Thursday, 19 May 2016

Is Vasculogenesis the reason for Tumor growth after Radiation?

Stephen and all -

What's your experience or opinion on anti-vasculogenesis following chemo and radiation therapy?

Research below is claiming that Radiation kills the angiogenesis mechanism and the tumor grows back not due to angiogenesis but due to vasculogenesis after standard therapy. So HIF-1 and SDF need to be inhibited. Plerixafor is one such treatment. More articles available on Google search.

http://www.ncbi.nlm.nih.gov/pubmed/20179352

3 comments:

  1. Plerixafor would be a good addition to a cocktail during and after radiation, for the reasons above, except that it's still on patent until 2018 and is very expensive (in the neighborhood of $7,500 for a single-use vial).

    There were 2 trials testing plerixafor in GBM but one was terminated due to low accrual and the other is still recruiting, but I've not heard any results for either of these.

    https://clinicaltrials.gov/ct2/show/NCT01339039
    https://clinicaltrials.gov/ct2/show/NCT01977677

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  2. Plerixafor is a very promising approach, the research is a bit scattered but suggests that it helps to address vasculogenesis (entirely new vessel formulation) vs. angio genesis (blood vessel formation from existing vessels). It is not the main reason for growth, but has been implicated to radiation specifically. It is possible that the tumor will bypass this and move to angiogenesis.

    Vasculogenesis is also a potential resistance mechanism to Avastin.

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  3. Thank you both for your insights.
    Outside the trial, how would you avail of treatment such as Plerixafor or Keytruda or Rintega? Would you request your NO or directly to the company sponsoring these medicines or some other solution? How would you go about securing any one of these if they were deemed useful based on your tumor gene analysis?
    I think someone had asked about Rintega before as well. Please comment.

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