Johns Hopkins University scientists led by urology professor Robert H. Getzenberg have developed a more accurate test for prostate cancer using a protein called Early Prostate Cancer Antigen (EPCA).
In the first clinical study of a new blood protein associated with prostate cancer, researchers have found that the marker, called EPCA or early prostate cancer antigen, can successfully detect prostate cancer in its earliest stages.
Greater sensitivity of cancer tests allows for earlier diagnosis and treatment and therefore better outcomes. Also, greater test sensitivity enables more rapid testing of anti-cancer drugs and of dietary and other interventions designed to prevent cancer in the first place.
The new test is much more accurate than the existing Prostate Specific Antigen (PSA) test.
The researchers found that EPCA levels were high in 11 of 12 prostate cancer patients (92 percent) and low in all the healthy individuals. Only two bladder cancer patients and none of the other patients had elevated EPCA levels, suggesting that for this study, the test was correct 94 percent of the time. In comparison, only one-quarter of patients who undergo biopsies because they have elevated PSA values are actually positive for prostate cancer, while as many as 15 percent of those with low PSA values were found to have prostate cancer as detected by biopsy, according to Getzenberg.
Larger clinical trials are under way to further refine the EPCA test, to make it more sensitive so it can pick up even the smallest traces of the marker and to verify its usefulness for detecting prostate cancer in a larger sample of patients, Getzenberg said.
Earlier cancer diagnosis will produce an unintended and yet ultimately beneficial consequence: The total number of people walking around with known cancer will rise dramatically. Therefore more people will feel the urgent need to support cancer research. A person who gets a cancer diagnosis and is told they have 6 months to live has little incentive to support cancer research and little time in which to do so. But a person who gets a cancer diagnosis 5 or 10 years before the cancer is going to reach the terminal stage has a lot of time and energy to devote to supporting cancer research.
This same phenomenon of increasingly earlier diagnosis years before a disease kills its sufferers is being repeated across many other types of diseases. Scanning technologies such as MRI, new blood tests, saliva tests, and other tests are leading to increasingly earlier diagnoses. In some cases this allows earlier and more successful treatment. But for incurable disorders this trend is also producing a growing body of people who now live for years knowing they have a fatal disease. This focuses more minds in support of developing better treatments.
A Henry Ford Hospital study shows use of antibiotics in babies dramatically increases the risk of allergies and asthma by age 7.
For the Henry Ford study, researchers followed 448 children from birth to seven years. The children were evenly divided by gender.
Data was collected prenatally and at the first four birthdays until the children were 6 and 7 years old, when they underwent a clinical evaluation by a board-certified allergist. The data included information about all prescribed oral antibiotics; blood tests that measure the antibody (immunoglobulin E) that causes allergies; and skin reaction tests that show whether a person is hypersensitive to an allergen. Researchers also collected data on all clinical visits and made home visits to collect environmental samples.
Of the 448 children, 49 percent had received antibiotics in the first six months of life. The most common antibiotic category prescribed was penicillin.
Among the findings:
- By age 7, children given at least one antibiotic in the first six months were 1.5 times more likely to develop allergies than those who did not receive antibiotics. They were 2.5 times more likely to develop asthma.
- By age 7, children given at least one antibiotic in the first six months and who lived with fewer than two pets were 1.7 times more likely to develop allergies, and three times more likely to develop asthma.
- By age 7, children given at least one antibiotic in the first six months and whose mother had a history of allergies were nearly twice as likely to develop allergies.
- By age 7, children given at least one antibiotic in the first six months and who were breast-fed for more than four months were three times more likely to develop allergies. However, breast-feeding did not influence the risk between antibiotics and asthma.
Note that between the second and third bullet items above the only difference was the reduction in pet exposure and the result was a higher incidence of allergies and asthma.
The oddest result that I see is the fourth item where breast-feeding increased the risk of allergies but not of asthma. One potential explanation: the breast milk might cause the immune system of babies to develop more rapidly and hence to be more likely to react to allergens. Given that breast milk probably has other benefits that makes its use a tough call.
Broader spectrum antibiotics increase the risk.
Overall, children given antibiotics in their first half-year were 2.6 times more likely to develop allergic asthma, the team told a meeting of the European Respiratory Society on Tuesday. With broad-spectrum antibiotics, which kill a wide range of bacteria, the risk was far higher: children were 8.9 times more likely to suffer from asthma.
Selection of an antibiotic more narrowly tailored for the target bacteria therefore would reduce risk of allergy and asthma among babies.
The new study also backs the growing belief that antibiotics disrupt the normal development of a child's immune system through a phenomenon known as the "hygiene hypothesis."
This "hygiene hypothesis" has been gathering strength in recent years. The latest result certainly strengthens the argument considerably. The idea is basically remiscent of the saying "idle hands are the devil's workshop". Remove the normal antigens that the immune system is exposed to and it starts reacting to things it ought not react to. Our ancestors lived in dirt floor dwellings and had much more exposure to animals, dirt, and nature in general. We live lives which bring us in much less exposure to the antigens we evolved to deal with. Exposure to those antigens appear to be necessary to instruct the immune system on what it should identify as a threat.
From a signal processing perspective you can think of the immune system as a sensor system that will incorrectly react to weaker signals in the absence of stronger signals to react to. The immune system never experienced enough evolutionary pressure to not react to weaker signals because there were so many stronger signals around for it to pay attention to.
Surely antibiotics are overused and this latest report is yet another reason to reduce the use of antibiotics in situations where they are not necessary. But some children will inevitably get bacterial infections in their early months of life that require antibiotic treatment. So what to do about this problem? One potential solution is to develop vaccines that will retrain the immune system to not react to allergens. It may some day be standard practice to give babies anti-allergy vaccines.
In the shorter term having dogs licking babies faces may be a good thing. Also, it might be possible to come up with formulations of beneficial bacteria to give to babies to replace normal harmless bacteria that are wiped out by antibiotic therapy.
The argument that cleaner environments cause problems in the immune system is especially interesting because it demonstrates how moving humans out of the environments they evolved in creates problems that can be quite subtle and that can go unrecognized for many years. This is not the only such problem of this sort. To take another but rather more obvious example, the higher incidence of obesity in affluent nations is a problem that has arisen because of the lifestyles that are the result of living in industrial societies. Obesity is even more interesting than the allergy/asthma problem because obesity is a behavioral problem. Obese people are driven by strong urges to eat more than what is good for them in modern circumstances.
There are other behavioral problems that arise from growing up in industrial society as well. To take another example, humans are obviously not evolved to handle recreational drugs. Recreational drugs interfere with mechanism of pleasure that evolved to guide learning and other activities. Drugs hijack pleasure systems. Many minds become too easily trained to crave the pleasures that the drugs give them and so the pursuit of pleasure becomes far more harmful than it was in our evolutionary past. Humans are going to have to develop methods of adapting themselves to the changes they are creating in their environment.
Update: In another example of the importance of the sensitivity of the immune system to the timing of exposures to various antigens researchers in the United States and Germany have just discovered that the date of first introduction of babies to cereals affects their odds of developing diabetes.
Babies with a family history of diabetes who were introduced to cereals before or after the recommended age of four to six months had a higher risk of developing a precursor to the disease, researchers said Tuesday.
US team lead researcher Dr. Jill Norris says early exposure to cereal proteins may cause an immature immune system to react inappropriately.
She hypothesizes that the youngest babies have extremely vulnerable immune systems. Older babies, denied solids for so long, simply ate more and overwhelmed still developing systems with foreign cereal proteins. The hypothesis has yet to be proved and Norris stressed the scenarios refer to at-risk babies.
Another theory is that children who don't start eating cereals by 6 months of age are more likely to be deficient in vitamins and that this causes their immune systems to malfunction and start making auto-antibodies (i.e. antibodies to ones's own proteins).
Ray Davies of the Kinks was on to something.
July 22, 2003 -- Researchers at the University of Toronto and St. Michael's Hospital have shown that a vegetarian diet composed of specific plant foods can lower cholesterol as effectively as a drug treatment. The study, published in the July 23 issue of the Journal of the American Medical Association, compared a diet of known cholesterol-lowering, vegetarian foods to a standard cholesterol-reducing drug called lovastatin. The special diet lowered levels of LDL cholesterol - the "bad" cholesterol known to cause clogging in coronary arteries - in subjects by almost 29 per cent, compared to a 30.9 per cent decrease in the lovastatin subjects. The special diet combined nuts (almonds), soy proteins, viscous fibre (high-fibre) foods such as oats and barley and a special margarine with plant sterols (found in leafy green vegetables and vegetable oils).
Lead author David Jenkins, a professor in U of T's Department of Nutritional Sciences and director of the Clinical Nutrition and Risk Factor Modification Centre at St. Michael's Hospital, believes the reason these foods work so well to reduce cholesterol is that humans may be evolutionarily adapted to what has been called the "ape diet," a diet very high in fibre, nuts, vegetable proteins and plant sterols.
He adds the study could have far-reaching implications for public health. "As we age, we tend to get raised cholesterol, which in turn increases our risk of heart disease. This study shows that people now have a dietary alternative to drugs to control their cholesterol, at least initially." Jenkins notes the diet can also be used to maintain normal cholesterol levels.
In this month-long study, a follow-up to one released December 2002, 46 men and women with raised cholesterol were randomly assigned to one of three vegetarian diet groups. The control group ate meals low in saturated fats (such as those found in animal products like beef and butter). The second group had the same low fat diet, plus a daily 20 mg treatment of lovastatin. The last group had a diet high in four foods known to have cholesterol-lowering properties. This special diet, designed to be easy to prepare and eat, included foods such as oat bran bread and cereal, soy drinks, fruit and soy deli slices. A typical dinner for people on the special diet was tofu bake with eggplant, onions and sweet peppers, pearled barley and vegetables.
The diet had 4 major categories of components.
The key components of the ape diet are plant sterols, found in plant oils and enriched margarines, viscous fibre, found in oats, barley and aubergine, and soy protein and nuts.
The margarines enriched with plant sterols (which compete with cholesterol for absorption) used in the study may have been the commercial brands Take Control, Benecol, and Benecol Light. To up your plant sterol content using natural foods one possibility is pecans with 95 milligrams of plant sterols per 100 grams. However, the level of plant sterols in the margarines is about two orders of magnitude greater (1.7 grams sterols in 14 grams of Take Control) and clinical trials in plant sterols have used about 2 grams per day. Still, the nuts have other heart-healthy benefits.
The researchers claim this diet works because it recreates the kind of diet humans evolved eating.
"We went right back in time to, hypothetically, five million years ago, when the diet would largely be leafy vegetables, fruits, nuts and seeds," Dr. Jenkins said.
While the researchers bill this diet as a return to the sort of diet that our ancestors ate for millions of years that is not exactly the case. First of all, it is unlikely that before the development of agriculture any humans or pre-humans ate soy as a major food source. If there are compounds in soy that have some sort of pharmaceutical effect upon cholesterol levels it is not clear (at least to me) that those compounds were present in diets thru some other food sources. Also, oats and barley would not have been major sources of calories. However, they are serving here as sources of soluble fiber and it does seem likely that whatever humans did eat provided a considerable amount of soluble fiber. So it seems likely there are elements in this diet which are not part of our evolutionary history while other elements have been added into the diet by using food sources that humans did not eat historically.
There is another important caveat to keep in mind when interpreting these results: various human subpopulations have split off from each other long enough and ate sufficiently different diets from each other to have evolved adaptations to local food sources. We see signs of this, for example, with northern Europeans who make more lactase enzyme for digesting milk. We also see it in the differing abilities of racial and ethnic groups to handle alcohol. It is unlikely that every ethnic and racial group has the same average ideal diet. Eventually declining costs of DNA sequencing and the identification of genetic variations that affect how we metabolise food will lead to the widespread practice of nutrigenomics where dietary recommendations will be personalized for one's specific genetic profile and risk factors.
The results of this study are sufficiently dramatic that JAMA recommends its use before cholesterol-lowering drugs are tried.
In an accompanying editorial, James Anderson, a professor of medicine at the University of Kentucky in Lexington, said the findings have dramatic public-health implications. He suggested that physicians prescribe the "ape diet" to patients before even considering drugs.
This deit is an improvement on the Garden of Eden diet the same researchers developed.
The daily volume of food was about a third of that of the Garden of Eden diet, Jenkins said, adding the people who followed it didn't complain about how much they had to eat but said they couldn't eat any more.
Those who lost weight were asked to, however.
Most of the reports on this study didn't pick up on one particularly interesting result the researchers observed.
Surprisingly, the diet also lowered the levels of C-reactive protein, considered a risk marker for heart disease.
Equally impressive was a 28 percent drop in C-reactive protein, a substance found in the blood that is a sign of inflammation and possible heart disease. The statin group had a 33 percent drop.
The fact that this diet lowers C Reactive Protein (CRP) levels is an added bonus. CRP is a marker for inflammation that has been found to be correlated with heart disease risk. While the importance of CRP as a marker is still debated among cardiology researchers it seems important because there is growing recognition among medical researchers of the role chronic inflammation plays as a cause of the development of degenerative diseases. Any diet that lowers inflammation markers likely will yield more benefits than just lowering the risk of heart failure.
As for how this diet lowered C Reactive Protein (CRP): there are a lot of possibilities. Vitamin E, omega 3 fatty acids, and vitamin B6 are a few of the factors that are thought to lower CRP. Losing weight helps lower CRP as well. However, statin drugs for lowering cholesterol also lower CRP. So is the cholesterol-lowering effect of the diet causing CRP to drop? Maybe.
The Scientist has a good recent survey of the many ways chronic inflammation appears to contribute to the development of many diseases. (requires free registration - and I really recommend taking the trouble as they are one of the better science news sites)
Centuries ago, this trigger was pulled on a more consistent basis as humans battled a harsher environment; Johnson attributes today's toll of inflammation on the super clean environments of Western society. Also, because humans are living longer than evolutionarily designed, and in larger numbers, says Johnson, the odds are increased for disease. "You have an immune system that's looking for something to do and is basically getting into trouble," he says. "I think the problems are caused by an ongoing, aggravated, chronic response to an immune problem that the innate system imagines is there, but isn't." Also, the various byproducts associated with immune system attack, such as reactive oxygen species that decimate joints, may be causing long-term, deleterious effects.
The argument here is that the immune system no longer has enough real enemies to attack and yet it is all hyped up ready to attack something and responds inappropriately. Of course there is a large assortment of auto-immune diseases but many scientists are looking at inflammation response (and it is hard to untangle inflammation response from immune response) as another manifestation of this general problem. However, in some cases chronic inflammation may be getting triggered by chronic infections. This can happen with helicobacter pylori in the stomach. Peridontal disease also causes arterial inflammation and increased risk of heart disease.
However, many clinicians were unclear of the cause of elevated CRP levels. A study published earlier this year in the Journal of Periodontology reported that inflammatory effects from periodontal disease, a chronic bacterial infection of the gums, cause oral bacterial byproducts to enter the bloodstream and trigger the liver to make proteins such as CRP that inflame arteries and promote blood clot formation.
Keep your teeth clean and your gums healthy.
The inflammation-lowering angle is a lot more interesting because the benefits of cholesterol lowering and the methods for lowering cholesterol are a lot more widely known in comparison. We still do not understand all the factors that contribute to chronic inflammation or the best strategies to use to reduce it.
A class of composite materials helps in the repair of natural teeth.
"Smart materials" invented at the National Institute of Standards and Technology (NIST) soon may be available that stimulate repair of defective teeth. Laboratory studies show that these composites, made of amorphous (loosely structured) calcium phosphate embedded in polymers, can promote re-growth of natural tooth structures efficiently. In the presence of saliva-like solutions, the material releases calcium and phosphate ions, forming a crystalline calcium phosphate similar to the mineral found naturally in teeth and bone. Developed through a long-standing partnership between NIST and the American Dental Association (ADA), these bioactive, biocompatible materials are described in a forthcoming paper in the NIST Journal of Research.
Plans are being made for clinical trials, and several companies have expressed interest in licensing the patented material once a production-ready form is available. Initial applications include adhesive cements that minimize the decay that often occurs under orthodontic braces. The material also can be used as an anti-cavity liner underneath conventional fillings and possibly in root canal therapy.
NIST and ADA scientists continue to enhance the material's physicochemical and mechanical properties and remineralizing behavior, thereby extending its dental and even orthopedic applications. For example, the researchers found that adding silica and zirconia to the material during processing stabilizes the amorphous calcium phosphate against premature internal formation of crystals, thereby achieving sustained release of calcium and phosphate over a longer period of time.
What would be handy would be a way to use this material to cause a gradual repair of cracks and pits and small chipped off areas.
Dr. Annette Fritscher-Ravens and colleagues at the University College London have successfully tested in humans a small swallowable gut camera that can be steered around in the gut.
Fritscher-Ravens and her colleagues say they have patented just such a method. Using technology very similar to that found in TV remotes or electronic car-keys, they attached tiny electrodes to the front and rear portions of the video capsule, along with a tiny antenna. Using a drive/reverse switch, they have been able to steer and propel the capsule through the gut, lingering wherever a lesion or other suspicious formation occurs
Passive camera pills known as capsule endoscopes are already available and in clinical and research use. But this new design allows doctors to tell the camera pill to move itself to areas of interest.
An existing passive capsule endoscope was recently used to discover greater side-effects from NSAIDs on the small intestine than had previously been reported.
The capsule endoscope, developed by Given Imaging, allows medical professionals to view the entire small intestine. The system uses a disposable miniature video camera contained in a capsule, which the patient swallows. The capsule passes through the digestive tract, transmitting color images, without interfering with the patient's normal activities. Capsule endoscopy diagnoses a range of diseases of the small intestine including Crohn's Disease, Celiac disease, benign and malignant tumors of the small intestine, vascular disorders, medication related small bowel injury and pediatric small bowel disorders.
The study enrolled 40 patients, with a mean age of 49.5, who had arthritis including osteoarthritis, rheumatoid arthritis and gout. Twenty patients took NSAIDS daily for three months. Twenty patients took acetaminophen alone or nothing at all. All patients fasted overnight and underwent capsule endoscopy. The pylorus, the sphincter muscle that controls the lower opening of the stomach where it empties into the upper part of the small intestine, was marked on each video. Two investigators who were not told which therapy the participants received, reviewed each video beginning after the pylorus, where the small intestine starts.
Severe injury to the small bowel was seen in 23 percent of NSAID users compared to no severe injury in the controls. Severe damage was associated with high doses of indomethacin, naproxen, oxyprozocin and ibuprofen.
Given the widespread long term use of NSAIDs this is an important result. A repeat of this study with a larger variety of NSAIDs and more test subjects could provide useful guidance in NSAID selection.
Update: this latest finding using a camera capsule to see the effects of NSAIDs on the intestines should not be surprising in retrospect. A 1999 study on mice found NSAIDs might be contributing to the development of inflammatory bowel disease.
A question raised by these experiments is the possible role of nonsteroidal anti-inflammatory drugs (NSAIDs) in promoting inflammatory bowel disease. In the researchers' mice, COX-2 inhibition by NSAIDs produced histologic changes reminiscent of human celiac disease. In view of the megaquantities of NSAIDs consumed worldwide, we'll need to delve more deeply into the full effects of COX-2 inhibition on immune homeostasis
Writing in the New York Times Bruce Grierson explores the potential use of individual genetic profiles to choose the ideal personalized diet.
A trip to the diet doc, circa 2013. You prick your finger, draw a little blood and send it, along with a $100 fee, to a consumer genomics lab in California. There, it's passed through a mass spectrometer, where its proteins are analyzed. It is cross-referenced with your DNA profile. A few days later, you get an e-mail message with your recommended diet for the next four weeks. It doesn't look too bad: lots of salmon, spinach, selenium supplements, bread with olive oil.
Once DNA sequencing costs fall far enough and more DNA sequence variations are tied to health risks and to interactions with dietary and other health habits personal dietary advisories will become possible to create. However, the most powerful use of personal genetic profiles will likely to develop therapies that reduce individual genetic risks and problems.
Suppose someone has a greater risk of getting heart disease on a high saturated fat diet. Well, people still want to eat fat. When the genetic variations that increase heart disease risk are all identified and the mechanisms by which they increase risk become better understood it is very likely that therapies will be developed to change the expression of the genes of high risk people. In the extreme one can imagine genetic therapies to fix the causes of genetic risks.
Gene therapy will even be utilized to make food consumption easier to do. For instance, one can easily imagine those with lactose intolerance getting a gene therapy via a swallowed pill to program intestinal cells to make more lactase enzyme to break down lactose.
By the time that nutritional genomics becomes possible it is likely that complete genetic variation mapping for each person will become possible. Therefore a person won't send a DNA sample off to be tested just for nutritional advice. Rather, someone will submit their genetic map to an advice service and the advice service will then respond with specific dietary and lifestyle recommendations. Also, the service will probably include a suggested list of preventative treatments including drugs to take regularly and preemptive gene therapies to undergo.
Normally if a cancer cell line is injected into a mouse the cancer cells grow. Some scientists at Wake Forest University discovered a mouse that was immune to injected cancer and have bred it and produced many generations of cancer-proof mice.
A cancer-proof mouse, which can survive being injected with any number of cancer cells, has been discovered by US scientists. The discovery of the resistant mouse could pave the way for future gene or drug therapies if the mechanism by which it fights cancer can be understood
This is amazing for a few different reasons. First, it is amazing that it is possible at all. An immune system that can kill such a large variety of types of cancer which does not appear to cause auto-immune disorders is not something I would have expected to be possible. Cancer cells look too much like normal cells and most cancers (perhaps virally caused cancers are an exception) are probably expressing only genes that naturally are expressed in human cells. So where does the specificity come from that lets an immune system knock out a large variety of cancers? Just figuring it out will reveal very useful knowledge.
What is also amazing about it is that the mutation happened and someone noticed. It is hard to say what the odds are for the occurrence of a mutant that would have the resistance to cancer.until it is discovered how the mechanism works and how many mutations had to happen for a mouse to have cancer resistance. Still, it seems amazing to me.
Here are more details.
WINSTON-SALEM, N.C. – Scientists at the Comprehensive Cancer Center of Wake Forest University have developed a colony of mice that successfully fight off virulent transplanted cancers.
"The mice are healthy, cancer-free and have a normal life span," the 10-member team reported in the Proceedings of the National Academy of Sciences online edition to be published the week of April 28.
The transplantation of the cancer cells in these special mice provokes a massive infiltration of white blood cells that destroy the cancer, said Zheng Cui, M.D., Ph.D., associate professor of pathology at Wake Forest University Baptist Medical Center and the lead scientist
"The destruction of cancer cells by these leukocytes is rapid and specific without apparent damage to normal cells," Cui said. "These observations suggest a previously unrecognized mechanism by which the body can fight off cancer."
The discovery of a genetic protection from cancer in mice "may have potential for better therapy or prevention of cancer in people," the team said. It also could help explain why some people are protected against cancer despite prolonged and intense exposure to carcinogens..
The discovery also could help solve another mystery. For years, scientists have been searching for the mechanism that permits spontaneous regression of human cancers without treatment. Cui said these cases are well-documented, but occur rarely. The new mouse colony gives the team the opportunity to study the mechanism in an animal model.
Cui and his colleagues began the mouse colony almost by serendipity. As part of ongoing cancer studies, they were injecting a virulent type of cancer cell that forms highly aggressive cancers in all strains of laboratory mice and rats. When injected into the abdomen, the tumor grows exponentially, causing the abdomen to fill with fluid within two weeks. The cancer can then progress by metastasizing into the liver, kidney, pancreas, lung, stomach and intestine.
But, said Cui, one male mouse unexpectedly remained free of the cancer despite repeated injections. The Wake Forest team was able to show this was genetic and to develop a colony from that single mouse. The colony, now about 700 mice, remains exclusively at Wake Forest. Meantime, the original mouse "remained healthy, cancer-free and eventually died of old age after a normal lifespan."
When the cancer-resistant mice were bred with normal partners, the researchers found that about half of their offspring were resistant to cancer cells, indicating that this genetic protection is dominant and is likely due to a change in one gene. The resistance continued in future generations.
Depending on the age of the mouse, some had complete resistance -- the cancer never got started -- while others displayed spontaneous regression -- the cancer started developing over a period of a couple of weeks, but then it rapidly disappeared in less than 24 hours.
"The mice became healthy and immediately resumed normal activities including mating," Cui said. They tested them again with another injection of the cancer cells. He said that once the mice developed the protection, they never again developed the cancer.
The researchers said the mouse model "represents a unique opportunity to examine cancer/host interactions."
Cui said the new mouse model also may help in solving another medical mystery -- why cancer becomes more common when people age. The usual explanation is that mutations accumulate in the body, leading to precancerous conditions that eventually become cancer.
But, he said, the mouse model suggests that the body's natural protection -- which scientists call host resistance -- declines with age.
Note that this result suggests another reason why the aging of the immune system is a significant problem. Luckily, it will probably be easier to develop rejuvenating cell therapy treatments for the immune system (also see this post) than for many other systems of the body.
How would a mutation that is found in a laboratory mouse strain be usable to create an anti-cancer therapy for humans? Well, the human and mouse genomes have both been sequenced and they have corresponding sections that can be lined up for 90% of their regions. Once the mutation location(s) responsible for this are found in mice then it is likely there will be a corresponding regions in the human genome. It may be possible to introduce equivalent mutations into the DNA of human leucocyte stem cell lines using gene therapy and then inject those stem cells into humans suffering from cancer. Then the cells would multiply and turn into immune cells that fight cancer. Many parts of the transfer of blood stem cells between humans is routinely done as part of leukemia treatments and for other disease treatments..
This mutation (or set of mutations - the capability may the result of a combination of mutations) is likely to have previously occurred in the wild. The fact that the mutation does not normally occur in wild type mice or naturally in other mammalian species suggests that either protection against cancer was not selected for by evolution because other things were killing mammals first or that the mutation has some cost in terms of reproductive fitness. It will be interesting to see how that shakes out.
Even if the mutation turns out to have some downsides it might still be useful as part of a therapeutic treatment. After all, when the downside of not getting treated is death then the side-effects (whatever they might be) of a revved up immune system may be worth it. Also, it might even be possible to add the mutation in a way that can be turned on and off. Attach the relevant gene to a regulatory region that can be switched on and off by a drug. Then even if there was a side-effect to this capability in the immune system it could be activated only long enough to wipe out a cancer.
Another thing that is great about this discovery is that it provides a model to figure out. Here's an immune system that can wipe out a large assortment of cancers. How? The detective work that will be done to figure that out will yield information that is useful by itself. It is even possible that the discovery of the knowledge of how these mice attack cancer will point the way to how to train an immune system to fight cancer with a method less drastic than gene therapy. Perhaps a vaccine could be developed that would train a human immune system to do the same.
The intent of the Personalized Medicine Research Project is to collect enough genetic and health record information about a large enough number of people that it will become possible to discover more genetic variations that contribute to disease.
Marshfield Clinic's publicly funded Personalized Medicine Research Project will collect DNA from 80,000 people and match the genetic profiles with medical histories and other information in a statistical database.
Researchers at the clinic, a not-for-profit health care provider southwest of Wausau, Wis., with 400,000 patients, and a pioneer in genetic research, said they hope to discover the genetic components of common disorders such as heart disease, cancer and diabetes and to tailor the health care of individuals based on their genetic profiles.
The medical records that the project staff will enter into databases will become more useful with time as the genetic assay technologies become cheaper and more powerful. As the number of people enrolled in this project increases and as the assay methods become more powerful an increasing number of medically important genetic variations will be discovered.