Cancer Covered Blog

Curing Cancer by Make and Model

People often ask me when we will cure cancer. I usually answer, “Which one?”

Cancer is not one disease, but a large family of different diseases. Under the microscope, cells from different cancer types look different, grow at different rates, spread to different places, and are powered by different machinery—sort of like different makes and models of cars.

Every year, we get a better understanding of what goes on “under the hood” of cancer cells. These insights then lead to the development of new drugs that sabotage cancer cells in ways that may cause minimal harm to patients.

The bad news? These new drugs may only work for a very specific “make” or “model” of cancer.

For example, some lung cancers have a “short circuit”, or permanent “on” switch, called the EML4-ALK signal. The EML4-ALK signal can be shut off by the new drug, Crizotinib, with minimal side effects. EML4-ALK-positive lung cancers shrink dramatically in response, and patients live two to four times longer than otherwise.

But, since Crizotinib—and drugs like it—are “make” and “model” specific, they only work for cancers with a specific kind of cellular machinery. And, in the case of EML4-ALK, that represents slightly less than 10% of all cases of non-small cell lung cancer.

Discouraged? Don’t be. We’re getting better (and faster) at decoding cancer’s genes and signals. Just compare Crizotinib’s development with the first molecular miracle drug: Imatinib, developed for chronic myeloid leukemia (CML):

Way back in 1960, the abnormal fusion of chromosomes 9 and 22 (called the Philadelphia chromosome) was identified as a key abnormality in CML. It took 13 years to figure out exactly what the Philadelphia chromosome was doing to the cellular machinery in CML. And it took 28 more years to turn that understanding into an effective drug. Finally, in 2001, Imatinib became widely available—a total of 41 years from lab bench to patient bedside!

Contrast that with Crizotinib: ALK abnormalities in cancer were first noticed 1998. The EML4-ALK fusion signal, specific to lung cancer, was identified in 2009. Crizotinib was approved on August 26, 2011. That’s just 13 years for Crizotinib, from the lab to the patient.

That’s progress, my friends.

Dr. Mitch Winkler signature
J. Mitchell Winkler, MD

Mitch has boundless energy and an unyielding approach to finding the most suitable solutions for each of his patients.

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