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Re: LNT and Bystander Effect
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Low dose effects are found to be higher in all experiments of this type
because the analysis is on surviving cells. More cells die at higher doses so
if you do not count these cells (they are dead so they cannot contribute to
later population effects) then you do not count the DNA effects. If you
follow the assumption that DNA damage is the CAUSE or INITIATOR of cancer then
you must assume that low dose effects are under predicted by the LNT.
What we may have is the looking-under-the-wrong-rock problem. The LNT and
low-dose crowd has
seized upon the 'assumptions' that alteration of the DNA initiates cancer and
aggressive growth is an inherent attribute of the cancer cell. Therefore,
since these assumptions are now fact (a basis for research funds) we can state
that since any dose may damage DNA, any dose may 'cause' cancer.
Perhaps I should revise my initial sentence to the looking-under-ONLY-ONE-rock
problem. If cancer initiation is epigenetic and/or lack of inhibition (by the
normal body mechanisms) allows growth of cancer cells then we have an entirely
different mechanism for radiation induced cancer. That mechanism is likely
deterministic, not stochastic. Note below what Bjorn quoted from John B.
Little.
Joe
Bjorn Cedervall wrote:
> There was quite much about bystander effects (the presentations I heard -
> although only a few - there were many parallel sessions - were quite
> convincining I must say) at the ICRR conference in Dublin in July 1999 (go
> to the Proceedings, Radiation Research, Vol. 2 for more information.).
> John B Little challenged the following central dogmas:
> 1. The cell nucleus is the target for the biological effects of radiation.
> 2. Biological effects occur in irradiated cells as a direct consequence of
> DNA damage.
> 3. Cancers are clonal in origin, arising from a radiation-damaged cell.
>
> The messeage was that these statements may not always hold.
>
> Bjorn Cedervall bcradsafers@hotmail.com
>
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