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Telomere damage activates autophagy to stop cancer

telomeres cancer autophagy senescence hayflick limit

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#1 QuestforLife

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Posted 25 January 2019 - 10:15 AM


So it turns out that replicative senescence, the process by which short telomeres arrest division, activates autophagy as a mechanism to prevent uncontrolled replicaton and chromosome damage (leading to cancer), whereas DNA damage away from the telomere activates apoptosis (if not repaired).

 

https://www.scienced...90123131706.htm

 

https://www.nature.c...1586-019-0885-0

(Abstract only)


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#2 Seganfredo

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Posted 11 February 2019 - 09:06 PM

Interesting. Besides research, have you found any way to promply apply that knowledge for cancer treatment?



#3 QuestforLife

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Posted 12 February 2019 - 10:58 AM

Interesting. Besides research, have you found any way to promply apply that knowledge for cancer treatment?

 

The main takeaways are that autophagy is good for cancer prevention, and that inhibiting autophagy (with drugs as is sometimes done to kill cancer cells), could be dangerous as it will increase the likelihood of more cancer cells appearing.


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#4 QuestforLife

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Posted 13 February 2019 - 11:46 AM

A fascinting and relevant paper:

 

http://emboj.embopre...embj.2018100492

 

Cardio-myocytes can become senescent and hypertrophic through telomere (length independent) damage. This presumably works via the fragments of telomeric DNA triggering (and eventually overwhelming) autophagy that was described in the paper that started this thread.  This new paper demonstrates this occurs in mice with age. They cleared such cells with senolytics, although with no ready replacements, this is possibly not a good idea (IMO). I wonder if upregulation of autophagy and reducing sterile inflammation might be a better therapy to address these hypertrophic cells. 







Also tagged with one or more of these keywords: telomeres, cancer, autophagy, senescence, hayflick limit

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