Cells and Aging

Thomas Mahoney excelife at earthlink.net
Fri Mar 5 05:41:38 EST 1999


In article <36dea957.757334 at news.springnet1.com>, fake at address.com says...
>
>>Dr Vaziri has done some research at the Ontario Cancer Institute, that 
shows 
>>that shortened telomeres lead to dicentric chromosomes.  By definition that 
>>would include a disruption of the heterochromatin.  It is at this point 
that 
>>the p-16/p-53 senescence block is initiated.  Whether the dicentric 
>>chromosome is itself sufficient to trigger senescence or whether senescence 
>>is induced by some intervening event, such as the altered genetic product 
>>produced by the loss of the heterochromatin silencing, needs to be tested. 
 
>>Each of these hypothesis are logically sound and we just need to do the 
>>research to to come to a valid conclusion.
>>   
>
>Would you mind briefly explaining to me what the p-16/p-53 senescence
>block is?  Is that the tumor suppressor gene?  Does it encourage
>replication or inhibit it?


P16 and p-53 are the primary genes responsible for stopping cellular 
proliferation in reproducing cells.

They are part of the cell maintenance machinery and are expressed when the 
cell detects damage to the genes or chromosomes in the cell.

They are considered to be tumor suppressent genes because they stop "damaged" 
cells from reproducing.

Many cancers show a defect in the p-53 gene which indicates that the gene 
failed in its role to stop proliferation of that cell line.

In most instances this alone is not sufficient to produce cancer in humans.  
a second brake on cell proliferation is the loss of the telomeres at the ends 
of the chromosomes.

Having by-passed the p-16/p-53 senescence block the cell proceeds on to 
crisis stage where the chromosomes literally fall apart because they have 
lost all the telomeres which hold them together.  This is usually sufficient 
to cause the cell to die.

In some instances, however, the enzyme telomerase is re-activated and the 
telomeres are stabilized.  It is these cases, where both the p-16/p-53 block 
of senescence is by-passed and telomerase is re-activated, that cancerous 
growth is seen.


Thomas Mahoney, Pres.
Lifeline Laboratories, Inc.
http://home.earthlink.net/~excelife/index.html








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