Comments on: Cancer Med Labels May Reflect Genetic Issues

By: Gregory D. Pawelski

Gregory D. Pawelski — Sat, 31 Jan 2009 07:13:13 +0000

I would not want to be denied treatment with EGFR antibody therapy because of KRAS gene testing. KRAS gene testing for EGFR is not a clear predictor of a lack of benefit from EGFR antagonist antibodies in colon cancer.

By: Insider

Insider — Thu, 25 Dec 2008 22:27:22 +0000

Unfortunately I’m afraid this type of information may be of has been applied selectively. If companies can show efficacy without testing they will, then when the patent life is running out we may see new information with drug-device co-labeling. Companies have been collecting genetic information for more than a decade. In spite of the fact that they were required by law to submit all information related to safety. Which this does fall under. Companies in the interim arranged with FDA to have a safe harbor to submit this genetic information to develop standards for approval and safety testing without it being revealed to the review staff under the voluntary genomic submission guidance (VGSG). While I agree with this approach for the future I’m afraid of the likely probability that during the past several years there has been a delay in release of critical information like this until it’s financially convenient. Even if the tests themselves were not ready for commercial sale we don’t know that this type of knowledge might have lead to switching therapies in the absence of a response for this or other conditions.

Salmon

By: Greg Pawelski

Greg Pawelski — Thu, 25 Dec 2008 17:59:12 +0000

I wholeheartedly agree, patients should be much better matched to their therapy and therefore improve their odds. However, molecular testing doesn’t tell you if one drug is better or worse than some other drug which may target a mechanism/pathway. There are differences.

Functional profiling with cell-based testing measures the response of the tumor cells to drug exposure. Following this exposure, it measures both cell metabolism and cell morphology. The integrated effect of the drugs on the whole cell, resulting in a cellular response to the drug, measuring the interaction of the entire genome.

No matter which genes or proteins are being affected, functional profiling is measuring them through the surrogate of measuring if the cell is alive ore dead. This kind of testing can save money and precious time to ensure that a patient is started on the right therapy up front.

By: former marketing exec

former marketing exec — Tue, 16 Dec 2008 00:51:16 +0000

This is a good thing and I applaud it. These cancer drugs, from what I have learned, are very expensive and if specific molecular testing up front can save money and precious time to ensure that a patient is started on the right therapy up front - then I say let’s do it.

Lately I have heard of a few stories of patients eroding their insurance caps until it was discovered that they were on the wrong treatment. Very often the disease can become even more resistant to other therapy making the chances for other therapies to work, less likely.

Drugs aside, this shows how far technology has come. With a variety of drugs to choose from, maybe it is not so impossible that patients will be much better matched to their therapy and therefore improve the odds for all patients.

Refreshing news in such dire economic times.

Bravo!

By: Greg Pawelski

Greg Pawelski — Mon, 15 Dec 2008 06:23:18 +0000

Mutations in the gene KRAS, which encodes a signaling protein activated by EGFR, are found in 15 to 30 percent of certain cancers. The presence of a mutated KRAS gene in a biopsy sample is associated with primary resistance to drugs. The change of a single base in DNA that encodes the mutant EGFR protein has been shown to cause drug resistance.

Tumor cells from patients who develop secondary resistance to a drug like Erbitux after an initial response on therapy did not have mutations in KRAS. Rather, these tumor cells have new mutations in EGFR. Drug resistance evolves by multiple mechanisms. This further indicates that secondary resistance is very different from primary resistance.

However, all the EGFR mutation or amplification studies can tell us is whether or not the cells are potentially susceptible to this mechanism of attack. They don’t tell you if one drug is better or worse than some other drug which may target this. There are differences. The drug has to get inside the cells in order to target anything.

The cell is a system, an integrated, interacting network of genes, proteins and other cellular constituents that produce functions. You need to analyze the systems’ response to drug treatments, not just one target or pathway.

No genetic profile test can discriminate differing levels of anti-tumor activity occurring among different targeted therapy drugs. Nor can an available it identify situations in which it is advantageous to combine a targeted drug with other types of conventional cancer drugs.