Male Breast Cancer

Male Breast Cancer

Men absolutely get breast cancer. It happens here in Green Bay.

I’ve treated it. So it’s absolutely a thing.

But men get breast cancer about 100 times LESS often than women do, for a very simple reason:

Most breast cancers develop from abnormal cells in the ductwork of the breast. But men have less breast ductwork to begin with – so they get breast cancer less often. It’s kinda the same reason you see fewer cheesehead hats in Florida…there are fewer Packer fans in Florida to wear them.

Since cancer screening only works in a high-risk population, and the risk for breast cancer in most men is so low–screening for breast cancer with breast exams and mammograms and such isn’t usually recommended (or even a good idea) for most men.

The exception is men who carry mutations that increase the risk of cancer, such as the BRCA mutation (specifically, the BRCA2 mutation). There are other mutations that also increase breast cancer risk, but that’s the most relevant one for men. The association between BRCA mutations and male breast cancer is so strong that having a male relative with breast cancer is usually a good enough reason to consider getting tested for the mutation.

Having said all that, once a man gets breast cancer–the treatment for it is remarkably similar to the treatment for women. This is because these cancers, whether they appear in a man or a woman, are driven by similar biological mechanisms, tend to spread in similar ways, and tend to respond to the same kinds of drugs.

One caveat to that general rule of treatments being more alike than different for men and women is that most men need mastectomy (removal of the whole breast) rather than lumpectomy (removing only the affected part of the breast) – but this is simply due to the fact that men generally have less breast tissue to work with than women do.

Estrogen blockers (like tamoxifen and aromatase inhibitors like arimidex and letrozole) work in most male breast cancers as well as they do for most female breast cancers. That surprises people because we tend to think of estrogen as the female hormone and testosterone as the male hormone, and tend to forget that both men and women have lots of both. It’s just the relative mix of the two hormones that’s different between the sexes–and that mix changes as we age.

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.