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Virus Tamed To Attack Cancer, Cancer Drugs To Treat Alcoholism

ScienceDaily is reporting that scientists at Oxford University seem to have adapted a virus so that it attacks cancer cells but does not hurt healthy cells. "Adenovirus is a DNA virus widely used in cancer therapy but which causes hepatic disease in mice. Professor Len Seymour and colleagues found that introducing sites into the virus genome that are recognized by microRNA 122 leads to hepatic degradation of important viral mRNA, thereby diminishing the virus' ability to adversely affect the liver, while maintaining its ability to replicate in and kill tumor cells." Relatedly, cancer drugs already approved for use may be cross-functional as a treatment for alcohol addiction. "Now, the researchers show that flies and mice treated with erlotinib also grow more sensitive to alcohol. What's more, rats given the cancer-fighting drug spontaneously consumed less alcohol when it was freely available to them. Their taste for another rewarding beverage -- sugar water -- was unaffected."

5 of 128 comments (clear)

  1. Replication is dangerous by toppavak · · Score: 5, Informative

    In any virus intended for therapeutic use in humans, allowing the virus to retain its reproductive mechanisms is just a bad idea. Viruses mutate rapidly and there's no guarantee that such a modified virus might not develop the right signals to enter and reproduce in healthy human cells. More promising efforts using engineered viruses involve the isolated production of viral structural RNA and coat proteins without the complete genome ever being copied or reproduced. This creates viral smart-particles that can be re-engineered to deliver payloads (therapeutics, contrast agents, nanoparticles etc) into targeted cell species. Nanovector is a recent start-up out of NC State University to commercialize this tech developed at a lab I used to work in as an undergrad.

    1. Re:Replication is dangerous by RDW · · Score: 4, Informative

      'Not as dangerous as you'd think...Viruses pick up DNA strands from the host as they are made by the hosts cells, this is primarily what causes rapid mutation and why H1N1 contains human, swine, and avian DNA-this strain has been transmitted between these three animals'

      The Flu virus is a rather unusual case - its genome (in fact RNA rather than DNA) is made up of 8 segments that can easily be swapped around ('reassorted') when two different strains infect the same animal (8 segments with 2 versions of each = 2^8 = 256 possible new viruses). This isn't true for the adenovirus used in the article, which has an unsegmented DNA genome, but there's still some concern that a therapeutic strain might 'recombine' with a wild-type strain:

      http://vir.sgmjournals.org/cgi/content/full/89/2/380

      This is one reason why you have to be careful when adding (e.g.) new genes to viruses of this type (as in gene therapy). It's rather less of a concern when doing the sort of experiment described in the original article, where the replication of the virus is partially blocked rather than enhanced, and where no new genes are added.

  2. John Titor by Niris · · Score: 3, Informative

    Along the same lines as I Am Legend, there was that whole John Titor thing back in 2000 where the guy writing it said stuff about using viruses to attack cancer. Yay internet culture to science.

  3. Re:Fungus in my cancer? More likely than you think by ShadowRangerRIT · · Score: 3, Informative

    By "alternative medical folk" do you mean quacks, or were you just misrepresenting their positions? Cancer as host cells gone awry (possibly due to an initial external influence, with the external influence not necessary for continued growth) is incontrovertible. If certain anti-fungals work on them, it's because it happens to work as an anti-cancer drug, it doesn't mean the cancer is fungus.

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  4. Re:I know that nobody cares, but... by MythoBeast · · Score: 3, Informative

    The basis of the treatment can be summed up fairly quickly. Drinking alcohol releases endorphins, and the endorphins addict us to the alcohol with a force identical to morphine addiction. Taking an endorphin blocker results in a reversal of this effect, where drinking makes you loose interest in drinking over time.

    The treatment that results from this effect is equally simple. You have the alcoholic take an endorphin blocker (naltrexone is typical) and then have them pursue their normal drinking habits. After about three to six months, 78% have significantly reduced desire to drink, 25% just stop drinking and have no desire to pick it back up again. I think you can see how this would put Betty Ford out of business and is indirect opposition to AA.

    The fine details are a little more complicated, but only because it goes against a lot of logic. For instance, most people expect it to have a "diet pill" effect where it suppresses your urge to drink, and that's how the naltrexone tends to be prescribed. Used this way you'd actually have better results with a placebo, and people give up when it doesn't work that way.

    But they wouldn't have to write a book if there were nothing else to say, would they?

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