. Allow me to sum up this timeline for you: I had the initial CT scans on April 26, showing the liver tumors. Liver biopsy on May 2. Our in-person consult was May 8. Dr. M called us that evening with the tumor marker results. My first chemo treatment was scheduled for May 10, exactly two weeks after that initial CT scan.
In short: this sucks, but I’m in very good hands.
Be sure to tune in for our next installment, where Herceptin hosts a cancer-killing party at my expense.
*CLEOPATRA stands for Clinical Evaluation of Pertuzumab and Trastuzumab, the official names of Perjeta and Herceptin. It also happens to be the name of the woman who ruled ancient Egypt, made some important Romans crazy with desire, and generally kicked a lot of ass. Seems appropriate.