I reaaaaally want to write about the presentations at the recent breast cancer conferences I’m been to – Lisbon and San Antonio. But before I get into all that I need to do a few basic breast cancer biology posts.
Breast cancer has several different subtypes. These subtypes dictate treatment decisions in terms of systemic (aka whole body as opposed to localized) treatment. A test is done on a breast biopsy for three different receptors.
My subtype of cancer is called “Triple Positive.” That means I’m positive for all three commonly tested receptors. I’m positive for the estrogen receptor, I’m positive for the progesterone receptor, and I’m positive for the Her2 protein.
Estrogen and progesterone are hormones. The most common type of breast cancer is hormone positive but negative for the Her2 protein. This cancer is treated with hormone-blocking drugs after surgery (and often chemo and/or radiation but not all the time – whether those methods are used depends on the Stage and aggressiveness).
What do hormone-blocking drugs consist? Well, it depends on menopausal status and how dangerous the cancer is.
For post-menopausal women, the standard of care is an Aromatase Inhibitor. A woman who has undergone menopause no longer has functioning ovaries, so her cancer is not fueled by estrogen from them. It is fueled by estrogen from other sources, like adrenal glands and fat cells. The AI, which is taken as a pill once a day, shuts down the estrogen from those sources.
What about premenopausal women who still have functioning ovaries? Well, there’s two options. For earlier-stage, lower-risk cancer, Tamoxifen is the standard of care. Tamoxifen does not shut down estrogen completely, but it attaches itself to the estrogen receptors. Then, for those with more advanced disease, they might be on ovarian suppression. This consists a choice of two shots, given either every four weeks or every twelve weeks and they are given either in the butt or stomach (fun!). Some women will also get their ovaries surgically removed to keep any breakthrough estrogen at bay. And remember above that I mentioned that there’s other sources of estrogen besides ovaries? A daily AI works in conjunction with the ovarian suppression to shut down the additional sources of estrogen. For metastatic patients, this therapy is often used in conjunction with new drugs called CDK 4/6 inhibitors.
For the record, I have been treated with ovarian suppression since November 2014, an AI from January 2015-April 2017 and a CDK 4/6 inhibitor as part of a clinical trial from January 2016-July 2016.
Above, I mentioned that I’m also positive for the Her2 protein. Her2 positive cancer can either be positive or negative for the hormone receptors. Her2 used to be the most deadly subtype, however Herceptin turned things around in one of oncology’s greatest success stories. Herceptin led to other targeted therapies, that target the specific protein while doing minimal damage to healthy cells. Herceptin is used either alone, with chemo, or in conjunction with a newer targeted therapy, Perjeta. Then there’s Antibody Drug Conjugates. They enclose potent chemo into a targeted therapy. The one available now is Kadcyla, but there’s a lot of interest and others in development. Then we get to Tyrosine kinase inhibitors. The one used these days is Tykerb, although there’s lots others in trials or available on compassionate allowance. Tykerb and similar drugs are important because they are small molecule drugs that can more easily pass the blood brain barrier.
I’ve been on Herceptin/Perjeta (March-June 2014), Kadcyla (September 2014-June 2015), Tykerb (November 2016-August 2017) and am currently on Herceptin/Perjeta again.
Then there is the Triple Negative subtype. Triple Negative breast cancer is characterized by its lack of receptors – i.e. it’s not positive for either hormones or Her2. That makes it harder to treat as hormonal and targeted therapies are not available for it. Triple Negative is treated by chemo. Other subtypes are often treated with chemo but they have the option of being treated with less harsh methods. I do not respond to targeted therapy or hormone therapy by itself so I am on chemo as well.
The chemos I’ve had are Adriamycin/Cytoxan (January-March 2014), Taxol (March-June 2014), Xeloda (March-August 2017) and am currently on Taxotere.
I sincerely hope my next treatment will be a targeted therapy or a combination of targeted therapies. It would be nice to have my hair grow back and be less exhausted. I say “next treatment” because that is the reality for most metastatic breast cancer patients. The cancer will eventually outsmart the treatment and they will have to switch treatment. There’s a small group of MBC patients who have a tremendous response to one particular treatment and stay on it for years or decades. I am doing my damndest to push for research to improve that number so many more people can live with MBC as a chronic diseases and not go through life switching treatments until they run out or their body no longer tolerates them and they die.