Friday, September 5, 2008

Finding the gene is only one part of a complex problem

Elaine Gottschall's comments regarding gene therapy. Elaine is the person who offers the carbohydrate-specific diet for intestinal dis-orders.
While I agree that cancers are complicated dis-ease states, espeically because of the oft overlooked variable by the name "emotional health", I certainly do not believe that 30 years of research to identify a gene pathway is moeny well spent.

There is a goodly amount of research available to support the basis of a theory to conclude that genes are not the cause of a dis-ease. The problem seems to be that this is the tunnel vision approach, and certainly the antithesis of what perspectivs I learned to evaluate while studying in my graduate level public health classes.

Maybe my lifelong creative streak gives me a window on research that is unlike the Newtonian way everyone else seems to be doing it.

While the scientific method may be fine, if you are really committed to finding a cure or coming up with prevention strategies then get you head out of the sand, somewhere out side the box or beyond the tunnel.

It is well known among geneticists that genes plus environment can cause disease or result in health. The fact that scientists have located the gene only gives fuel to the new hype that we will soon be able to cure everything by injecting a virus carrying the correct gene. People should not continue to hype the idea that finding the gene is the b-all and end-all.

Finding this gene is only one part of a complex problem. For example, testing the DNA of Crohn's patients might show a "bad" gene but that gene CAN BE THE RESULT OF MALABSORPTION. This malabsorbtion has been researched by Dr. Haas and is discussed in Breaking The Vicious Cycle.

The building blocks of DNA require the formation of 4 base pairs (adenine, cytosine, thymine, guanine; ATCG) The cells cannot form thymine if the person is deficient in certain vitamins and minerals. All dividing and mutiplying cells are constantly forming these base pairs but if a person is deficient in certain vitamins and minerals (particularly folic acid and B12), they will not form the perfect molecule of thymine thereby resulting in a "bad" gene. With a thymine molecule that is not formed perfectly as cells divide, we have a mutation. Therefore, it is a vicious cycle of what comes first, the chicken and the egg.

(Not many people are aware of this but I took 3 years of genetics and did a graduate course in cytogenetics and gave a report on it. It is important to print the news of gene advances but it also important to give a fair shake to all science. Just being told that we are making advances so that we can someday inject a perfect gene into you to substitute for the bad gene is not enough.)

Dr. Ebringer's work has shown that genetically, (according to tissue typing) some people are more vulnerable to an attack against intestinal bacteria by the antibodies produced by the immune system. Dr. Ebringer showed about 15 years ago that histocompatibility genes (genes that confer on certain people a certain tissue type, eg. HbA-27) can make one susceptible to the antibodies that are trying to kill certain bacteria in the gut. He also showed how a diet similar to SCD got rid of the bacteria and stopped the immune system producing all those "lethal" antibodies. from Elaine Gottschall

Now, back at the ranch, none of this may matter if patients aren't getting preventative and curative care through such effective approaches offered by the Kelley or Bruzynski methods.

Trying to pin the tail on one gen seems to fail to consider all possible vectors in a person's situation and, to me, fails to find the cause. Maybe it is just my idealism or my lean toward quantum mechanics and string theory.

Arthur Koestler may have been a spy, so they say, but he sure as hell had some damn good thoughts on creative thinking.
Gene domino effect behind brain, pancreatic tumors
Thu Sep 4, 2008

Scientists have mapped the cascade of genetic changes that turn normal cells in the brain and pancreas into two of the most lethal cancers. The result points to a new approach for fighting tumors and maybe even catching them sooner. Genes blamed for one person's brain tumor were different from the culprits for the next patient, making the puzzle of cancer genetics even more complicated.

But Friday's research also found that clusters of seemingly disparate genes all work along the same pathways. So instead of today's hunt for drugs that target a single gene, the idea is to target entire pathways that most patients share. Think of delivering the mail to a single box at the end of the cul-de-sac instead of at every doorstep.

The three studies, published in the journals Science and Nature, mark a milestone in cancer genetics.

"This is the next wave," said Dr. Phillip Febbo of Duke University's Institute for Genome Sciences and Policy, who was not involved with the new research. "What's really important is that finding those common elements within the landscape suggests there are therapeutic interventions that can help the whole group."

Despite 30 years of laborious work, scientists until now have found only a fraction of the genetic alterations required to cause any of the 200 diseases that collectively are called cancer. Different tumors require a different domino effect of genetic changes to arise, and to determine their severity and even which treatments will work.

The new maps do not include just mutated genes. They cite missing ones, extra ones, and overactive or underactive ones, too, in the most comprehensive look ever at human tumors.

Teams led by Johns Hopkins University examined more than 20,000 genes in tumors taken from 24 pancreatic cancer patients and 22 patients with the most dangerous brain tumor, called glioblastoma multiforme. Separately, The Cancer Genome Atlas project — a government-funded network of 18 medical centers — analyzed 600 genes in glioblastomas from 206 patients.

The Hopkins teams found hundreds of genetic changes, including a particularly intriguing gene named IDH1. Twelve percent of glioblastoma patients, mostly young ones, harbored a mutated version that brought longer survival: a median of 3.8 years compared with the 1.1 years for patients without the mutation.

If additional study proves that effect, doctors soon might use an IDH1 test to help determine prognosis, said Hopkins' Dr. Victor Velculescu, who led the glioblastoma work. If so, the next question is whether certain drugs work better in those patients as well.

The bigger discovery involved cancer's genetic chaos. No tumors were identical. The typical pancreatic cancer contained 63 genetic alterations and the average brain tumor 60, Hopkins researchers reported in Science.

Fortunately, "genes don't work alone," said Hopkin's Dr. Kenneth Kinzler, who led the pancreatic work. Figure out which genes cluster in which pathways and "a simpler picture emerges."

The Hopkins team identified 12 core pathways that were abnormal in most pancreatic tumors. In Nature, The Cancer Genome Atlas researchers reported three core pathways at work in most glioblastomas.

The pathways do different things. Some allow damaged DNA to escape repair. Some switched off protective factors meant to suppress tumors.

Finding drugs that block those pathways will not be easy, said Dr. Bert Vogelstein of Hopkins and the Howard Hughes Medical Institute, who oversaw the research. They also may cause more side effects than current "targeted therapies" that work against only a specific gene defect.

But companies already are researching drugs to block a particular enzyme pathway implicated in the studies.

Also, pathway blockers should work in larger groups of patients, Vogelstein said. One particular pancreatic cancer pathway contains a variety of genes mutated in only a few people, but regardless of which gene ran amok, the whole pathway was broken in every tumor studied. "Even though it sounds complex, it's actually allowing us to simplify the complex into pathways that will allow us, I think, to truly understand cancer for the first time and take a much more rational approach to treatment," said Dr. Anna Barker of the National Cancer Institute, who co-directs the cancer atlas project. "I'm more optimistic."

Moreover, the work suggests possible ways to catch cancer earlier, by tracing mutant DNA floating through the bloodstream well before tumors themselves start to spread, Vogelstein added. "I don't think that's any longer science fiction."

On the Net:
The Cancer Genome Atlas:
Copyright © 2008 The Associated Press. All rights reserved

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