New Therapeutic Options for Cancer Patients

New Therapeutic Options for Cancer Patients

By Clifford Reid, PhD

Some recent scientific publications further support the value of Travera’s approach to determining which cancer drugs to give to which cancer patients by direct testing: that is, removing cancer cells from each patient and directly measuring the response those cancer cells to many different cancer drugs.

In a recent publication (Lin et al, Science Translational Medicine, October 11, 2019, summarized by the New York Times, October 11, 2019), researchers ran experiments on ten targeted therapies that ostensibly work (their “mechanisms of action”) by eliminating a protein that is essential for cancer cell growth but not essential for normal cell growth.

The researchers used another method (CRISPR) to eliminate those proteins from a living cancer cell line, and then made two startling discoveries: (1) the cancer cell lines grew just fine without the ostensibly essential proteins, and (2) the drugs worked just fine in killing the cancer cells, even though their protein targets were completely missing.

This is an elegant experimental demonstration of the well-known “off target” effects of many targeted cancer therapies: yes, they work at killing cancer cells, but their mechanism of action described in the published literature (and used to achieve FDA approval) is only one of their many mechanisms of action. They kill cancer cells many different ways.

How many different ways? We do not know exactly, but another recent study gives us a reasonable estimate (Klaeger et al, Science, December 1, 2017). Researchers measured how many different proteins (called “kinases”) the targeted therapies called “kinase inhibitors” (which represent most of the FDA-approved targeted therapies) actually inhibit. They tested 243 clinical and preclinical targeted therapies and reported three important results: (1) most of them inhibited more than one protein (2) about a third of them inhibited more than ten proteins, and (3) a few of them inhibited more than 100 proteins.

These recently published results reinforce how much we have left to learn about how cancers and cancer drugs actually work.  They suggest that matching cancer drugs to cancer patients by sequencing genes involved in their known mechanisms of action will fail to identify many (possibly most) of the effective targeted therapies for each patient.  By contrast, Travera’s approach will match effective cancer drugs to each cancer patient regardless of whether the mechanism of action is known or unknown.