How Anderson Transformed Multiple Myeloma Care

Published: Thursday, Nov 12, 2015
Kenneth C. Anderson, MD

Kenneth C. Anderson, MD

When Kenneth C. Anderson, MD, began his studies at Johns Hopkins Medical School, he fully intended to abandon the basic biological research he loved and focus instead on the sort of general clinical practice that would provide “real benefits to real people.”

Then he met Richard L. Humphrey, MD, a legendary pathology professor, who convinced him that research could provide even greater benefits to real people, if Anderson always followed two simple rules: make science count for patients, and treat patients like family.

Humphrey could not have imagined at the time how right he was. The discoveries that Anderson has made over the past 34 years at the Dana-Farber Cancer Institute have helped spur a revolution in the treatment of multiple myeloma— nine new treatments in less than 15 years.

When Anderson began that work, multiple myeloma was not only incurable, it was basically untreatable. Now, for many, it’s a chronic disease. “I’ve always enjoyed the intellectual challenge of discovering how the disease works and what can disrupt its workings,” said Anderson, who is now the director of the Jerome Lipper Multiple Myeloma Center and LeBow Institute for Myeloma Therapeutics at Dana-Farber in Boston.

“But the real joy has come from watching patients live long enough to enjoy birthdays and graduations and other milestones they would have missed,” he said.

Setting Practical Goals

When Anderson came to Hopkins, Humphrey was culturing multiple myeloma cells in test tubes and bombarding them with potential treatments. The effort did little to change myeloma care, but it did change Anderson’s life. That one experiment illustrated that very basic research could have very practical goals. It also convinced Anderson that myeloma research might prove particularly fruitful.

By that time, bone marrow aspirations made it easy to gather myeloma cells from patients, and even the simplest cultivation techniques kept those cells growing. Myeloma thus ranked among the easier cancers to study in the laboratory, but when Anderson turned his attention to the disease, virtually no one was doing so. After completing his internal medicine residency at Hopkins, Anderson began a medical oncology fellowship at Dana-Farber in 1980, pitching in with ongoing efforts there to develop and test treatment protocols for the first generation of monoclonal antibodies.

Anderson first used antibodies to deplete tumor cells from bone marrow taken from patients with multiple myeloma, which was then returned to them to restore blood and immune function after high-dose therapy.

Fewer cancer cells in the transplanted marrow led, in turn, to fewer relapses for transplant patients.

Such work illustrated the breakthrough potential of treatments that prevented tumor cells from interacting normally with their microenvironments and inspired Anderson to embark upon a multidecade quest to understand and model the workings of multiple myeloma. For example, Anderson and his colleagues slowly discovered how multiple myeloma cells used cytokines to develop resistance to many treatments, and they speculated that a cytokine- inhibiting substance could retard the development of drug resistance.

Turning to Thalidomide

The problem was finding a drug that could interfere with cytokines. Anderson gathered as much information as he could about existing and experimental compounds. He tested possible candidates. Nothing offered much promise—until 1997, when Anderson heard that Bart Barlogie, MD, PhD, had undertaken a trial of thalidomide on 84 patients with previously treated multiple myeloma.

The idea for using thalidomide as a cancer treatment came from one of Anderson’s most eminent colleagues at Harvard, the pioneering angiogenesis researcher Judah Folkman, MD, a recipient of the Scientific Advances award of the 2013 Giants of Cancer Care.®

Folkman believed the drug would slow disease progression by depriving cancer of blood. The results, however, far exceeded anyone’s dreams, and Anderson soon suspected that thalidomide acted not only as an angiogenesis inhibitor but also as an immunomodulator, one that prevented the cell-signaling mechanisms that lead to drug resistance.

Research at Anderson’s laboratory confirmed that thalidomide does interfere with cytokines and does delay drug resistance. Better still, all that Anderson had learned about multiple myeloma’s biology over the years enabled him to create models of myeloma in its bone marrow microenvironment that helped predict how to administer the drug for maximum effect, first in animals and then in human patients.

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