Dr. Mills Discusses the Field of Targeted Therapeutics

Gordon B. Mills, MD, PhD
Published: Tuesday, Oct 18, 2011

Gordon B. Mills, MD, PhD, chairman, Department of Systems Biology, chief, Section of Molecular Therapeutics, Professor of Medicine and Immunology at the University of Texas MD Anderson Cancer Center, explains that the field of targeted therapeutics was initially heralded as a "magic bullet" against cancer.

The ultimate paradigm at the onset of targeted therapy was the use of imatinib (Gleevec) for chronic myeloid leukemia (CML). This therapy incurred an incredible response in patients and the idea in place at the time was that this would be the standard for future targeted therapies.

Unfortunately this paradigm has not been realized in all cases of target therapies. Mills mentions that almost all other new agents are restricted to a subpopulation of patients and from those with the correct marker only a few will transiently respond.

This disappointment is the direct result of two mechanisms:
  1. Researchers failed to embrace that a clean and clear link showing a benefit to patients needs to be established between a combination of sensitivity and resistance markers and the drug to be used before you go to the clinic and needs to be modulated and modified within the clinic.
  2. It needs to be fully understood which resistance mechanisms are already in place or can be derived or evolved over time before the study moves to clinical trials in patients.
Gordon B. Mills, MD, PhD, chairman, Department of Systems Biology, chief, Section of Molecular Therapeutics, Professor of Medicine and Immunology at the University of Texas MD Anderson Cancer Center, explains that the field of targeted therapeutics was initially heralded as a "magic bullet" against cancer.

The ultimate paradigm at the onset of targeted therapy was the use of imatinib (Gleevec) for chronic myeloid leukemia (CML). This therapy incurred an incredible response in patients and the idea in place at the time was that this would be the standard for future targeted therapies.

Unfortunately this paradigm has not been realized in all cases of target therapies. Mills mentions that almost all other new agents are restricted to a subpopulation of patients and from those with the correct marker only a few will transiently respond.

This disappointment is the direct result of two mechanisms:
  1. Researchers failed to embrace that a clean and clear link showing a benefit to patients needs to be established between a combination of sensitivity and resistance markers and the drug to be used before you go to the clinic and needs to be modulated and modified within the clinic.
  2. It needs to be fully understood which resistance mechanisms are already in place or can be derived or evolved over time before the study moves to clinical trials in patients.

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