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A Protein That Terminates 70% Of Common Cancers

Orne writes "BBC News reports here that researchers at the Washington University School of Medicine in St Louis have located 'a protein CUGBP2 (that) interacted with the mRNA for Cox-2 in eight types of human cancer cells.' Cox-2 (which is already known to affect inflammation in arthritis sufferers) is involved in growing blood vessels to feed cancer cells, leading to their uncontrolled growth. Raising CUGBP2 to normal levels puts the cancer's 'death' cycle back on track."

5 of 48 comments (clear)

  1. good, but... by C21 · · Score: 3, Interesting

    what are the side effects with flooding tissue with this protein?

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    this is not a sig.
  2. Any way to volunteer for tests? by Cyclone66 · · Score: 3, Interesting

    It's probably to early but anyone who knows people with inoperable cancer would probably love to try anything.. just the hope it would give them would make there last days/months/years of life more bareable.

  3. UD.. by olman · · Score: 3, Interesting

    I wonder if all those UD packets I crunched had anything to contribute. Probably not.

  4. I wonder... by Gamasta · · Score: 3, Interesting

    if cancers can evolve, eventually becoming immune to these proteins. I think not, but nature is often quite surprising.

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    reason defies logic
    1. Re:I wonder... by wilgamesh · · Score: 3, Interesting

      Very insightful. You would be describing the case of Gleevec, among I'm certain other cases. Gleevec is the wonder drug that's been shown to have great effects on leukemia (CML). However, patients will develop resistance to it during the course of treatment. The source of resistance, it turns out, is the mutation of the Gleevec target (a protein) such that it binds Gleevec differently.

      One story: http://www.researchmatters.harvard.edu/story.php?a rticle_id=510

      There's also the common idea that many cancers are multi-mutational events. That is, many mutations conspire in the cellular network to produce a cancerous cell. What that means is one cancer cell may have one method of producing all the right cell factors to proliferate wildly, while another cell employs a slightly different mechanism of doing so. This would mean that any single-prong approach to treating cancer would not be entirely successful. Hence, the article mentions that "multi-prong" approaches are a possible next step.