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As we are all quite aware, this method is incredibly damaging to the body, and doesn’t always lead to the results that we desire. Researchers found that restoring normal levels of a human colorectal cancer gene in mice stopped tumor growth and re-established normal intestinal function within only 4 days. Up to 90% of tumors of this variety contain a particular mutation inside called the Adenomatous Polyposis Coli (referred as APC from here on). What they found however, was that by precisely and reversibly disrupting the APC activity in a small mouse which had colorectal cancer, they found that the cell began functioning properly again, and actually stopped its cancerous activity.
By doing so, the tumor cells stopped multiplying, and intestinal cells recovered to behave normally. Currently, it is unclear whether this method will work on other forms of cancer, as the genealogy is often slightly different. Besides the fact that these scientists are AWESOME and deserve a round of applause, and encouragement to continue the research and get this formula out to the masses, I’d say that there is something special and interesting about this information. It seems to me that no matter what the problem, no matter how bad something gets, there is always something deep down that, if you can make a shift at that core level, you can return things to a natural, harmonic state. George Klein, Professor Emeritus at the Microbiology and Tumor Biology Center at the Karolinska Institute in Stockholm, Sweden, has been teaching and researching since the mid-1940s.
As Klein explains, the suffering of cancer patients and their families has inspired most cancer researchers to focus on the genetics of cancer susceptibility. In a previous discussion, Klein and his coauthors identified five kinds of anticancer mechanisms. The third mechanism is epigenetic, which involve changes in gene expression, rather than changes in the DNA text itself. Klein predicts that intercellular surveillance by neighboring cells, the fifth known anticancer mechanism, plays a major role in tumor resistance. While the first four anticancer mechanisms are known to be influenced by genetic variation, little research has been performed on possible genetic or developmental variations in the efficiency of the intercellular anticancer mechanism.
It turned out that tumor incidence in the normal mammary gland derived from the high cancer parent was tenfold higher than in the mammary gland from the low cancer strain.
Klein urges researchers to investigate this intercellular issue, along with the genetics of tumor resistance that act in multiple ways. Researchers have built a computer model of the interaction between different bacteria, and between bacteria and the gut wall.
Many of the drugs we use in hospitals a€“ antibiotics, antifungals and anti-cancer drugs, to name but a few a€“ are produced by bacteria that live in the soil beneath our feet.
VIRUSES specifically designed to battle superbugs are being trialled in a South Australian hospital. A naturally-occurring mutation in a rabbit-specific virusa€”related to the smallpox virus a€”weakens the virus and may give insight to understanding pathogen evolution, according to a Kansas State University study. Supercomputers have helped scientists find a surprising link between cross-shaped (or cruciform) pieces of DNA and human cancer, according to a study at The University of Texas at Austin (UT Austin). Like top musicians, songbirds train from a young age to weed out errors and trim variability from their songs, ultimately becoming consistent and reliable performers. A biomedical breakthrough published today in the journal Nature reveals never-before-seen details of the human body's cellular switchboard that regulates sensory and hormonal responses. Imagine you wanted to know how much energy it took to bike up a mountain, but couldn't finish the ride to the peak yourself. Well googleplex, I don't know if they've identified any beneficial viruses yet, but IIRC the vast majority of viruses that live in humans are not harmful to us. I asked myself long ago, before applying to grad school, the same question and i wrote a small paper expressing my ideas.
You know, we could spend all the effort figuring out a cure for cancer now, or we could just be patient and wait a few thousand years for Darwin to do his thing and give us natural cancer resistance. Death is required for evolution to work, and evolution actively regulates longevity of every species including humans.
The only thing I hope is that 15 years from now (and hopefully much sooner), the medical establishment will look back and realize that chemotherapy as a cancer treatment was the greatest medical mistake in modern history. One more thing as it seems to me you might be referring to my theory that human aging is the direct product of evolution, in that case you should keep in mind that not all species are in the same situation, the relative importance of aging as a mechanism of removing old individuals depends on the evolutionary setting, if other factors constantly limit the population more then what would be optimal from evolutionary POV then aging might even be non existent.
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This site is my hobby, and I do not accept donations, though I appreciate those who have offered to help. List the three most common cancers in men and in women, and the three most common fatal ones. Tumors arise from single cells, and they recapitulate, more or less, the things that cell did in health. I'd insist that there be two different pathologists' signatures on every positive cancer biopsy.
Tumor cells are locally invasive; the tumor grows into the surrounding tissue and destroys it. Much of the day-to-day work of a surgical pathologist is figuring out the cell of origin of poorly-differentiated cancers. Look for cells with elongated nuclei running parallel, with at least a modest amount of cytoplasm. Thanks to the decline in deaths from atherosclerosis, cancer is now the leading cause of death in U.S.

The grade and stage of a cancer are determined to offer a prognosis and to determine treatment. TUMOR GRADE: assigned by the pathologist to reflect the cancer's degree of differentiation. I personally know many people who underwent Chemo therapy and never came out of it, and I know that i’m not the only one. Despite the fact that this method is incredibly young, it is clear that there is something to it that may hold the key to healing cancer all over the world. Remarkably, tumors were eliminated within 2 weeks, and signs of cancer were prevented months later. Colorectal cancer is the second leading cause of cancer-related death in developed countries, accounting for nearly 700,000 deaths worldwide each year. For a long time, it was thought that these mutations were the cause of colorectal cancer, and it had not been clear whether the inactivation of this gene also played a role in the growth of tumors and the survival of said tumors once cancer had been developed. Tumors pulled back and soon vanished, or reintegrated with normal tissues within only 2 weeks, and by the 6 month follow-up period there was no sign of cancer anywhere. However, this method does open up many new potentials for exploration within other cancers to find other opportunities for facilitating the transformation of the cells back to normal. Whether you’re dealing on a physical, emotional, or mental level, equilibrium can always be found. In a recent study called a€?Toward a genetics of cancer resistancea€? published in the Proceedings of the National Academy of Sciences, Klein highlights evidence of several biological cancer resistance mechanisms that some individuals have that seem to prevent them from developing cancer. On the other hand, the genetics of cancer resistance has been largely unexplored, possibly because it is assumed to be merely the other side of the susceptibility coin. Perhaps most people have various protective mechanisms that counteract the development of cancer cells and stop the disease from progressing beyond the earliest stages. Studies have shown that there are individual variations in the efficiency of DNA repair, which is highlighted in cases such as the specific DNA repair deficiency called xeroderma pigmentosum.
Studies have shown that when mice that carry a paternal precancerous mutation inherit a maternal imprinting defect, normal parental imprinting is impaired, which can increase the probability of cancerous development.
As part of an intracellular defense, a cell can trigger apoptosis, or cell death, if it detects extensive DNA damage, so that the cell doesna€™t reproduce and spread the damage.
Cells that are in direct physical contact with each other can detect precancerous conditions in one another, and together act as a microenvironmental control system to prevent the development and progression of unhealthy cells.
However, Klein mentions a group of largely forgotten experiments from the 1950s and a€?60s, where scientists crossed mouse strains that had a high incidence of cancer in a given tissue (due to inbreeding and selection for that particular type of cancer) with mice from a low incidence strain. Evolution seems to have favored some relatively common resistance genes that protect the majority of humans against cancer development. Zheng Cui (IIRC) at Wakeforest found cancer resistant mice and people whose neutrophils and macrophages and maybe natural killer cells gang up on cancer cells and kill them. Imagine we have an organism which never dies, as it procreates it will soon completely fill it's environment and what then? Are you unable to explain this aparent contradiction with your theory that death is essential to life? The findings provide proof of principle that restoring the function of a single tumor suppressor gene can cause tumor regression and suggest future avenues for developing effective cancer treatments.
Moreover, this approach was effective in treating mice with malignant colorectal cancers with the Kras and P53 mutations. That is, two out of three people never get cancer, and more than half of heavy smokers dona€™t get cancer, either.
Perhaps, Klein says, there are cancer-resistant genotypes that a€?nip cancer in the buda€? and keep most of us healthy.
For example, if cancer is caused by mutations in genes that control cell division, then it logically seems that cancer resistance is simply a low occurrence of these mutations. For instance, researchers have compared the antibody responses of the squirrel monkey and the marmoset when infected with Herpesvirus saimri, a virus that is endogenous to squirrel monkeys but that the marmoset never encounters. Individuals with this deficiency are highly sensitive to ultraviolet light, and even with careful protection they develop multiple skin carcinomas due to the genetic deficiency. In humans, this same imprinting defect occurs spontaneously and increases tumor incidence, affecting 10% of humans, and increasing their risk of intestinal cancer about threefold. In the experiments where they studied mammary cancer, hybrid females were taken from this case. This genetic difference could either act at the level of the cancer cells or at the level of their microenvironment. One day, finding out how nature keeps most of us cancer-free could help identify and repair specific genetic mechanisms in the large minority of individuals who do suffer from cancer.
It's doubtful that having old people around consuming resources and generally not being of much use other than information storage is worthwhile in a hunter-gatherer society. When you, or your loved ones get it, you may care! Understanding cell function and malfunction is worth far more than "space travel" or photo cells, or YOU! An organism that lives indefintely, will create more copies, than one that doesnt, and so evolution, if its true, should have organism living longer and longer, so they can have more offspring. But not for all people or old people or people in the winter or people who have had a great upset in the last few days.
As for evolution it's goal is not to cure every disease, only to bring them down to manageable levels, evolution is all about *economy*, if the cost of additional resources required to further lower incidence of the disease outweights benefits such outcome is of course not desirable and will be selected against.Death is required for evolution to work, and evolution actively regulates longevity of every species including humans. The fact that the treatment is often as bad or worse than the disease, its poor success rate, and, probably most importantly, that it has such poor affinity to cancer cells, makes it a Dark Ages treatment.

These mutations are found in about half of humans who have been found with colorectal cancer. A recent study points out this overlooked fact, and suggests that researchers might discover something by asking why so many people are resistant to the often deadly disease.
When exposed to the virus, the marmosets, but not the squirrel monkeys, develop rapidly growing lymphomas. For example, individuals who carry the genetically mutated tumor suppressor p53 run an increased risk of inheriting Li-Fraumeni syndrome, a rare disease in which patients develop multiple tumors. However, Klein says that ita€™s premature to speculate exactly how understanding genetic resistance could help people who are susceptible to cancer. However nobody rushes to the doctor to say they feel particularly well today and has a viral analysis. Think of it this way: the more complicated a machine, the harder it is to fix when it breaks.
Then, when the cell divides into 2, one of the cells takes *all* of the damage, leaving the other cell undamaged ("young"). He should be starting clinical trials in June or so this year using neutrophil rich centrifuged blood from cancer resistant people to transfuse into cancer victime. The lengthy series of random reselections of whole chromosomes until one set reproduces faster is why the result may take decades after the insult. To evolve old organisms need to be removed somehow, unless you assume the environment has unlimited resources which is unrealistic.
The researchers found a striking difference in the timing of each animala€™s antibody response. One mammary gland from the high cancer strain parent and one gland from the low cancer strain parent were then transplanted to two opposite flanks of the hybrids. That now-damaged bacterial cell continues to divide, taking all of the cumulative damage onto itself, until it is too damaged to function, then it dies. Sometimes it's called LIFT for Leucocyte InFusion Therapy, but the clinical trial hasn't begun yet.And Peter Duesberg, the hero, has shown that cancer is NOT a genetic disease. Of course, other damage to the repair enzymes like p-53 do make it more likely, eventually.
In the tumor-resistant squirrel monkeys, the antibodies rose to a high level just three days after the infection, but, for the marmosets, the response took three weeks.
Dealing with two inbred strains and their hybrid progeny, there is no problem with graft rejection, Klein explains. If you were to limit your statement to simply "Death is not desirable to any organism" then I would be more inclined to believe you. And cigarette smoke likes to damage two particular spots on the P-53 DNA with some biphenyls. Under ideal conditions they could live for 1000's of years. Clearly the sea urchin evolved from something else, but it does not have death programmed into itself. Today in the world of research funding you need to conform otherwise be ostracized as a crackpot. As for studying why people don't get cancer, if they think this is a good idea, then perhaps they would also be interested in why people without lungs full of fluid don't drown! As it stands, it would seem that for survival of the race as a whole, it becomes less efficient to prolong an individual's survival beyond a certain point.
For example in humans, mitochondrial damage is a byproduct (cause?) of aging, and in terms of overall species fitness, it does not make sense to have those kinds of members kicking around. Cui at Wakeforest has discovered many humans with neutrophils and macrophages which seek out and kill any cancer cells not suppressed in other ways.
Hence your hypothesis is disproven. Your comment that cancer is "all about chance" is puerile.
Cancer happens when the cellular program gets corrupted to the point that failsafe mechanisms which should kill the cell in such a case also fail and the cell goes on a progressively more chaotic dividing spree following it's more and more erratic code.
I am talking from a purely scientific stance. Why are we not over run with sea urchins even though they don't die of old age. Your immune system does an incredible job of catching cancer many, many times over the course of your lifetime. Clinical trials for his Leukocyte InFusion Therapy (LIFT) are expected to start in June.Malthus guarantees that deaths will occur eventually if fitter survivors who reproduce well consume all the food, but otherwise evolution only requires that fitter offspring reproduce more successfully. To respond to paulthebassguy's comment: Sorry, we already have natural cancer resistance that works incredibly well. But major evolution of big slow animals like us will usually take many thousands of years, not just a few.
Take a look at how many people actually have cancer, then consider how many DNA base pairing events occur over the course of each person's lifetime.
Under ideal conditions they could live for 1000's of years.Clearly the sea urchin evolved from something else, but it does not have death programmed into itself.
Ah well, it's the nature of humans to focus on the times things go wrong, rather than the number of times things go perfectly well undetected. Age is obviously not the only source of death, you can always get killed!It's very easy to see why evolution requires death.

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