Drug Doesn't Work, You've Failed & Need A Gene Fix: Modern Medicine's View

by Heidi Stevenson

23 February 2010

In a strange twist of logic, scientists have determined that the reason Tamoxifen doesn't always work is that the victim...uh, patient is at fault. Therefore, the solution is to "fix" the miscreant gene. In this strange new world of medicine, toxic drugs are normal, someone whose body doesn't respond the way they think it should is abnormal, and the gene identified as abnormal must be fixed.

The gene involved is called FGFR1 (fibroblast growth factor receptor 1). It's a critical gene in development of the fetus, and it's a factor in a chromosome that's deeply involved with bone marrow, as shown here:

Based on the idea that women who don't respond to Tamoxifen have too many FGFR1 genes, scientists have done lab experiments using drugs—Of course!—to switch off the FGFR1 gene in cancer cells. That resulted in Tamoxifen's continued cytotoxic effect on the cells, the goal they were hoping to reach.

It sounds good, but let's examine this. Experiments have only been done in labs. What will happen to noncancerous cells is unknown.

Animal studies have not been done. Drugs generally don't target their effects; that is, they have effects on cells other than the ones that are targeted. Tamoxifen is an exceptionally toxic drug, and these scientists are proposing to add at least one more drug to the regimen of the one-third of women who don't benefit from Tamoxifen.

That's just for starters. Consider that Tamoxifen, though it does treat breast cancer, does so at a huge cost. Its toxicity results in greater risk of cataracts, deep vein thromboses, endometrial cancer, uterine sarcoma, and strokes. The fact is that, on average, little, if any, life extension is gained by taking Tamoxifen.

So, to gain a rather dubious benefit from Tamoxifen, another drug, with whatever risks it carries, will be given. This drug is hoped will destroy what what have been deemed to be excessive numbers of a gene. There is otherwise no problem with these so-called "excess" genes. These genes' chromosomes are critical in bone marrow function, which is a major part of the blood manufacturing system. No one knows what effects will result from killing off the "excess" genes. And, of course, the use of Tamoxifen has little benefit anyway.

The lead researcher, Dr. Nick Turner, stated:

We have known for some time that breast cancer patients with too much of the FGFR1 gene in their cancer are more likely to have a poor prognosis, but we did not know if FGFR1 was behind this. Understanding how this gene can cause tamoxifen resistance reveals a new drug target for treating breast cancers in patients who would otherwise have a poor outcome.

There are a number of drugs in development that stop FGFR1 working, and clinical studies are investigating whether these drugs work against cancers with too many copies of this gene.

The next step is to set up a clinical trial to see whether a drug that blocks the action of this gene can counteract hormone therapy resistance in breast cancer patients. If these trials confirm our lab work we could be on the verge of a potentially exciting new treatment for breast cancer.

At best, Turner is hyping his own research. He's gone public with something that is, at best, in the early stages of development. The chances of its success in humans is unknown. The risks that might be associated with the proposed treatment are completely ignored. Yet, he is giving the impression that this is a great and exciting development that has nothing but benefits associated with it.

It seems that modern medicine has gotten itself trapped in a loop. When a drug isn't effective, then the solution is seen as finding another drug. To do that, ever more twisted logic needs to be used—like suggesting that there's something wrong with the patient when their drugs don't have the desired effect. And then, looking for another drug to fix the newly-defined abnormality in the patient.

This "abnormality" is defined as abnormal only because it manages to defeat the effects of a drug. There is no other negative effect associated with it. Can there be any greater hubris on the part of modern medicine than to define a gene as abnormal simply because it defeats the toxicity of a drug?

Normality is not defined by gaining benefit from a drug! Perhaps these doctors and researchers need to take a look at a more sane viewpoint. Perhaps they should consider the idea that some patients have the ability to negate the toxic effects of their drugs. That changes the whole picture, doesn't it?

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