Hi, I think aging as a concept is hard to be applied to describe cancer cells. They are not normal in the first place. Many tumor cells emerge as a result of progressive accumulation of mutations, which is quite accepted to be age-dependent. 

I recommend you read Prof. Robert Weinberg's landmark reviews on cancer hallmarks:

http://www.ncbi.nlm.nih.gov/pubmed/21376230

http://www.sciencedirect.com/science/article/pii/S0092867400816839

The telemerase activity merely allows the cancer cells to repeatedly re-enter the cell cycle when in fact they should be denied to. Telemerase activity then cannot be a measure to predict genomic integrity. 

Rather cancer cells are like zombie cells that refuse to rest and die. In that sense, they do age, but only the telemerase activity deceptively makes them appear "forever young" (or immortal). If you ever do live cell imaging of cancer cells, you will find that they are a highly heterogeneous and disorganized lot. 

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To sidetrack a bit, I would think it has been quite recognized that the "biological clock" is not only installed in the limited telemerase activity, but also in the mitochondrial DNA, which depletes with age and becomes progressively poorer in quality as we age. With poor mitochondrial DNA, for sure we will have worse and worse mitochondrial metabolism; aging will be an inescapable fate. 

Sir is it possible that we activate telomerase in normal cells to increase the life span of individual slightly more??

Or due IVF technology n gene engineering  we engineered telomerase activated zygote to increase the life span??

Nice questions. Unfortunately, I am really not very knowledgeable about telemere and telemorase. 

However, you may take your chance to write to Prof. Elizabeth Blackburn. She's expert in that. I met her once during public lecture. She's very nice, and patient to answer young researchers' questions. 

http://biochemistry2.ucsf.edu/labs/blackburn/index.php?Itemid=3

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As a word of caution, however, actually, a lot of our biological processes involve precise and temporally controlled apoptosis. Development and differentiation depend on selectively programmed cell death, to weed out unwanted cells. Imagine, that we suffered multiple viral infections during early childhood, and our genomic DNA somehow acquired more mutations than we want to, but for the fact that our telemerase has been engineered to be perfect and intact throughout life, we are going to have defective cells to undergo replicative cycles just as efficiently as do the normal cells. It may not be a nice and problem-free thing. In other words, even if we have super-high telemerase activity, we ALSO NEED super-efficient DNA and other cellular repair mechanisms to be installed, in order to make better and  healthier prolonged life happen. Cheers

• i have another que regarding to this if telomerase protect the telomere in cancerous cell then what is the life span of the cancerous cell??
• and we know that this much area is infected with cancerous cell so why we dont have any mechanism to remove the telomerse? telomerase is an enzyme n enzyme could be inactivate if appropriate condition is changed like temp. pH salt conc. etc.......
• plz give me ans thanking you 

This link provides a generalist answer: https://answers.yahoo.com/question/index?qid=20090131202531AAwrUFs

Although theoretically cancer cells can keep proliferate and persist despite their abnormal physiology, it is known that under some conditions (e.g. chemotherapy) cancer cells are forced to commit suicide -- either by apoptosis or differentiation. A differentiated cell means end of immortal life. Various types of leukemia models have been "treated" by inducing tumor cell differentiation. 

So far the best known mechanisms for regulating telomerase activity is transcriptional control. 

See this review on why its activity goes down with age.

http://mmbr.asm.org/content/66/3/407.full

Hi Vaishwik, I agree with Nai-Kei Wong. It is possible to induce telomerase activity in a zygote; however, in the case of humans, zygotes are telomerase positive. The telomerase enzyme is then down regulated further along in the gestation period. However, with increased telomerase activity you are now giving cells the ability to divide indefinitely. All cells will eventually gain mutations that should die via the apoptotic response. One way the cell ensures that these mutations do not accumulate, eventually turning into cancer, is by allowing a finite amount of cellular divisions due to a decrease in telomere length. Once telomeres get to a critically short length, the cell will enter senescence and eventually apoptose. Some cells in the human body (e.g. gametes and stem cells) are telomerase positive, but according to the cancer stem cell theory, the telomerase positive stem cells are likely to be the root for cancer development. There currently are several anti-telomerase drugs in the trial phase for cancer therapy, however it is more likely that anti-telomerase drugs alone will not be sufficient. This is because it takes many cell divisions for telomeres to shorten, so there is not an immediate response to the drugs. Even without the presence of telomerase the tumor will still continue to grow and divide. There have also been reports that anti-telomerase drugs have induced ALT or alternative lengthening of telomeres. ALT is a telomerase-independent method to maintain telomere length via homologous recombination.

Mr.Miles,

Do this alternative lengthening of telomere turns normal cell into a cancerous one?

Hi Shivang, I do not want to mislead anyone and assume that telomerase upregulation/reactivation or ALT is the cause of cancer, but it is a key event. There are several mutations and changes in cellular function that are necessary for the propagation of cancer. ALT is present in 10-15% of all cancers, but is common in those of mesenchymal origin. If you're interested in ALT, I would highly suggest reading Anthony Cesare & Roger Reddel's review in Nature Genetics here: http://www.nature.com/nrg/journal/v11/n5/full/nrg2763.html

Thank you sir.

My one more question about this is, can we reduce the rate of cell proliferation of a cancerous cell?

As we know that cancerous cell is immortal because it's telomere gets regenerated due to activity of telomerase enzyme. The cancerous cell then starts to divide rapidly.

If we can reduce the rate or speed of that cancerous cell then we can stop the formation of tumor and thus it can also help in decreasing the senescence.

Miles Mckenna Sir, telomerase is one kind of enzyme so is it possible that is inactivated by something change in pH temperature or change in the protein folding etc...

What are you planning to do Mr. Vaishwik???

If you want to inactivate or denature that particular enzyme by changing the pH or temperature, you can do that in an in vitro condition.

But if you are planning to do it in an in vivo then the change in temperature and pH against normal body temperature and pH will affect the other cells or tissues or organs of the body. I mean it may lead to other consequences which can be harmful.

I dnt knw about protein folding but i think the above parameters are not applicable for in vivo experiment!

but individual enzyme has a particular temp pH and other parameters at which they work more efficiently and inactivated and in case of cancer we can take a small amount of risk to heal the cancerous cell to preventing the life time damage n for experiment  we can experiment this in vitro then we go further