David Clancy may or may not have Chuck E. Cheese to thank for catching his acute myeloid leukemia early.

It was June 29, 2024, and Clancy and wife Tammi had driven to Colorado Springs from their home near Taos, N.M. The idea was to pick up building supplies for a casita they planned as an outbuilding of their future forever home. Plus, they could also visit their son Nick’s family in the city where the Clancys themselves had lived until 2012, raising Nick and three daughters along the way.

At the urging of their grandson Talon, they had dinner at the Chuck E. Cheese on the south side of town. The next day, they drove the three-and-a-half hours back home. The day after that, Clancy stayed in bed, where he would remain for the better part of a week. They speculated that it might have been bugs picked up from kids at the pizzeria.

Clancy, then 66, is a former masonry foreman and realtor. He had recently built most of a 2,100 square-foot home on his own, including laying some 11,000 bricks as flooring.  He and Tammi had just spent three weeks in Italy. So, Tammi wasn’t accustomed to seeing her husband being listless, achy, and in bed all day.

On July 4, she finally convinced him to visit the local hospital’s emergency department. There he was diagnosed with bacterial pneumonia and sent home. A lousy night of intense headaches and night sweats brought the Clancys back the next day, and low blood-oxygen levels led to his being admitted. By then, blood test results had come back with low white blood cell counts.

An AML diagnosis and some timely advice

Leukemia ran in Clancy’s family – his father and four of his dad’s siblings had been diagnosed with some form of it. It took a couple of days for the doctors in Taos to get past the pneumonia as principal diagnosis. A staffer – perhaps a charge nurse, the Clancys aren’t sure – had already arrived at that conclusion. She told them Clancy needed a bone marrow biopsy, a procedure beyond the capabilities of the 25-bed rural hospital. (The white blood cells that become cancerous with leukemia are produced in the bone marrow.) And she told him that, if it’s leukemia, they should request a transfer to “Anschutz.” She had been treated there for cancer after being told she wouldn’t survive, and here she was.

“It was divine feminine intervention,” Tammi said.

The Clancys had never heard of Anschutz – University of Colorado Hospital on the Anschutz Medical Campus. But a few days later, a bone-marrow biopsy done at Albuquerque’s Lovelace Medical Center had come back with the acute myeloid leukemia (AML) diagnosis. They asked for a referral to Anschutz.

Days later, the Clancys drove the five hours to Aurora. They met with University of Colorado School of Medicine blood cancer specialist Dr. Dan Pollyea at the UCHealth Blood Disorders and Cell Therapies Center. Pollyea ordered another bone marrow biopsy, and they met with him again when the results were in. The test confirmed the AML, and it noted a mutation of the DDX41 gene as the probable trigger.

“DDX41 is a gene mutation that we’ve only recently noted to have significance in AML,” Pollyea said later. “It’s of particular interest, because, unlike most other gene mutations implicated in AML, this one can be inherited.”

He told Clancy this: “This can be cured, and we are going to try our best to do that.”

“He really put me at ease,” Clancy recalled.

Venetoclax-azacitidine treatment: Take out the cancer, replace the bone marrow

The cure would unfold in two steps. The first would involve two drugs: the first a low-dose chemotherapy treatment, azacitidine, and the other a pill, venetoclax. The combination could eliminate the AML without Clancy having to spend a month in the hospital undergoing intensive chemotherapy – historically, the standard of care. The second step would be a bone marrow transplant. That’s essentially a precaution in the event that rogue AML cells survived the venetoclax-azacitidine treatment. For that he would have to spend weeks in the hospital.

Pollyea knows venetoclax as well as anyone. He was part of a team led by CU School of Medicine PhD cancer biologist Craig T. Jordan that laid the groundwork for the drug’s emergence as an AML treatment. Jordan had recognized that venetoclax worked by essentially starving AML stem cells to death. The very first venetoclax clinical trials occurred at CU, and based on this work, the U.S. Food and Drug Administration approved venetoclax-azacitidine for AML patients in 2018– but only for patients 75 and over or those who couldn’t withstand chemotherapy.

Venetoclax’s impact on patients was so profound that Pollyea launched and now leads a second clinical trial for patients ages 18 to 59. That trial, which enrolled 36 patients including and former world-champion triathlete Siri Lindley, is scheduled to wrap up in 2026.

Pollyea’s clinical trial was already fully subscribed by the time Clancy arrived at his clinic, and, at age 66, Clancy wouldn’t have qualified anyway. So Pollyea prescribed venetoclax off-label.

“We have learned that this regimen can be so effective – and better-tolerated than the alternative treatment with intensive chemotherapy – that we’re moving toward prescribing it more commonly in situations like this,” Pollyea said.

Feeling good, and headed home

Rather than chemotherapy infusions, Clancy took two six-week rounds of pills. By acting on the AML stem cells that drive the cancer, venetoclax-azacitidine has the effect of pulling AML out by the roots. On Nov. 13, he had a stem-cell transplant under the care of Dr. Jonathan Gutman, a CU School of Medicine hematologist who teams with Pollyea on AML cases. This time, Clancy spent more than three weeks in the hospital as his immune system was chemically destroyed and then reborn through stem cells from a donor in Germany.

For 100 days after the bone-marrow transplant, the Clancys were to stay within 30 miles of UCHealth University of Colorado Hospital. To accommodate their Sheepadoodles Jax and Finn, they rented a furnished house not far from Sloan’s Lake in West Denver. There were bumps in the road as he recovered, in the form of atrial fibrillation, a blood infection, and a stark drop in his white blood cell counts with the reintroduction of venetoclax after the transplant – a new use of venetoclax post-transplant that can act as an insurance policy against AML’s unlikely reemergence, Pollyea says. But as day 100 approached, Clancy’s hair was coming back in in wisps, and he was feeling himself again.

“I feel good, and I sleep good,” he said. “I wouldn’t even know I was sick.”

As their mid-February return to Taos approached, Clancy was more than ready to relaunch the work on the casita he had paused all those months ago. When that’s done, he’ll start on the 3,600 square feet of forever home. That plus six grandchildren ought to keep him plenty busy in what has been – and will again become – a very active retirement.

Regarding Pollyea and Gutman, Clancy said, “Both of those guys and the nurses are all phenomenal. Just super people.”

But he was looking forward to heading back south. On the way through, they may skip the pizza place.

“I’m excited to go home,” he said. “It’s been a process.”