The triage nurse had written: “Forty-five-year-old man, chief complaint: not feeling himself, blurry vision. Fell three days ago. No loss of consciousness. Skin intact.” So here he was in the emergency department at 10 p.m. on a Sunday night. Why now? I wondered.

Jadesh, my resident, went into the examination area to visit Mr. Sullivan. Twenty long minutes later, Jadesh returned. “I think the spleen is very enlarged,” he said, a trace of awe in his voice. The spleen, located just under the left lower ribs, filters debris and abnormal cells from the bloodstream. You normally can’t feel a spleen.

“You sure?” I asked.

“He has been having night sweats for the past three days since he fell. Changes his clothes several times a night.”


“How did the fall give him night sweats?”

Jadesh shrugged. Add night sweats to an enlarged spleen and most doctors guess a diagnosis of lymphoma or leukemia. Missing, however, was the usual story of weeks or months of fatigue and weight loss, and maybe some easy bruising. “But he’s here because of the fall, right? He was fine until he fell?” I asked.

“So he says.”

As we walked over, Mr. Sullivan eyed us expectantly. With a puckish belly and thin limbs, he couldn’t have weighed more than 120 pounds. I introduced myself, then laid a hand on his abdomen. On the right, the liver edge felt OK. Moving across, my fingers kneaded the soft, thin flesh until they hit an edge as hard as a two-by-four. Stretching from rib cage to pelvis, the spleen filled half his abdomen. Straining to keep my eyebrows from hitting my hairline, I carefully asked, “You were OK until three days ago?”

“That’s right, doctor. I slipped walking down the stairs.”

I motioned for Jadesh to follow me out of the room. “He’s been carrying a watermelon around in his abdomen,” I said. “Must have been there for months. Good pickup on your part. Could be mistaken for his entire abdominal wall.”

“But why no symptoms?” Jadesh asked.

I flipped to the chart’s face sheet. Mr. Sullivan owned a small business and had no health insurance. Stoicism, American style. His white blood cell count had come back a whopping 318,000 white cells per cubic millimeter—30 times normal.

“CML, right?” Jadesh asked.

“Looks like it,” I told him. “But I’m no cancer expert.”

CML, chronic myelogenous leukemia, stems from white blood cells’ multiplying like rabbits in the Australian outback. During my internship complainers were told: “Could be worse. You’re not in blast crisis.” That doomsday term refers to a stage in CML when, after three to five years of steadily increasing white cell counts, the dam bursts: The bone marrow spews huge numbers of blasts (immature cells), the immune system collapses, and eventually you die. Chemotherapy, I knew, could slow the disease, but only a bone marrow transplant—grueling and sometimes fatal—could cure it. And only about 30 percent of patients find a good donor match. There were newer treatments, but I hadn’t followed the long-term survival data. My guess was, Mr. Sullivan had three or four years to live. “We need to tell him,” I said to Jadesh.

Back in the room, Mr. Sullivan had been joined by his partner. I looked from one to the other, then started in. “Your white count is very high. White cells are the infection-fighting cells in your bloodstream.” I paused. “You very likely have leukemia.”

Mr. Sullivan didn’t flinch. More puzzled than scared, he said, “That’s pretty serious.”

“Yes. We need to admit you for more tests.”

“Leukemia,” he repeated. I held his gaze and nodded.

CML is a peculiar beast. The first human cancer to be tied to a visible (under a microscope) chromosomal abnormality, it has become to cancer research what the Galápagos were to Darwin: a stripped-down, elegant illustration of how bigger, messier systems work. Chromosomes—we humans have 46 of them—are the big packets of DNA in a cell’s nucleus that contain hundreds of genes apiece. Every time a cell divides, the chromosomes duplicate. Sometimes they swap chromosome chunks with each other. The genetic scramble known as the Philadelphia chromosome (because it was discovered there in 1960) is one such hybrid. As bad luck would have it, the improper swapping of two gene fragments—from chromosomes 9 and 22—produces a mutant protein, a type of tyrosine kinase, which triggers the leukemia.