This sounds like it could be a really important breakthrough!

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dlb823
dlb823 Member Posts: 9,430
edited July 2014 in Clinical Trials, Research News, Podcasts, and Study Results

Quoting Integrative Oncologist Brian Lawenda... "Hundreds of millions-to-billions of dollars have been spent on drugs designed to shut down a key protein instrumental in promoting cancer cell growth. Turns out we had the science totally backwards. In fact this protein (Cyclin D) actuallySTOPS cancer cell growth. Time to rewrite all the textbooks. I know this sounds like nerd stuff but it is actually game-changing in the fields of oncology, drug development and cellular biology. Take home point: never accept anything as dogma."

http://medicalxpress.com/news/2014-07-bizarre-cyclin-d-believed-cancer.html

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  • farmerlucy
    farmerlucy Member Posts: 3,985
    edited July 2014

    That IS very exciting!

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  • dlb823
    dlb823 Member Posts: 9,430
    edited July 2014

    I wish I knew which drugs fall into the category of blocking Cyclin D.  Any pharmacists or chemists or MDs among us???     Deanna

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  • SpecialK
    SpecialK Member Posts: 16,486
    edited July 2014

    Here is some more info on trials and drugs, check the date on that last ASCO cite - it is 2005:

    http://www.ncbi.nlm.nih.gov/pubmed/22475046

    http://www.ncbi.nlm.nih.gov/pubmed/18347178

    http://www.medscape.com/viewarticle/823158

    http://jco.ascopubs.org/content/23/18/4215.full

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  • primrose83
    primrose83 Member Posts: 2
    edited July 2014

    The scientific paper in discussion is extremely important because it challenges the way entering the cell (division) cycle was believed to happen.

    Long story short, the role of cyclin D:CDK4/6 is better understood now : it doesn't shut down the tumor suppressor protein Retinoblastoma (shortly Rb) but instead activates it , however shit still happens and Rb is inactivated through a mechanism mediated by the cyclinE:CDK2, a complex which researchers don't understand how it gets activated. They tend to believe that "Cyclin D:Cdk4/6 activity combined with other signal transduction pathway mutations contributes to increased cellular metabolism that we speculate is monitored by an unknown metabolic sensor. Once the metabolic threshold has been exceeded, the sensor activates cyclin E:Cdk2" which will inactivate the Rb protein. Complicated stuff I would say....

    The researchers clearly still miss important pieces from the "how cancer is driven" puzzle. So even though the newly emerged cancer drugs that inhibit Cyclin D:Cdk4/6 complexes are based on a dogma that is now seriously shaking, for some reason they seem work! They significantly prolongue PFS in clinical trials that enrolled patients with metastatic HR+ breast cancer. So if Lawenda insinuates that all that money was wasted, I beg to differ.

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  • toomuch
    toomuch Member Posts: 901
    edited July 2014

    This is indeed interesting and I agree with primrose83 that is supports how little we know about the cell cycle and cancer. I know that palbociclib, which has been shown to prolong PFS, is a CDK4/6 inhibitor. Lilly has a similiar drug in clinical trials right now but Ii don't know it's name. While new findings are always encouraging. There is so much scientisits still don't understand. I hope that thse findings don't interfere with the clinical trials that are underway or instill a sense of dread in the women participating in the trials. There is still so much unknown.

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