In late summer of 2010 Jason was diagnosed with Hodgkin’s lymphoma.
It’s a cancer of the immune system. The word lymphoma refers to the lymphatic system, the network of nodes where the immune cells gather. In Hodgkin’s—named for the nineteenth-century English doctor who discovered it—B cells have mutated into malignancy.
Cell mutations take place all the time inside the body. All of us get cancers. You might well have one now. Most of these mutations die off, simply because they are too mutant to survive or because the immune system identifies them as alien and destroys them. In the case of Hodgkin’s, the cancer takes advantage of the immune system, dupes it, and even uses it to thrive.
The cancer cells “look like self in disguise,” said Dr. Alexander Lesokhin, an expert in blood cancers and a hematologic oncologist at New York’s Memorial Sloan Kettering, one of the leading research institutes in the world. Part of the way that Hodgkin’s and other cancers disguise themselves is by tricking the T cells that would ordinarily help kill off the mutation. What the cancer does is send a signal to the T cell to self-destruct.
Why would the T cell do that? Why would it even have such a receptor on its surface capable of receiving a self-destruct signal?
It’s because the immune system has many mechanisms that are aimed at slowing it down, shutting it off, keeping it from overheating. Cancers take advantage of these fail-safe mechanisms to survive.
The self-destruct receptor on the T cell is called programmed death. For short, PD.
On the cancer is a molecule called PDL-1, a programmed death ligand that binds to or connects to the PD receptor on the T cell.
Inside Jason’s body, malignant B cells had grown and were using PDL-1 to put the brakes on the killing part of his immune system. At the same time, now that the immune system had received a message that the cancer was “self” and not alien, the immune system actually set out to protect and support the cancer.
Dr. Lesokhin said it appears that “the tumor co-opts the immune system and says, ‘I’m okay. I just want you to help me grow.’”
It’s tempting to anthropomorphize the cancer and think of it as cunning, or strategic, but, really, cancer is a product of the same evolutionary processes that lead to our own survival, or that of any other species or organisms. When a mutation occurs inside us, it thrives if it has developed the ability to evade our body’s defenses. Over the course of our lifetimes, we’re being thrown tons of twists by malignant cells, and it takes only a handful to turn on the immune system’s brake and start a cascade of malignancy.
“It’s basically evolution at work in real time, a Darwinian survival system,” Dr. Lesokhin said.
In the case of blood cancers, the exact mechanism is still being explored, but Dr. Lesokhin hypothesizes that the successful cancers result from an evolutionary process in which the surviving mutations are the ones that evolve a key adaptation that allows them to “use the immune system or avoid the immune system.”
Jason had this growing inside him. A cancer had figured out how to turn down his defenses, mute them, while using the might of the immune system to build the infrastructure—the blood and tissue roadways and constructions—to help the cancer grow.
In Jason’s immune system, there had been a coup. Left untreated, the malignant cells would’ve reproduced unchecked, voraciously eating up more territory, invading organs, causing normal bodily functions to slow or cease. Jason would’ve lasted only four months. Fortunately, there was a veritable nuclear bomb to deal with those rogue cells—or so it would have seemed.
Chemotherapy is brutal. “When you have cancer, you spread napalm on it and burn everything to the ground,” Jason’s oncologist, Dr. Mark Brunvand, told me.
Mostly through dumb luck, scientists had at least found an effective version of napalm for Hodgkin’s, the kind of cancer Jason had. It provides a 90 percent survival rate.
The chemotherapy drugs target cells that are fast dividing, which is a marker of cancer. The malignant alien cells reproduce quickly, just like those healthy cells in a wound that are being fed by blood and protected by the immune system itself. The evil malignancies co-opt the system, and in an odd way, they get treated to the privilege of dividing quickly. There are other cells in the body that also divide quickly, including hair follicles and cells in the gut and mouth.
A fire hose was spraying Jason’s Festival of Life with poison. That terrible toxic cocktail called ABVD was effective against all these cells, but its list of possible side effects reads like a who’s who of extreme irritants and dangers: bruising, bleeding, tiredness, constipation, flulike symptoms, hair loss, mouth ulcers, sore eyes, dizziness, and on and on. On top of this is insomnia, which can be a byproduct less of the chemotherapy than of the use of steroids. These are used, as you know by now, to limit inflammation and cut down a massive immune system response. Why, you might ask, would you limit an immune response in a time of cancer?
In this case, you want toxins in your body. Poison is your ally, and the more it can be allowed to flow freely, the greater the chance it will target these fast-dividing cells. But part of the way that steroids suppress the immune system is by activating the adrenal glands (remember that when stress and adrenaline get activated, they suppress the immune system).
In short, there is nothing good about chemotherapy other than the fact that it can save your life. A trade-off, often, worth making.
Chemotherapy, Jason discovered, is also expensive. The first clinic he visited told him that the terrible toxic cocktail known as ABVD entailed “twelve chemos at $8,500 a pop. They realized I had bogus insurance, and they cut me loose.”
He was two days away from treatment and needed a safety net. He found it at Denver General Hospital, a catchall for the uninsured or poorly insured, the place where you end up when they find you on the street with a gunshot wound or an opioid overdose, or where you go when you’ve got cancer and no money to treat it. It was October 2010. Jason jumped in, sort of. During his first round of chemo, he had trouble getting to his appointments on time.
He was “always on the road, always busy,” said Dr. Michael McLaughlin, his first oncologist. “I thought: This guy is on the run.”
Jason’s chemo didn’t work. He was one of the unlucky 10 percent whose cancers manage to survive the toxins. Sometimes this happens because cells mutate in the face of the drug’s onslaught and become resistant to treatment. Relatedly, for the best chance of attaining good results, the treatment needs to be given in the proper doses at the right times. Jason thus didn’t do himself any favors by missing some appointments, potentially giving the cancer more time to adjust to the treatment. Whatever the reason for the chemo’s failing, and there can be no way of knowing for sure, the race to save Jason’s life had begun.