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When there is 'excessive' cell growth 'ordered' by the human body in some specific part of the body that is not part of the usual repairing mechanisms, does this cause extra telomere 'shortening' or damage even though a lot of cell growth and repair is 'required'. If a lot of cell growth is 'activated' with problematic telomeres does this cause telomerase to be formed which then might shut down the apoptosis mechanisms and keep the cell 'going' indefinately. Note; I read some acid reflux problem causes parts of the throat to scar or be damaged causing excessive cellular repairs on those parts of the throat where tumors have later developed. When someone gets sunburned on the shoulders say, and this damages the skin there, then does every future time the persons shoulders get in the sun ,do those same areas get further damage causing excessive growth and repair of skin cells on the shoulder. With a lot of excessive repair tumors might develop. SO could excessive cell growth (that might be caused by many different factors ) help to cause cancer??

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Long story short: Absolutely.

Short story long:

While your intuition that growing a lot of cells can increase the risk of damage that might cause cancer is spot on, your specifics are a little off. It's not the telomeres themselves that are the problem, but broad spectrum DNA damage and transcriptional changes. The condition of the telomeres doesn't directly affect the likelihood of a cell growth becoming more cancer-like. A cell with perfect telomeres fresh from a telomerase-expressing stem cell and cell with shortened telomeres have an equal chance of becoming cancerous. Cell populations with longer telomeres have 'more time' or more chances to develop mutations and cell expression damage, however. You're more likely to get in a car crash if you go to the store across town than the neighborhood convenience store, even though it's not intrinsically more dangerous per mile driven.

The sunburn example can be a little misleading. It's not cell regrowth that's the key carcinogenic factor, but instead the direct DNA damage UV radiation can cause. In a particularly bad sunburn your skin cells may be killed or commit suicide(apoptosis) because of the DNA damage they've sustained. If the cells are damaged but do not die, they're likely to recover. Over time and repeated sun exposure, the skin cells that are most resistant to orders from the body to stop growing or die stick around and may grow and divide. Freckles are when this happens to a population of skin cells that ignore orders about how much brown pigment to be, but still listen to the orders that instruct them on how to be skin. When they stop listening to the skin orders, they officially become precancerous.

The acid reflux example is excellent. There are populations of stem cells throughout the adult body that produce skin cells and hair follicles and blood cells and all the other kinds of cells that are more or less expendable. Generally speaking these stem cells don't have do very much work replenishing esophagus cells, so when they are taxed by something killing off the esophagus lining regularly, they can 'break down' and lose control of their own replication.

It seems like you're both pretty interested in cellular mechanisms of cancer and a little shaky on current theories of cancer formation(there are a few), so if there's a section of this answer that needs to be more detailed or followup questions please let me know.

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  • $\begingroup$ Are there ways to retard or slow down excessive cellular growth? Can telomere damage cause the apoptosis mechanisms to malfunction? I'm fascinated with Biology but am shaky on a lot of theories.. $\endgroup$ – user128932 Sep 29 '14 at 2:12
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    $\begingroup$ Depends on the kind of growth. In the case of acid reflux, no. You need to replenish that lining once it is damaged. Telomeres are rarely 'damaged', as they're very long highly repetitive sequences. Think of them as 'margins'. When the margin is missing, you start to lose words off the page, and indeed telomere shortening is used as a trigger for apoptosis. If damaged or short telomeres interfered with apoptosis, very little apoptosis would every happen. $\endgroup$ – Resonating Sep 29 '14 at 19:44

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