That title should really be movin’ on down, because this post is all about my metabolic markers…which are moving down!!! As a child of the 70s and 80s, however, I couldn’t resist a reference to one of the best television theme songs ever, as sung by the lovely Ja’net Dubois.
The big news is that my liver function is steadily improving. The suite of enzymes used to assess liver function — APT (alkaline phosphatase), AST (aspartate aminotransferase) and ALT (alanine aminotransferase) — were very high before I started treatment, ranging from 2 to 5X above normal. But the levels are all coming down, and even approaching normal levels. Check it out for yourself.
The other two measures on this chart, CEA and CA 27-29, shown by the orange and purple circles, are liver tumor markers. You’ll recall that Dr. M wanted to get chemo moving on the double once he saw these results. I had to create a second y-axis to show these tumor markers above, because their values are in the 1000s, rather than the 100s. CEA, or carcinoembryonic antigen, is used as a marker of response to treatment for a few different cancers. CA 27-29 is used specifically for breast cancer. The normal range for CEA is 0.0 – 2.5 ng/mL, while normal for CA 27-29 is 0-38 U/mL. My levels were 4272 ng/mL and 1218 U/mL, respectively. So, yeah…kind of high.
They only measure the tumor markers every 3 weeks, which means I’ll get new results this coming Wednesday. Based on the weekly metabolic results, though, I expect these to have moved on down, too.
Otherwise, things are going well. No problems with the chemo treatments, and the side effects have been mild. Last week I had an isolated skin rash and some blurry vision for a couple days, but that subsided. No mouth sores yet, which is great news, and my appetite is much improved, though still unpredictable.
I’ve found that the first day after treatment is an excellent day. The steroids I receive on treatment day have the effect of making me feel sort of superhuman the next day. But this wears off quickly, and the second and third days after treatment are usually far more subdued. This week I made the mistake of doing a little too much on the first day, which meant I was utterly exhausted on day 2. I’m learning how to navigate this cycle, though, and grateful that it’s not been too bad thus far.
Thanks for all the love, everyone. We’re feeling it.
One of the major and most well known side effects of chemotherapy is hair loss. It’s important to note that not every type of chemo causes total hair loss, and even when it’s expected, individual responses vary.
You may wonder why hair loss is so common with chemotherapy. It’s pretty simple, really. These drugs target fast-growing cells, but cancer cells aren’t the only ones that grow quickly in our bodies. Hair follicles, especially, grow very fast, thereby attracting the attention of the chemo drugs.
The informational website breastcancer.org offers a handy summary of the typical hair loss responses from a few common chemotherapies used for breast cancer.
As you can see, Taxol (my treatment), is the jackpot of hair loss, generally causing complete loss of hair all over the body. Yippee.
I have long hair. Thick hair. A lot of it. I’m one of those people who is often described by my hair. In fact, I’ve long argued that my long brown hair is the reason people often tell me I look “just like” their cousin/sister/aunt/best friend/brother’s ex-girlfriend, etc. People see a woman with long brown hair and glasses, and they see nothing else. I even gave this a name many years ago: “long brown haired woman syndrome.”
It is noteworthy, then, that I am going to lose this defining attribute as part of treatment, even if only for a little while. This is, of course, one of the most challenging outward aspects of chemotherapy for many people, especially women. It shouldn’t be too surprising that there is research underway to try to counteract this psychologically significant side effect. You may have heard of the cooling head caps that are said to minimize hair loss during chemo treatment, or perhaps the development of topical agents using nanoparticles that might reduce the accumulation of chemo drugs in hair follicles. That’s all well and good, but I won’t be using any of those things. I’m going whole hog, baby.
Don’t get me wrong: I know I’m going to freak out when I start losing my hair. I decided that it would be least traumatic for me to take some control of the situation by getting my hair cut short. I have this image of standing in the shower and sobbing as handfuls of hair come out of my head. This is the worst case scenario for me, and I want to avoid it. At least I can start by making sure that only small handfuls of hair come out. Plus, this allows me to try out a short haircut in a very low pressure way (I’ll probably only have it for a couple more weeks) and then donate the remainder.
This brings me to my Hair Loss Plan, or HLP.
HLP Step 1: take photo of self with long hair. Note length, texture, color and current status of brown to gray ratio. I think I’d give myself a B:G of 20:1 overall, with a 2:1 ratio over my forehead. I’m tracking that B:G ratio (sort of) for two reasons: wig makers don’t want hair with more than 5% grays (whew! Just made the cut), and I’m curious about how things will look when my hair grows back in a few months from now.
HLP Step 2: ask friend and awesome hairstylist to give me a short haircut. Pause while she squeals with glee. (No, not really. She was appropriately heartbroken, but you know how it goes with people who cut hair. Hairstylists gonna cut, just like surgeons.)
HLP Step 3: look at photos of short hairstyles to try to find something that…maybe?…will look good on me. Let’s pause for a moment to note that I have never had short hair in my life. Gulp. I have absolutely no idea what short hair will look like on me. I decided to shoot for something like this Michelle Williams look. But will my hair even do that??
HLP Step 4: down a couple of shots
Just kidding. No drinking for me right now. But if you want to get yourself one before proceeding, please go ahead.
HLP REAL Step 4: go for the haircut. Listen to friend’s expert opinion on short hair, including the fact that thin blonde hair is not likely to respond like thick brown hair. Hold breath. Marvel at the sheer quantity of hair that has been removed from your head.
HLP Step 5: look in mirror. Pick jaw up from floor. Breathe big sigh of relief that I don’t look like a circus clown. In fact, as Mom pointed out, maybe I sort of look like Rachel Maddow.
Hmmm. Am I now afflicted with short brown haired woman syndrome?
HLP Step 6: order a scalp prosthetic
In one of our earlier meetings with Dr. M in May, he gave me a prescription for a “scalp prosthetic,” or what we normal people would call a wig. I will use this prescription, not least because wigs can be very expensive, and this will reduce the cost significantly. But I don’t expect to wear a wig very often. As my mom pointed out, wigs are hot, and even though this has been an atypically cool and rainy spring for southern New England, summer will arrive eventually.
HLP Step 7: wait for the inevitable.
So that’s the HLP. Depending on how I’m feeling, there may be a step 8, which could be “do your best Telly Savalas impression with a rousing rendition of ‘Who Loves Ya Baby?'” or “find some Star Trek: The Next Generation togs and dress up like Captain Picard.”
Or, you know, just wrap up my head and wait to see what happens on the other side of this madness.
That stands for Taxol, Herceptin, Perjeta, although I actually receive them in the reverse order.
Week 1 of chemo is an experiment for everyone. It’s my first time receiving these drugs, so no one really knows how I’ll respond. It’s the first time Husband and I have been in the infusion center at DF, so we are meeting all the nurses for the first time. This is the most obvious statement of all time, but I’ll go ahead and say it: that first chemo treatment is horrifying.
That said, I was pretty amazed by all they do to make patients comfortable.
The visit starts with a measurement of my
weight and height. It’s critical to have up-to-date measures each week, since the medicinal dosage is based on body surface area. One of the side effects of my rapidly dividing liver tumors was a significant loss of appetite, which means that I’ve been steadily losing weight. NOTE: I do not recommend this weight-loss plan. It’s stupider than the Cigarette Diet.
A few minutes later, Husband and I were ushered into the infusion center, which consists of 4 or 5 large rooms, each separated into small individual units by large hospital curtains. I was directed to a big chair outfitted with massage and heating functions. Husband’s chair was not so great, but he endured. (My word, not his!) Perhaps because it was our first time, or maybe just because we got lucky, our Week 1 position happened to be along the outside wall, giving us a fabulous view of the Boston skyline through the large plate glass windows.
Then began the parade of visitors/caregivers. First my chemotherapy nurse, M, who is absolutely wonderful. I was raised by an RN and spent a good deal of time surrounded by nurses as a kid. I have immense respect for this profession, and I know that a good nurse can make a great difference in a person’s medical outcomes. M is one of those special nurses who immediately put me at ease with his competence, curiosity, and compassion.
He explained that things would unfold slowly over the day, according to this plan:
pharmacy prepares my THP infusions based on the weight/height data
M delivers the pre-meds (anti-nausea, steroids, etc.)
Perjeta infusion followed by observation period
additional pre-meds as needed
Herceptin infusion followed by observation period
additional pre-meds as needed, including Benadryl
I would only get this “long treatment” every 3 weeks, with Taxol-only infusions every week. All told, we could expect the long THP day to take a good 4-5 hours, in addition to the 4 hours or so of driving we had to get to and from Boston. Alrighty, then!
While we waited for the pharmacy, a volunteer came by to offer me a hand massage! I happily accepted. She has been volunteering there for six years, and gave us the low-down on the many services volunteers provide. They come by with snacks (yogurt, goldfish crackers, etc.), lunch (itsy bitsy little sandwiches suitable for chemo-sized appetites, etc.), and books and magazines.
M periodically came over to check on us and see if we needed anything, until finally the show got started. The Perjeta infusion went beautifully! Nary a problem and I felt just fine. I was feeling very confident at this point.
Then Herceptin. Oh boy. Almost immediately after the infusion started I felt a warm flush in my throat and into my stomach, much like the feeling I get from a contrast injection during a CT scan. I was quietly observing these sensations, trying to determine whether they were real or imagined, and whether they were a problem. M told me before each infusion what I might expect in terms of sensations, and he didn’t mention this flush. I then noticed a mild feeling of nausea and a growing pain in my back, so I hit the call button to alert M.
Ok, he said. Let me know if it becomes more intense.
Within another 5-10 minutes, it had. Before we knew it, a full-on exorcism started. Over the course of about 60-90 minutes, during which time they stopped and started the Herceptin infusion multiple times, I vomited, got intense chills that caused me to shake violently for 15+ minutes, and spiked a 103 degree fever. During all of this, there were at least 5 nurses who came by to assist in various ways and they threw a bunch of meds at me to slow or stop the various reactions.
They called down Dr. M at some point in the madness and he said something like, “this could be happening because the meds are already killing cancer cells.”
In my drugged-up, demon-ridden stupor, it seemed that the nurses looked at him a little dubiously, but they didn’t argue. I recalled Dr. M’s early statement that fast-growing tumors tend to respond very quickly, but this was ridiculous. Could it possibly start to happen this fast?
Once we finally got through the Herceptin infusion and observation period, we started the Taxol, which went well. They gave me a massive Benadryl dose at the start that knocked me out for the duration, and for the rest of the night.
So that was it. Week 1 down, 11 to 17 more to go.
Some good news here is that they give the largest dose of Perjeta and Herceptin in Week 1. Hopefully this means my response won’t be quite so crazy in weeks 4, 7, 10, etc.
The best news of all is that I started to feel better as of the very next day. I’m still amazed by this. The liver and back pain receded for the first time in months and weeks, respectively. I was tired, but had far more energy than I had in ages. Nurse M gave me a call to see how I was doing, and was actually surprised to hear that I felt so great, given my bad response to the Herceptin. I became a little more tired over the next few days, but still felt much better than I’d expected.
This past week , week 2, was a very busy one, starting with outpatient surgery to place a Power Port in my chest on Tuesday.
The port is a way to avoid having IVs placed in my arms or hands each week. My once great veins have already become pathetic from past cancer treatment, and chemo is sure to make this worse. The Power Port is like an artificial vein. It’s a small plastic triangle placed under the skin, which connects to a catheter directed into a large vein near the heart. They can use the port to take blood samples as well as deliver meds. It’s far less painful than getting poked for a regular IV (IMHO), but they even make a special numbing cream for use over the port if needed.
The next day was Taxol day, which went very well. They halved the Benadryl dosage, which left me sleepy, but not zombified like last week.
The best news of the week is that my appetite started to return as of Wednesday night. I’m still nowhere close to my normal level of hunger, but this is the first time I’ve wanted to eat anything more than a small cup of soup in quite a while. Also, the expected side effects have not yet begun to affect me. I think I’m in a Goldilocks zone right now where the cancer is responding to treatment (as Dr. M suspected), immediately lessening the effects of all those liver tumors. I know that things will get more difficult as treatment wears on, of course, but I’m thrilled to be in this moment.
Finally, I had a visit with a social worker yesterday and those two MRIs (thoracic spine and brain) that had been scheduled a while ago. A friend and I were just joking about the fact that the MRI techs ask if you want to listen to music while you’re in the machine. I said yes, please. Classical. Of course, this had the ultimate effect of sounding like someone was using a jackhammer next to my head for an hour while the polite sounds of a piano plinked in the background. Not super relaxing, but you take what you can get when you’re wrapped up like a burrito in a hot, shaking, jackhammering coffin.
We’re anxiously awaiting the results of these new scans, of course. I will let you know, but I’m trying to stay positive. I figure we’re due for some good fortune at this point.
Husband and I went to visit a local azalea garden yesterday. They have countless varieties of both azaleas and rhododendrons there, with an array of colors that is both gaudy and perfect. Along the way Husband spotted this tulip tree. Clearly the gardeners had tried to stunt this tree’s growth, but it would not be stopped. That’s me, folks. I will not be stopped.
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.
The fact that breast cancer recurred in my liver has caused some confusion for a few people. Cancer is a strange beast. The type of cancer a person has is named based on where it started. My leiomyosarcoma, for example, was called uterine leiomyosarcoma b/c that’s where (we think) it started. According to the Liddy Shriver Sarcoma Initiative, soft tissue sarcomas account for 0.7% of all cancers. About 5-10% of sarcomas are leiomyosarcomas, meaning they arise from smooth muscle cells lining small blood vessels. Or, in the case of uterine leiomyosarcoma, they arise directly from the uterus. About 1% of women who get uterine cancer are diagnosed with uterine leiomyosarcoma, specifically.
Breast cancer starts in the breast, obviously, but when it recurs, the metastases tend to show up in the liver, bone, lungs, or brain. This is the same cancer. It was just sitting in wait, trying to find a comfortable place to set up shop. I can’t help my oceanographic worldview affecting how I think of this process, so bear with me for a marine-themed analogy.
I imagine a rogue cancer cell that managed to get loose from the area of the breast that was targeted for surgery, and then further managed to float through my circulatory system until it found a nice spot to settle. In my mind, this is akin to oyster larvae, floating along with the current until they find a place to settle where they can grow into big, delicious oysters.
Just don’t ever say I told you to eat cancer cells.
But I’m going to write a whole bunch of them, anyway.
I’ve had a recurrence.
With a normal person, it would be obvious what that means. But with me, the originator of two primary, unrelated cancers, this begs the question: which one?
The short answer is breast cancer, which is actually a great stroke of luck. If this were my other cancer, uterine leiomyosarcoma (ULMS), I would be facing a far worse scenario. As it is, I’m preparing to fight a disease that is one of the best studied cancers in existence. The fact that I’ve got metastatic HER2+ breast cancer (more on this in another post) gives me more opportunities and a far better prognosis than I would have with other types of breast cancer or with ULMS.
A word of warning before we get started. I have kept previous posts on this blog PG-rated, meaning I’ve refrained from cursing because I shared the blog with a broad range of family, friends, and colleagues. I will warn you, gentle reader, that round 3 of this cancer journey will not be as family-friendly. There are going to be some F-bombs in here on occasion, because I’m mad. It’s well known that swearing is a sign of honesty and can make a person feel better. Plus, a new study says swearing can boost strength and reduce pain. So, to sum up: there’s a heck of a lot of research on the benefits of swearing, and it all proves that swearing is good.
That said, here’s the backstory.
I started experiencing an evolving suite of abdominal pains in January of this year. They began as occasional, stabbing pains. At the time, I thought these pains might be one of my patented stress responses. I was feeling despondent about Donald Trump’s ascendancy, and I’ve been known to physically manifest stress ever since high school, when I developed a very obvious and embarrassing eye twitch that often made people think I was winking at them. I can’t begin to recall what could have been so stressful at that moment in my life, but it was the beginning of a recurrent pattern in terms of my physical responses to stress.
These pains carried on for a few weeks, and then I went to my primary care doc in mid-February after an especially mean stomach bug, just to be sure that all was ok. At that time they ran a bunch of tests, all of which came up normal, including liver function. For whatever reason, the abdominal pains stopped after that stomach bug. I thought maybe I had been experiencing some tenacious virus that I’d finally expelled through an unpleasant, but ultimately productive, 36-hour period of vomiting.
But over the course of the next 6 weeks or so, the pains returned, becoming localized in the upper right part of my abdomen and evolving from occasional to constant. I had also become increasingly tired over those months, and had gotten to the point where I was exhausted by the smallest activity, even filling up Kit’s bowl with kibble in the morning.
I went back to my PCP in early April to discuss the evolution of my abdominal pains, and they couldn’t make sense of it. The doc advised that I get a CT scan of my abdomen and pelvis, “given my history,” and I chose to do this at Dana Farber, since they’ve been doing regular scans of my abdomen and pelvis since 2011 (and also the chest since 2015).
I had the abdomen/pelvis CT on April 26. Ray and I met with my sarcoma oncologist to review the scan that afternoon. She informed us, with no small amount of sadness and surprise, that there was a good explanation for the pains I’d been experiencing…my liver had 20+ tumors in it, ranging from 1 to 5 cm in size. She showed us the scan, and it was shocking. My liver looked like a bag filled with marbles. Here a marble, there a marble, everywhere a marble.
It’s important to remember that my last CT was last November. I actually graduated to annual CT scans at that point, but even if I had still been on a 6-month schedule, I wouldn’t have been due for another scan until this month. This, combined with the fortuitous testing I had done in mid-February, indicates that these tumors grew very quickly.
Well, it turns out that collecting samples from an organ is a little bit more painful than collecting them from breast tissue. The constant liver pain I’d been experiencing prior to this was now compounded by a miserable soreness from the biopsy.
The point of this biopsy was to figure out which of my cancers this was. Husband and I joked that this could be yet a third cancer (because cancer humor is an essential tool in our coping toolbox), but the odds were that the liver tumors were metastases of one of my original cancers. But which one? Breast cancer seemed most likely, because breast cancer tends to metastasize to the liver or bones. But my 2015 breast cancer diagnosis was only micro-invasive, and I did all the appropriately aggressive treatment at that time. The ULMS seemed unlikely, too, since I’m now 5.5 years out from treatment for that one. In either case, this was a very unusual situation.
A very unusual situation. Is anyone picking up on a theme here?
I had that biopsy on a Tuesday, and we had another appointment scheduled with my sarcoma oncologist for the following Tuesday to get the results. I was surprised, then, to get a call from my breast oncologist on the intervening Saturday. I happened to be in the middle of a pedicure with two of my best pals when he called, so I asked him to call back later. My friends were duly impressed that a doctor was calling me on a Saturday afternoon.
Dana Farber is the bomb.
Dr. M, the breast oncologist, finally caught up with me Saturday evening. He had gotten the results of the biopsy, and they showed that this was, in fact, breast cancer. The good news is that the pathology showed this to be the identical breast cancer I first experienced in 2015. It’s very weakly estrogen positive, progesterone negative, and very strongly HER2 positive. The weak hormone receptors (estrogen and progesterone) made the oncologists focus on the HER2+ status rather than the hormone status. This blogger provides an excellent summary of these aspects of breast cancer if you want to read more about it.
Having a HER2+ breast cancer is good for a couple reasons. First, breast cancers sometime show “discordance” between the original cancer’s response to hormones and the hormone receptivity of the recurrent cancer. This discordance can cause some additional challenges for treatment, so it’s nice that this was one thing we didn’t have to worry about. Second, HER2+ breast cancer is very well studied, and there have been great advances in its treatment over the past 10-15 years. In fact, a landmark paper in 2015 has led to the inclusion of a particular antibody as a standard part of treatment, brand name Perjeta (again, more on this later), that, combined with another antibody (brand name Herceptin) and chemotherapy, significantly extends “progression-free survival.”
I can’t overemphasize the good fortune of having a recurrence of HER2+ breast cancer over ULMS. I mean, none of this is especially lucky, but at least I didn’t pick the shortest stick. But speaking of short sticks, here is one of the most astounding things I’ve learned over the last few weeks.
Remember that I was diagnosed in 2015 with a micro-invasive “ductal carcinoma in situ,” often referred to as DCIS. Here’s the kicker: Dr. M told us that, in DCIS cases where there was a very small area of invasion (1-2mm, in my case), the risk of spread is 1-2%.
Let me restate that. There was a 1-2% chance that I would develop metastatic breast cancer based on scale of the initial occurrence.
Dr. M went on to explain the treatment options, and the various statistics regarding their outcomes. But before he started, he made a comment that perfectly sums up his particular brand of practical, tempered, yet appropriately sarcastic medical guidance. It also demonstrates why I’m so glad he’s my oncologist. “You’ve had two rare developments, which leads to incredulousness regarding all statistics.”