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Oncothyreon Inc Message Board

  • ows_1 ows_1 Apr 16, 2013 10:38 PM Flag

    PX-866: How it works

    The followin describe how I believe PX-866 works
    =================================================
    The bottom quotes are probably very accurate.
    My summary, well what can I say, it is my understanding.

    summary : pi3k -- pten -- atk -- tsc -- cell division
    A messed up pi3k lipid can lead to hyperactive cell division.

    px866 helps in binding with the pi3k damaged receptor in such a way as to not trigger cell division and eventually allow the cell to die.

    Foward looking: If px866 ends up being something that can be widely used in most cancer treatments,
    or to complement other treatments (x-ray, chemo, other drugs, surgery, gene therapy,...) you could end up
    with a drug with a huge market. At the moment Onty should have a clear idea of possible potential.
    =================================================
    Some medical quoted concerning pi3k

    "The most common therapeutic approach for many cancers is chemotherapy. However, many patients relapse after treatment due to the development of chemoresistance. Recently, targeted therapies represent novel approaches to destroy cancer cells. The PI3K/PTEN/AKT pathway is a key signaling pathway involved in the regulation of cell growth. Dysregulated signaling of this pathway may be associated with activating mutations of PI3K-related genes. Analyses of these mutations reveal that they increase the PI3K signal, stimulate downstream Akt signaling, promote growth factor-independent growth and increase cell invasion and metastasis. In this review, we summarize the PI3K/PTEN/AKT pathway genetic alterations in cancer and their potential clinical applications"

    "Since its initial discovery as a proto-oncogene, the serine/threonine kinase Akt (also known as protein kinase B or PKB) has become a major focus of attention because of its critical regulatory role in diverse cellular processes, including cancer progression and insulin metabolism. The Akt cascade is activated by receptor tyrosine kinases, integrins, B and T cell recepto

 
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