I’ve been talking a lot lately about immunotherapy — with family, friends, neighbors, anyone who asks me how my treatment is going. But when someone politely inquired the other day about my “amino acid therapy,” I realized that I’ve been spending too much time in Club Cancer! Not everyone speaks this lingo (and I’m glad they don’t have to).
So, let’s take a step back and I’ll try to explain the basic difference between chemotherapy — which a lot of people are familiar with, at least the word itself — and terms like “precision medicine” and “immunotherapy,” which are getting a lot of press in the past year or two.
Chemotherapy kills cancer cells…and plenty of healthy cells as well. It’s kind of like conducting a bombing raid to kill a snake. Knowing that snake has a deadly bite, you want to attack it as fast and hard as possible, and this can be quite effective in some cases. Unfortunately, collateral damage is almost inevitable: side effects can include everything from extreme nausea and fatigue to permanent numbness and tingling in one’s fingers and toes. It’s debilitating and exhausting and scary as hell to go through, and in most cases, it only sends the snake into hiding temporarily. Scientists have been searching for a better weapon for decades, and it’s starting to look like they’re on the verge of finding at least parts of it.
Immunotherapy is based on the recognition that we’ve already got our own skilled team of assassins inside our bodies: Our immune system. The trouble with cancer cells is that through various complicated tricks, they come up with innocent-looking disguises so that our immune systems fail to recognize them as The Bad Guy Cells and let them mosey on past internal checkpoints to start building a full-scale Evil Empire undetected. Scientists have been working on disabling those disguises for decades — no easy task, since there are many, depending on the specific type of cancer and each individual’s personal genetic mutations. And they’ve had some major breakthrough successes with certain lymphomas, lung cancers and melanomas in the past few years (hooray for Jimmy Carter!).
Yet while those breakthroughs are real and amazing, so far they largely do not apply to my particular type of cancer.
This gets us into another bit of cancer lingo: One of the first things colorectal cancer patients ask each other in online forums is whether their tumor has been tested for “microsatellite instability,” because a minority (15 percent or so) of colorectal tumors are MSI-high (microsatellite-instability high). Instability may sound like a bad thing–and it can mean that such patients have devastating hereditary conditions such as Lynch Syndrome–but it turns out to have a silver lining when it comes to immunotherapy. It seems that the more mutations a tumor has, the more potential targets there are for the immunotherapy drugs to hit and essentially unmask to the immune system.*
However, my colon cancer, like most, is MSS (microsatellite stable). So while there have been some super-exciting successes with immunotherapies for MSI-high colorectal cancers, attempts to apply the same approach to MSS patients like me have largely fallen flat so far.
My lucky/unlucky twist is that my tumor tested positive for a mutation called BRAF V600E, which is quite rare in colorectal cancers, and considered a poor prognostic indicator. But it’s pretty common in melanoma, as it turns out, so in the past couple of years a few researchers have started to pay attention to whether some of the successes achieved with new treatments for melanoma might be translatable to BRAF-mutated colon cancers. Trials that involved simply using the melanoma drugs by themselves in colorectal patients largely didn’t work, however. So now the latest approach for cases like me is to try combining tried-and-true chemotherapies with more novel drugs, meaning immunotherapies and/or drugs that target specific genetic mutations. (UPDATE: I’ve edited this after realizing that I was incorrectly lumping together immunotherapy and targeted therapy, although they often work together and both fall under the umbrella of precision medicine. Sorry about the confusion.)
I started my cocktail approach three weeks ago, after my awesome doctor convinced my equally awesome insurer to cover this BRAF-inhibitor drug even though it’s currently only FDA-approved for melanoma (this is called “off label” use, and if my insurer hadn’t agreed to cover it I’d be looking at something like $25,000 a month out of pocket). Things got off to a rocky start with severe side effects, but I restarted at a lower dose this week and it’s going okay so far.
The hope is that I can tolerate it for at least a month or two, and then I can have another CT scan to see if it’s doing any good. Best case scenario, it will make my tumors “melt away” (my doctor’s words, not mine, but aren’t they lovely?) and reunite me with good old NED.
And I’ll leave it there, because best-case scenarios are all I’m interested in thinking about right now.
*Disclaimer: Remember that I’m a journalist, not a scientist! Here’s some additional reading to check out.