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Astex Pharmaceuticals, AŞ Message Board

  • kyjellie kyjellie Apr 5, 2013 3:26 PM Flag

    Interesting item at AACR

    Didn't catch this the first time, but it might be very good news. Apparently they are looking at sgi-110 having an impact on how cancer metastasis. This drug maybe given to help other drugs work better and follow up by treating patients to insure that their cancer doesn't metastasis.

    SGI-110 prevented TGFβ-induced EMT and reduced by two-fold the number of cells with stem cell characteristics (ALDH1+). These results demonstrate that DNA methylation is a dynamic process involved in regulation of genes implicated in EMT and metastasis.

    Yahoo needs to add a sentiment greater than Strong Buy.

    Sentiment: Strong Buy

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    • Found this piece on EMT and metastasis. Maybe just maybe sgi-110 is the answer? Fun to think about. Here is part of an article that address the situation with how cancer metastasis:

      They found that inhibiting cells with the NF-kB inhibitor switched off a reporter in that pathway, but not one in the other pathway, indicating that TGFß activation was independent of NF-kB activation, while the effects were synergistic.

      And finally, here’s the piece de resistance of the paper; they showed that blocking TGFß secretion in megakaryocytes and platelets or wrecking the TGFß pathway was enough to prevent metastasis, they did this using mice in which TGFß expression was knocked out where seeding with cancer cells prevented metastasis to the lungs. They also showed that even cells pre-treated with wild type platelets for a while before introduction into TGFß fl/fl mice wasn’t enough to trigger metastasis.

      This basically confirms that platelet derived TGFß signalling is absolutely necessary, while NF-kB signalling in synergy with it renders tumour cells potentially more metastatic, but isn’t per se sufficient for metastasis.

      They note that this could have therapeutic implications, since TGFß inhibition in platelets doesn’t have physiological effects on normal cells, and if this could be replicated in humans it might serve as a brilliant therapeutic strategy.

      However, as always, blocking metastasis, it would appear, would only really be useful in tumours where metastasis hasn’t occurred, how established metastatic disease should be dealt with is still a very open, and problematic question.

      Sentiment: Strong Buy