From: Damien Broderick (d.broderick@english.unimelb.edu.au)
Date: Wed Aug 28 2002 - 23:27:03 MDT
At 12:00 PM 8/28/02 -0700, Robert Bradbury url'd:
>Life preserver floods cancers:
>Cancer cells let telomerase loose.
>http://www.nature.com/nsu/020819/020819-13.html
< When normal cells' DNA was broken into pieces by radiation, cells quickly
impounded free telomerase into a compartment called the nucleolus. This
prevents it attaching ends onto the DNA and allows the correct repair
mechanisms to mend the gap. >
Oh, oh, oh. What about this:
When tumor cells are damaged by radiation or chemical attack, might the
breaching of their boundaries allow a gale of telomerase to `infect'
adjacent cells, and maybe render some neoplastic that had all the
preliminary malign mutations *except* for a switched-on telomerase gene?
Might this give enough of them breathing-space *until* that needed mutation
occurs by chance in one of the clones? Hence the disheartening finding that
often the removal of a tumor is followed by new tumors springing up all
over the place? I understand that this is currently explained by a
*suppressive* influence exerted by the primary while it's in situ, but
maybe...
Damien Broderick
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