This article appears in the July/August issue of The American Spectator. To subscribe, please click here.
SCIENTISTS THESE DAYS TEND TO BELIEVE that almost any trait can be attributed to a gene. The gene obsession, showing up in science journals and on the front page of the New York Times, culminated in the Human Genome Project. The human genome was sequenced, then that of the fruit fly, the rat, the mouse, the chimpanzee, the roundworm, yeast, and rice. Computers cranked out their mindless data. It has been a bonanza for techies and the computer industry but the medical benefits have remained elusive.
Now they are talking about a Cancer Genome Project. It would determine the DNA sequence in 12,500 tumor samples and is supposed to reveal cancer-causing mutations by comparing the order of the letters of the genetic code in tumor cells with sequences in healthy tissue. But there is no single cancer genome, and the project will not improve our understanding of cancer.
Cancer has proved resistant to every “breakthrough” and treatment hype, and the new approach will only sustain the error that has dominated cancer research for 30 years. Since the mid-1970s, leading researchers have doggedly pursued the fixed idea that cancer is caused by gene mutations. I believe it will prove to have been one of the great medical errors of the 20th century.
WHERE TO BEGIN? One place is a story in the Washington Post, a few months back, headlined “Genetic Test Is Predictor of Breast Cancer Relapse.” The test “marks one of the first tangible benefits of the massive effort to harness genetics to fight cancer,” Rob Stein wrote. No real benefits yet? I think that is correct. Two well-publicized genes supposedly predispose women for breast cancer, but in over 90 percent of cases these genes have shown no defect.
Genes that (allegedly) cause cancer when they are mutated are called oncogenes. They were reported in 1976 by J. Michael Bishop and Harold Varmus, who were rewarded with the Nobel Prize. Varmus became director of the National Institutes of Health (NIH) under President Clinton; Bishop, chancellor of the University of California in San Francisco, one of the largest medical-research institutions in the country. The two scientists had “discovered a collection of normal genes that can cause cancer when they go awry,” Gina Kolata later reported in the New York Times. About 40 such genes had been discovered. Normally harmless, “they would spring into action and cause cancer if they were twitched by carcinogens.” When mutated, in other words. This was “a new era in research.”
The following week, on October 20, 1989, Science magazine also reported the award. The article claimed: “…the work of the Bishop-Varmus group has had a major impact on efforts to understand the genetic basis of cancer. Since their 1976 discovery, researchers have identified nearly 50 cellular genes with the potential of becoming oncogenes.” Their work was “already paying off clinically.”
And so it went. Researchers began to find more and more of these oncogenes; then “tumor suppressor genes” were added. Now, in the Washington Post article, we read that “researchers sifted through 250 genes that had been identified as playing a role in breast cancer.”
So, up to 250 genes are “playing a role.” The Sanger Institute, which was also involved in the human genome project, claimed recently that “currently more than one percent of all human genes are cancer genes.” The latest figure is 25,000 genes in total for humans, so that is surely where the 250 “cancer genes” came from.
At the beginning, the oncogene theory posited that a single gene, when mutated, turned a normal cell into a cancer cell. We have gone from 1 to 250, the latter “playing a role.” This “multiplication of entities” — genes — is the hallmark of a theory that is not working. It’s what philosophers call a “deteriorating paradigm.” The theory gets more and more complex to account for its lack of success. The number of oncogenes keeps going up, even as the total number of genes goes down. Six years ago some thought humans had 150,000 genes in all. Now it’s one-sixth that number. How long before they find that all the genes “play a role” in cancer?
IT ALWAYS WAS unlikely that a single mutated gene would turn a cell into a cancer cell. Mutations occur at a predictable rate in the body. As the cells of the body number perhaps trillions we would all have cancer if a single hit was sufficient. Then came the “multiple hit” theory. Three or four, maybe six or seven genes would all have to mutate in the same cell during its lifetime. Then, bingo, your unlucky number had come up. That cell became a cancer cell. When it divided it just kept on and on dividing.
Meanwhile, the underlying theory never changed. The research establishment remains in thrall to the idea that cancer is caused by gene mutations. It was and is unable to lay its hands on the genes responsible, but it believes they are in there somewhere.
There are several problems with the theory, but the most basic is this. Researchers have never been able to show that a mutated gene, taken from a cancer cell, will transform normal cells in the petri dish. They are unable to show that the allegedly guilty party is capable of committing the crime. They can transport these mutated genes into test cells. And the supposed deadly genes are integrated into the cell’s DNA. But those cells do not turn into cancer cells, and if injected into experimental animals, they don’t cause tumors. That’s when the experts said, well, there must be four or five genes all acting at once in the cell. But they have never been able to say which ones, nor show that in any combination they do the foul deed.
There is even a genetically engineered strain of mice called OncoMouse. They have some of these oncogenes in every cell of their small bodies. You would have thought they would die of cancer immediately. But they leave the womb, gobble up food, and live long enough to reproduce and pass on their deadly genes to the next generation.
I have a suggestion for Gina Kolata, who still works on these issues for the New York Times. Why not try asking Varmus or Bishop exactly which genes, either individually or in combination, cause cancer in humans or anything else? I tried calling Bishop at UCSF a few months back but couldn’t get through. He will respond to the New York Times, surely. But maybe not with a straight answer.
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