No Illusions

No Illusions

Though I’m an oncologist and not an infectious disease expert I’m getting bombarded with questions about the pandemic. Patients and staff are asking me and every one of my partners similar things, over and over:

How long until things go back to normal?

How much danger am I in?

Is it all going to be ok?

Though I’m supposed to have all the answers, I haven’t felt too sure of anything lately. It must show on my face, because recently one of my patients (a young woman living with incurable breast cancer) asked “how you doing there, doc?”

“Honestly, I’m not sure,” I said. “My regular routine is wrecked, I don’t feel as safe as I used to, and I don’t know what’s coming.”

“Welcome to my world,” she said, with a wry smile.

I suppose like everyone else in my privileged corner of the planet, where war is remote and epidemics are rare, I’ve been fooled into believing that the world is a safe place, that nature wants the best for us, and that we have control.

Somehow I’ve mistaken privilege for entitlement.

But the pandemic has stripped those illusions from me, just as cancer stripped them from my patient long ago. I’ve had to accept that there’s no such thing as safe – only safer. I’ve had to admit that I don’t have as much control as I’d like. And I’ve had to consider the very real possibility that I or someone I love might not survive.

And even if we and all our loved ones come through safely, somehow I doubt we can ever go back to the sleepy (and false) security of before. We may well divide our lives into distinct sections: “Before COVID” and “After COVID”, just as many patients have distinct lives before and after cancer.

And maybe we’re better off living without illusions of safety.

If life becomes more precarious, maybe it’ll also be more precious. Maybe in facing the truth of our mortality we’ll learn a deeper compassion for all survivors, everywhere – since every human breathing is a survivor of something. And if I’m spared, perhaps the me that comes after will have learned to live with more dignity and courage.

Maybe my patient will teach me.

Curing Cancer by Make and Model

Curing Cancer by Make and Model

People often ask me when we will cure cancer. I usually answer, “Which one?”

Cancer is not one disease, but a large family of different diseases. Under the microscope, cells from different cancer types look different, grow at different rates, spread to different places, and are powered by different machinery—sort of like different makes and models of cars.

Every year, we get a better understanding of what goes on “under the hood” of cancer cells. These insights then lead to the development of new drugs that sabotage cancer cells in ways that may cause minimal harm to patients.

The bad news? These new drugs may only work for a very specific “make” or “model” of cancer.

For example, some lung cancers have a “short circuit”, or permanent “on” switch, called the EML4-ALK signal. The EML4-ALK signal can be shut off by the new drug, Crizotinib, with minimal side effects. EML4-ALK-positive lung cancers shrink dramatically in response, and patients live two to four times longer than otherwise.

But, since Crizotinib—and drugs like it—are “make” and “model” specific, they only work for cancers with a specific kind of cellular machinery. And, in the case of EML4-ALK, that represents slightly less than 10% of all cases of non-small cell lung cancer.

Discouraged? Don’t be. We’re getting better (and faster) at decoding cancer’s genes and signals. Just compare Crizotinib’s development with the first molecular miracle drug: Imatinib, developed for chronic myeloid leukemia (CML):

Way back in 1960, the abnormal fusion of chromosomes 9 and 22 (called the Philadelphia chromosome) was identified as a key abnormality in CML. It took 13 years to figure out exactly what the Philadelphia chromosome was doing to the cellular machinery in CML. And it took 28 more years to turn that understanding into an effective drug. Finally, in 2001, Imatinib became widely available—a total of 41 years from lab bench to patient bedside!

Contrast that with Crizotinib: ALK abnormalities in cancer were first noticed 1998. The EML4-ALK fusion signal, specific to lung cancer, was identified in 2009. Crizotinib was approved on August 26, 2011. That’s just 13 years for Crizotinib, from the lab to the patient.

That’s progress, my friends.