SAN DIEGO, CA – In 1977, when David R. Parkinson, MD, graduated from medical school at the University of Toronto and moved to McGill University to train in internal medicine and eventually hematology, the idea of medical oncology was in its infancy. In Canada, the profession didn’t exist.
“In Canada, there were no medical oncologists,” Parkinson told Inside Precision Medicine. “Radiation therapists administered what little chemotherapy existed. They resisted the development of medical oncology as a specialty.”
Through the ensuing 49 years, Parkinson didn’t just see the rise of kinase inhibitors, antibodies, and cell therapies in real-time—he helped create the world of modern cancer therapeutics.
In reflecting on his remarkable career, which was recognized with the 2026 AACR Outstanding Achievement Award for Service to Cancer Science and Medicine, Parkinson said, “I’ve essentially grown alongside the field.”
From scarcity to structure: Oncology’s early years
When Parkinson arrived in Montreal, there were only a handful of chemotherapeutics available. “In those days, there were only one or two drugs available for hematologic malignancies across the entire field,” Parkinson said. “The main treatments were cyclophosphamide and nitrosoureas.”
Even supportive care lagged. “Initially, we had no effective way to control chemotherapy-induced nausea,” he noted of the standard of care for testicular cancer. “Some patients stopped treatment because they couldn’t tolerate it.”
Parkinson explained that early cancer drugs worked best on rapidly dividing tumors, like leukemias and testicular cancers, because that’s what the animal models represented. These therapies targeted DNA and cell division broadly, often with severe toxicity, and were far less effective against slower-growing solid tumors.
After his residency at McGill, Parkinson moved to Boston, first to Tufts New England Medical Center on a modest Canadian fellowship that placed him at the edge of a field just beginning to coalesce. “I was on a Canadian fellowship earning $12,000 a year,” he said. “The exchange rate fluctuated significantly, which made things difficult, and I couldn’t work due to my student visa.”
What he found, however, was momentum. Through connections with Dana-Farber, Parkinson entered formal training in medical oncology as the specialty began to take shape. “I connected with Dana-Farber and took their introductory course for fellows—that was my entry into medical oncology.”
At the same time, breakthroughs in specific cancers hinted at what might be possible. “What really shaped my thinking was the emergence of treatments for testicular cancer just as I entered oncology,” he said. “Platinum-based therapies—and later combination regimens—felt like miracles. We had never seen anything like it. These were often young patients, difficult to manage, but suddenly there were real cures.”
Targeted therapy and the Gleevec moment
Parkinson’s career soon intersected with early efforts to harness the immune system against cancer—decades before immunotherapy became a dominant paradigm. “I became deeply involved in immunotherapy, particularly interleukin-2 and early tumor-infiltrating lymphocyte studies,” he said.
Working at the National Cancer Institute (NCI), he collaborated with leaders, including immunotherapy pioneer Steven Rosenberg, MD, PhD, maintaining a hybrid role that combined research with clinical care. “At the same time, I continued clinical work for a couple of months each year, collaborating with Steve Rosenberg in the surgical branch.”
These early approaches were technically challenging and often unpredictable, but they laid the groundwork for later advances. “We started with basic approaches, moved to tumor-infiltrating lymphocytes, and eventually to engineered CAR T cells,” Parkinson said. “Progress has been steady, though often slower than those treating patients would like.”
If immunotherapy represented one trajectory, targeted therapy represented another—one that depended on a deeper understanding of cancer biology.
“When I joined Novartis in the late 1980s, we were among the first developing kinase inhibitors,” Parkinson said. At the time, the idea was controversial. “Early skepticism suggested kinase inhibitors wouldn’t work due to high intracellular ATP levels and structural challenges.”
But advances in molecular biology were beginning to change the landscape. The discovery of the Philadelphia chromosome and its associated oncogene created a clear therapeutic target. “The Philadelphia chromosome had been known since the 1960s, and by the 1980s the responsible gene was identified,” Parkinson explained.
The result was imatinib (Gleevec), a drug that would become a prototype for precision oncology. “Eventually, a small molecule inhibitor was developed that targeted it precisely.”
The clinical results were extraordinary. “By the third cohort in a Phase I trial, patients with chronic myelogenous leukemia showed dramatic responses—some within 24 hours,” Parkinson said. “It’s probably the only Phase I oncology trial where essentially every patient achieved remission.”
For Parkinson, the implications extended far beyond a single drug. “Of course, [Gleevec] was a unique case,” he said. “But it proved an important point: what once seemed impossible can become possible.”
Since then, the field has expanded dramatically. Hundreds of kinase inhibitors have been developed, with thousands more explored, reflecting a broader shift toward therapies grounded in specific molecular mechanisms.
Precision medicine—and its limits
As oncology evolved, so too did its language. “For years, we called it ‘personalized medicine,’” Parkinson said. “I used to joke that medicine has always been personalized—you’re always trying to determine what’s best for a specific patient in a specific context.”
He credits industry with popularizing a more precise term. “Although Pfizer popularized the term ‘precision medicine,’ I think it’s a better term,” he added, with a note of humor: “I have a few good Pfizer jokes—best shared over a drink.”
Yet the reality of precision medicine has proven more complex than its promise. “The evolution of therapeutics mirrored the models and biological understanding available,” Parkinson said. “Targeted therapies only emerged once we understood the biology. Diagnostics, however, lagged by about two decades.”
That lag remains a structural challenge. Parkinson founded a diagnostics company based on single-cell signaling technology developed at Stanford. “Technically, it worked—we solved major challenges in instrumentation, standardization, and analysis,” he said. “But we couldn’t establish a viable business model.”
The core issue was reimbursement. “Without adequate reimbursement from Medicare, even highly sophisticated diagnostics struggle commercially,” said Parkinson. “Better diagnostics can reduce the use of expensive drugs by identifying who won’t benefit—something that doesn’t always align with pharmaceutical business models.”
In recent years, Parkinson has focused increasingly on large-scale data integration, including his involvement with the GENIE consortium. The initiative aggregates genomic and clinical data across institutions, aiming to accelerate discovery and improve clinical decision-making. “GENIE has been a technical success,” he said. “But its long-term sustainability remains uncertain.”
The broader challenge, he argues, is conceptual as much as technical. “Looking forward, the field is evolving toward integrating multiple data types—genomics, transcriptomics, imaging, and more—to better understand tumor biology,” he said. “Sequencing alone isn’t enough. The challenge now is not a lack of data, but making sense of it—something where artificial intelligence will play an increasingly important role.”
Back to basics
Across academia, government, and industry—including roles at the NCI, Novartis, Amgen, and Biogen Idec—Parkinson sees a single throughline. “I remember an interview with a biotech company where an HR representative told me, ‘You seem to have done a lot of different things,’” he said. “I responded that I had really only done one thing: trying to improve cancer treatment, just from many different angles.”
Not every effort succeeded. “In one case, we developed a drug that performed beautifully in mice but failed in human trials,” he said. “That’s common in oncology—most ideas don’t translate. You don’t think of it as failure but as learning. Still, there’s a limit to how many ‘learnings’ one can appreciate.”
Reflecting on decades of progress, Parkinson emphasizes both how far the field has come and how much remains unresolved. “Outcomes have improved dramatically across several cancers, especially hematologic ones,” he said.
Yet he underscores a fundamental principle: that progress in cancer treatment comes down to understanding biology. “The better we understand it, the more effectively we can develop targeted therapies,” said Parkinson. “Without that understanding, we’re essentially guessing.”
At AACR 2026, Parkinson’s recognition underscores not just past achievements but a continuing trajectory—one shaped by the interplay of discovery, failure, and persistence. “Despite all the challenges,” he said, “[precision medicine] is still the most promising path forward.”
The post AACR 2026: David Parkinson and the Arc of Modern Cancer Therapy appeared first on Inside Precision Medicine.
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