Dedicated to Discovery. Committed to Care.

2000s

"Smart" drugs like Gleevec and technology such as gene-expression arrays are important cancerfighting tools today.

The age-old goal of oncology research – to devise treatments that strike and kill cancer cells and only cancer cells – remained a distant prospect until scientists learned the source of cancer's alarming idiosyncrasies. From the outside, cancer cells and normal cells often appear more like siblings than strangers, their surface markings strikingly alike. Those similarities proved baffling to most traditional chemotherapy agents: Drugs that kill fast-growing tumor cells often wind up harming normal fast-growing cells, such as those in the digestive tract and scalp, producing the nausea and baldness so often associated with cancer therapy.

Scientific and technological advances in the 1980s and '90s enabled researchers to read the instructions embedded in the genetic "hard drive" of cells, the DNA programming that directs their behavior, and to pinpoint where those instructions differ in cancerous and normal cells. The result is a new generation of "targeted" therapies that are the biological equivalent of smart missiles used in warfare. (In truth, "smart" drugs are no more clever or discerning than conventional drugs. It's their developers who have the smarts.)

Dana-Farber scientists have played a role in the success of at least two targeted therapies so far.

The era of targeted therapy has only just begun, but Dana-Farber and its scientists can justly claim a role in the success of two of them: Gleevec and Iressa. Gleevec, a breakthrough treatment for chronic myelogenous leukemia (CML), was developed by Novartis Pharmaceuticals based on studies of chemical signaling led by DFCI's Thomas Roberts, PhD, Charles Stiles, PhD, and James Griffin, MD. Brian Druker, MD, of Oregon Health University, who had learned of the drug as a fellow in Roberts' lab, made headlines when he showed that Gleevec can produce long-lasting remissions in many patients with CML. And it was Dana-Farber's George Demetri, MD, and colleagues who proved that the drug is equally successful against the rare digestive-tract cancer GIST (gastrointestinal stromal tumor).

A similar kind of molecular sharpshooting led Institute researchers to discover in 2004 that lung tumors containing a particular mutated gene could be halted by Iressa, a finding that may benefit tens of thousands of people around the world.

The future

Prediction-making is a notoriously flawed business, but all signs point to the coming decade at Dana-Farber and cancer centers around the world as the beginning of an era of more personalized medicine in cancer research and care. The days of "one size fits all" cancer therapy are long gone: With every new discovery, the ability of doctors to treat the unique features of each patient's disease improves. The types of therapy given, and their order, timing, and dosage, are increasingly calibrated to individual circumstances and forms of disease.

Such trends are accelerating as researchers uncover the genetic and genomic "signatures" of various types of cancer. The practice of classifying tumors by their organ of origin – colon cancer, lung cancer, etc. – may seem antiquated by the year 2017, replaced by a system for identifying them by patterns of gene activity. Treatments will likely become ever more precise, and ever easier for patients to tolerate.

Dana-Farber's Strategic Plan, adopted in 2003, is designed to make the Institute not only the place where important basic-science breakthroughs happen, but also where such advances are put to practical use in the form of better therapies and cancer-prevention techniques. Many of the concepts and terminology in the plan would be unrecognizable to Dana-Farber's founders, but the goal – the defeat of cancer – would not.