In my local cancer support group, a member revealed that her cancer had metastasized, and she would be getting immunotherapy to counter that. Which lead to a bunch of various questions, which, as an unethical, opportunistic writer, I seized upon to form the core of this essay. First up, we all thanked her for letting us know about recent developments and remarked on her courage — which it does take a bit of guts to open yourself up to people like that, but, at the same time; when you’re going through the abyss, you want to consult people who’ve been there — everyone immediately wanted to know if she wanted someone to sit by her in the infusion center, if she needed help with food — all the nuts-and-bolts stuff of daily living that only your fellow sea monsters know is important and gets neglected after the words, “Stage 4.” As they say at Stupid Cancer, “Hang out with the people who ‘get it,’ because we’ve already gotten it.” And, it’s worth noting that, as in LGBTQ culture (which, I guess I’m sort of part of, as a demisexual)(but that’s an entire series unto itself), cancer culture is fragmented into major subcultures and subcultures within those (I’ll discuss that in just a second). First big question, as a survivor, and to address every newly-diagnosed survivor’s concerns…

What if this treatment doesn’t work?

This is the biggest, hardest, scariest question all new survivors ask. I know I absolutely annoyed my oncologists by opening and closing all consultations with that question. Head Warlock in Charge (HWiC)(my original oncologist’s research partner who wound up being my primary neurooncologist) annoyed me just as much by calmly saying, “Then we’ll explore other treatment possibilities.” Halfway through active treatment, I stopped asking him this, because it started becoming clearer that treatment was working. So, in the glioblastoma nation of Planet Cancer, the big go-to urban legend is off-label multi-drug cocktails. It’s what Ben Williams (Patient Zero in GBM Land) credits his recovery with; there are professional oncologists who dabble in it, and even HWiC mentioned he’d done some research on them. My own experience, as a grad student and survivor is that not everyone is going to have the constitution and support necessary to just say, “Sure, I’ll add Drug X to my regimen” until you have a 14-drug cocktail that keeps the disease at bay. However, if you’re in the thick of it, that can seem horrible or daunting. And you do have to pass yourself off as physically healthy enough to add yet another med onto a bloated treatment regimen (that’s a chore unto itself). Be prepared to be adaptable, don’t pin your hopes on any one single treatment, and be prepared to gnaw through as many different drugs/treatments as are needed to win. So, there’s a horrifying amount of random chance involved, I won’t lie; but the “proper mind-set/positive attitude” comes into play when your first-line treatment doesn’t work, and your oncologist discusses other treatment options. My own experience is, my life got simpler (and better) when I made it my primary directive to get more treatment. Remember, anything that hurts you probably also hurts the cancer.

Why do we get cancer?

I’m paraphrasing several questions/ideas/interjections; and, to answer it, I’m compressing multiple years of grad school courses (this also plays into the “What is immunotherapy” question that’s coming up, so you might want to read this one).

In order to understand this one, you need to understand that life originally evolved as a single-cell . Multi-cellular life is the exception to the rule, and, as such, there are certain single-celled adaptations that kick in inconveniently. See, when you’re a single cell, you have to be as big as you possibly can, live as long as you can, and have as many offspring as you possibly can in order to do well, evolutionarily (these are also the rules that cancer cells play by). It’s like being a lone child on the playground, or a one-man band. Multicellular life is a little different, in that it’s like being part of a symphony (or the E Street Band). Sure, there are some instruments and melodies that are more critical than others at certain times, but you want a balanced orchestra, playing in time and tune with the other musicians. Even if Bruce Springsteen is chattering with audience members, everyone has to stay on task or things break down. In your own body, you want cells to grow appropriately, divide appropriately, and then die (this is why you don’t have webbed fingers — those embryonic cells die off and shrivel before your born). In your cells, this is done by activating certain genes (protooncogenes) and deactivating others (tumor suppressor genes) at appropriate times. Once you have a cell that has a protooncogene permanently turned on, and the corresponding tumor suppressor gene turned off, you have cancer. Now, it may take a few years for that cell to spread those “constantly-divide-grow-spread-and-invade” qualities to its neighbors (in a process we don’t really understand, called recruitment)(also, in single-celled organisms, this is not a problem, because getting bigger, invading your neighbors’ territory, and having lots and lots of babies just means that you and your army are winning)(that’s a problem when you’re in the strict confines of, say, a human body). So, after that dual-mutation, cancer cells have to keep hidden from your body’s immune system (which normally catches and corrects these things in the very early stages due to some biochemical phenomena that we may or may not get to in this essay) long enough to spread their cancerous properties to neighboring (or distal cells). Eventually, you get enough cells with the ability to grow, divide, and outlive their cellular expiration date (the cellular limits on division and life are called “the Hayflick limit,” for everyone curious, and its usually believed to be the driving force in aging), and you have detectable tumors. It’s at this point usually that survivors start noticing symptoms and getting misdiagnosed (I’m a really bizarre freak in Planet Cancer in that they’ve caught all of mine in incidental scans before I had any real symptoms). So, to make a long story short; you’re born with the genetic means to get cancer (even though some of us may have genetic predilections to certain cancers); all it takes is exposure to enough carcinogens long enough. It’s a simple proposition, right? Just avoid all carcinogens. So, as a public service announcement, I will now give you, dear reader, the complete list of all substances documented by science as not being carcinogenic at all:

That was fast, wasn’t it? To give you an idea of how impossible it is to avoid carcinogenic substances, oxygen and sunlight — in the right doses — are carcinogenic. Try and live life without them. My immunology/cancer biology professor claimed he’d once tried to calculate cancer rates if we all lived in biodomes without any major known carcinogens (in other words; some sunlight and minimal oxygen exposure are okay, asbestos and cigarettes are out). He said he figured we’d only cut cancer rates by a third to a half. Again, as a society, we need to get really comfortable with this concept that, if you live long enough; you will get cancer. This not only would be helpful in removing the stigma, but also in reframing survivors’ initial (unhelpful) response as, “Why me? What did I do?” to, “Oh, I guess it’s my turn in the hot seat. How do I get out of it?” (I could also write an entire series on the helpfulness of various questions to survivors — “Why” is a useless, exasperating question that wastes time, “How” is the question that gets shit done). Even though people like me, who develop it at age 17, are a rarity, everyone will experience this group of diseases, if they live long enough. Again, it’s just modern cells that are playing by a much older, harmful strategy that’s built into our cells through millions of years of evolution.

As far as being able to spread; the defining trait of cancer is its ability to spread to distal organs (or, in the case of brain cancer, distal parts of the same organ); again, we’re not sure on the specific mechanisms of this; last time I checked, the popular theory was that it was a biochemical process (read: the cancer cells secrete some sort of substance that “recruits” other cells). It’s at this point that concepts like “primary tumor” and “secondary tumor” come into play — a primary tumor is the original one, the matriarch, if you will. If it metastasizes or regrows elsewhere, that’s a secondary tumor, and has some different characteristics. Usually, secondary tumors tend to be a little less aggressive and slower-growing, but each cancer is unique (GBM also tends to be the exception to the rules — it tends to metastasize or recur worse than the original). My latest tumor — in one of those weird, “it could only happen to me” moments that have defined my life — is a secondary tumor, probably derived from one of my (numerous) lower-grade primary brain tumors. Again, these seem like minutiae, but they’re critical when making medical decisions.

What is immunotherapy?

Basically, it’s using your own immune system to fight cancer. In one of my pharmaceutical manuals in my personal library, there’s the statement, “Drugs can only speed up or slow down certain biochemical reactions.” Which is true, and the point of that point is that the modern biopharma industry can’t create entirely new functions or reactions. Which is still mostly-true of biotechnology products, but immunotherapy is more like “reprogramming certain systems to do the same old job in a slightly different way.”

You remember that bit about cellular biology? Well, all cells have biochemical “tags” on them that signify what they’re doing and what’s going on inside of them (this is why most cancer cells get destroyed by the immune system long before they become problematic). In most cancer cells, the immune system no longer responds appropriately and destroys it. Immunotherapy is usually “teaching” the immune system to retarget those cells based on specific biochemical markers. And this can range from the “Jurassic Park” end (I was initially signed up for a clinical trial that would’ve involved reprogramming my own white blood cells to attack recurring low-grade gliomas) to the relatively uninteresting (interleukins are just immune-stimulating chemicals that are naturally made by the body). For all the anti-vaxxers out there, I do have some really, really bad news: almost all immunotherapies count as a form of vaccination. And, like a vaccination, they tend to work longer than traditional chemotherapy.

The side-effects of immunotherapy tend to be similar to chemo — you’re really just attacking cells, either by getting the immune system to do it for you, or by targeting them with chemicals. Which brings up another point to pay attention to: chemotherapy is far more targeted and effective than in previous generations. Just as we can teach the immune system to target certain cellular “tags” associated with a specific tumor, we’re making highly-targeted chemo agents that only work on specific markers, and in an extremely specific fashion. Take the experimental chemo I was on; Marizomib. It was “designed” (really, it was yet another accidental discovery) to target cells with an IDH mutation and p53 mutations (those are both specific genes)(or proteins, to be a little more specific), and stop them from growing and spreading. I haven’t heard of it doing much to “attack” cancer cells — in the trial I was in, it was only being used in patients who had the tumor completely removed and nuked.

Immunotherapy is almost as well-targeted — when I was in market research, the company I was indirectly working for was researching the possibility of reengineering T-cells to attack two possible mutations in glioblastoma (yes, the irony of the fact that I’d be diagnosed with GBM just two years later is not lost on me); the question being, “How common are these molecular ‘tags’ in GBM cases?”

The bet that you, the survivor, are making with any treatment — is that every cancer cell will have those same markers, and whatever treatment you’re on will wipe it all out. Because, by definition, if just a few of those of those cancer cells survive, they will have different biochemical markers that make this treatment ineffective.

I strongly suspect that the reason why “good” cancers are more survivable isn’t that we have better or more effective treatments than for “bad” cancers; it’s that we just have more treatments available. If the “first line” drugs for breast cancer don’t work, there are other chemo options. Right now, if the first line drugs for brain cancer don’t work, there are a “second line” group (lomustine), but very little after that. Immunotherapy would undoubtedly help, because it would offer another shot at the disease.

As always, though, I am not to be considered an expert here, and am not a valid alternative for consulting an oncologist. If you are experiencing a medical emergency, hang up and dial 911.

Written by

Science journalist, cancer survivor, biomedical consultant, the “Wednesday Addams of travel writers.”

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