[ RadSafe ] Cancer
JPreisig at aol.com
JPreisig at aol.com
Tue Aug 19 11:03:21 CDT 2014
Mohan/Radsafe:
If one can model computationally radiation scattering from DNA,
cells etc., one could probably also model the adaptive response you mention.
Adaptive Estimation --- I seem to remember a book by Widroe/Widrow???
Take Care.
Regards, Joe Preisig
In a message dated 8/18/2014 2:50:54 P.M. Eastern Daylight Time,
Mohan.Doss at fccc.edu writes:
Dear Joe,
The basic concept you are implying, that DNA damage causes cancer, is not
consistent with evidence. Of course DNA damage is needed to have cancer,
but it is not sufficient. In fact almost everyone has covert cancer
http://www.nature.com/nrc/journal/v14/n4/full/nrc3703.html , i.e. cells with
carcinogenic mutations, but a majority of us are not diagnosed with cancer even
in all of our lifetime. What gives rise to clinical cancer is the
depression of the immune system, which allows these covert cancers to grow
uncontrollably. If the immune system is not depressed, the slightly increased
number of mutations from any cause, e.g. radiation, would not affect cancer
risk. Low-dose radiation boosts the immune system and so would reduce
rather than increase cancers. The adaptive response due to low-dose radiation
would boost defenses like DNA repair enzymes and so would reduce the damage
to DNA over the longer term, since the increased protection would reduce
the endogenous
DNA damage that would have occurred otherwise. I have described this
briefly in the recent debate on health effects of low-dose radiation in Medical
Physics
http://scitation.aip.org/content/aapm/journal/medphys/41/7/10.1118/1.4881095.
So, doing MCNP, etc. to calculate the DNA damage, without including the
adaptive response of the body, may not help with estimating cancer risk from
radiation.
There is evidence cancers have resolved spontaneously, and this is
probably because the immune system got rid of the cancer cells.
With best regards,
Mohan
Mohan Doss, Ph.D., MCCPM
Medical Physicist,
Associate Professor, Diagnostic Imaging,
Fox Chase Cancer Center,
333 Cottman Avenue,
Philadelphia, PA 19111-2497.
Phone: 215 214-1707
Website: http://www.fccc.edu/research/pid/doss/
Blogs: http://mohan-doss-home-page.blogspot.com/
-----Original Message-----
From: radsafe-bounces at agni.phys.iit.edu
[mailto:radsafe-bounces at agni.phys.iit.edu] On Behalf Of JPreisig at aol.com
Sent: Sunday, August 17, 2014 11:20 PM
To: radsafe at agni.phys.iit.edu
Subject: [ RadSafe ] Cancer
Radsafe,
I guess in cancer production, the carcinogen is in some volume within the
body, and this volume can grow if the carcinogen continues to be
introduced into the body. The cancer is probably in the vicinity of this
carcinogen volume. One question I might ask is that once the cancer grows
outside of the carcinogen volume, will the cells (upon cellular division)
continue to be cancerous? I expect bodily circulation and other processes could
also cause the carcinogen volume to diminish in size. Quite a dynamic
process....
I guess cancer production via radiation is a whole different process,
mostly a scattering process of the various forms of radiation by cells, DNA
and so on. Any new science on single strand breaks, double strand breaks
etc. in the literature lately???
Maybe someone (a young person) could start to use MCNP, MCNPX or some
similar computer code, to model computationally (on a supercomputer these
days) the scattering of radiation from DNA strands, whole human cells,
groups of cells, various human tissues and so on. Computationally
setting up
the first DNA strand or human cell would be pretty daunting. The
repeated
structures capability of MCNP might be helpful. Doing some studies
computationally may allow us to avoid doing all the studies via lab
experiments on various animals. I guess animal studies would still be required
for important intellectual steps...
Has it ever been observed that a cancerous human cell has reverted to a
non-cancerous state????
Have a good week. Regards, Joseph R. Preisig
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