An Introduction To Telomere and Telomerase

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The telomere-telomerase hypothesis of aging and malignant neoplastic disease is based on the findings that most human tumours have telomerase activity while normal human bodily cells do non.

An emerging hypothesis is that the up ordinance or reexpression of telomerase is a critical event responsible for uninterrupted tumour cell growing. In contrast to normal cells, tumour cells show no loss of norm telomere length with cell division. Through this suggestion immortalization may happen through a mutant of cistron in the telomerase repression pathway leting the look of telomerase in malignant neoplastic disease cells.

Telomerase is a ribonucleoprotein enzyme which stabilizes telomer length by adding hexametric ( TTAGGG ) repeats to telomeric terminals of the chromosomes, therefore counterbalancing for the continued eroding of telomeres that occurs in its absence. Telomerase is usually merely in cells that give rise to sperm and egg or in some root cell lines, it maintains the unity of the chromosomes. the sex cells are the lone portion of the organic structure that are biologically required to be immortal, because if there was a progressive loss of chromosomes with each coevals so this would take to extinction. However when cells become cancerous, the enzyme telomerase is activated, this enables the cancerous cells to retroflex without a bound and this procedure makes the cells immortal.

Harmonizing to a research done by a squad of research workers at the University of Texas,

An rating of cell lines from 18 different human tissues revealed the presence of telomerase in 98 of the 100 immortal cell lines, telomerase was non found in any of the 22 person cell lines.

Telomeres is a perennial Deoxyribonucleic acid sequence ( TTAGGG ) found at the terminals of additive chromosomes that protect the terminals of the chromosome from debasement, or telomere can be defined as Deoxyribonucleic acid sequences found at the terminals of eucaryotic chromosomes which maintain the fidelity of familial information during reproduction. At birth as determined by terminal limitation fragment analysis, telomeres consist of about 15,000 base brace of repeated TTAGGG DNA sequences, which become shorter with each cell division owing to the terminal reproduction job. Every clip a cell divides it loses 25-200 DNA base pairs off the telomere terminals. one time this pruning has occurred about 100 times a cell ages and does non go on to split. It has been proposed that telomere shortening may be a molecular clock that count the figure of times a cell has divided and determines when cellular aging occurs ( cellular aging is the limited capacity of cells to split beyond a finite figure of population duplicating. In a ballad adult male’s understanding this means cellular decease. Normal diploid human cells have limited capacity to proliferate ( are mortal ) .

There look to be two mechanisms responsible for the proliferative failure of normal cells. The first, mortality phase 1, occurs when there are still at least several thousand base brace of telomeric sequence left at the terminal of most of the chromosomes. It is possible that mortality phase 1 may be induced by the activation of cistrons located in the instantly

subtelomeric part of the chromosomes.

The 2nd is the mortality phase 2 which represent the physiological consequence of critically short telomeres when cells are no longer able to protect the terminals of the chromosomes, so that the terminal debasement and terminal to stop merger occurs and causes genomic instability and cell decease ) .

While researching on a subject like this, twosome of of import inquiries came to mind, so I made attempt to research and turn to some of these inquiries which might be considered of import.

One of such inquiries is why do telomeres shorten?

the mechanism of DNA reproduction is different in additive chromosomes is different for each of the two strands, known as prima and lagging strands. the lagging strand is made as series of distinct fragment, each one necessitating a new RNA primer to originate synthesis. the Deoxyribonucleic acid between the last RNA priming event and terminal of the chromosome can non be filled in. { this procedure is known as the terminal reproduction job } since a strand can non copy its terminal, telomeres shortening is required to happen during progressive cell divisions. the sawed-off telomeres are inherited by girl cells and procedure repetitions itself once more.

The head may ask if halting the shortening of telomeres whether that will forestall the organic structure parts from aging ; harmonizing to research workers, decelerating down the rate of telomere shortening might assist cut down the extent at which the organic structure ages. An experiment done by a group of research workers from the University of Texas helps clear up this statement in full, loanblends between immortal cells that express telomerase, and normal cells that lack telomerase, creates a cell with limited lifetime. Besides experiments show that intervention of immortal human cell lines with oligonucleotide will ensue in telomere elongation.

Using this determination, the research workers tested the hypothesis that elongation of telomeres could widen the lifetime of a cell, this was done by handling an immortal homo cell line with oligonucleotides to lengthen its telomere, and so blending the cell to a person cell. this experiment showed that the intercrossed cells had a longer lifetime, than the loanblends without extended telomeres. This gives the hypothesis that telomere length may find the human lifetime.

Many might non cognize, but telomerase pays an of import portion the length of service of malignant neoplastic disease cells, which makes it one of the outstanding AIDSs in the ability of malignant neoplastic disease cells to boom. The enzyme telomerase AIDSs malignant neoplastic disease cells by holding the telomere shortening in malignant neoplastic disease cell, thereby leting the cell to split indefinitely. Scientist are fighting to develop a therapy to suppress telomerase activity in malignant neoplastic disease cells which they believe will coerce the cells into a normal form of aging and de


Person might inquire if it where possible to return old cells into immature cell: harmonizing to my research, technically its possible, therefore if cells are wholly aging it may non be possible to acquire them to turn once more even if the telomere is elongated, nevertheless telomere’s are rate restricting for growing, so a few division may make the fast one of resetting the clock.

Due to the fact that telomerase AIDSs malignant neoplastic disease cell, an single might inquire why the debut of telomerase non lead to malignant neoplastic disease?

First a fact should be stated that telomerase are found present in specialised generative cells and most malignant neoplastic disease cells that appear to split indefinitely, but the chief map of telomerase is to keep telomeres and license continued cell growing.

So its of import to understand that malignant neoplastic disease is caused by accretion of several changes that occur over a life-time, and which affects processes commanding cellular growing rates, and ability to occupy and undergo metastasis, while telomerase merely affect the numeration of the figure of times a cell has divided, non the rate of cell growing. therefore all telomerase do is allow continued cell growing that would otherwise be limited by sawed-off telomeres, so that does non do it a cause of malignant neoplastic disease.

Another inquiry that personally i was interested in while researching about telomerase is? would telomerase therapy onslaught other cells such as generative cells?

Harmonizing to my research anti telomerase therapy could impact germ line { generative cell and perchance stem cells of reclamation tissues { basal cells of tegument } . but fortunately the telomeres of such cells have longer telomeres than malignant neoplastic disease cells, so it might be possible to suppress telomerase in malignant neoplastic disease cells and do their decease, without doing the other cells to run out of telomeres.

Another state of affairs, one feel will be of great enquiry among cognition filled heads is ; harmonizing to multiple researches, its been proven that non all malignant neoplastic disease sells express telomerase, if so how are they keeping their telomeres growing?

Scientists province that about 85-90 % of malignant neoplastic disease cells displays telomerase activity, which brings us back to the chief inquiry. Harmonizing to scientific research workers malignant neoplastic disease cells, which do non demo mark of telomerase activity, may be involved in one of these activities:

1, the cell may non hold yet been immortalized, thereby doing the visual aspect of telomerase activity absent.

2, besides batch of scientist believes that some malignant neoplastic disease cells have an alternate tract for keeping telomeres. This telomere is believed to be of heterogenous length, changing from large to little, and this aiding as confusion to the construction responsible for cell decease.

One of the chief focal point of research workers in the survey of malignant neoplastic disease is utilizing the sensing of telomerase activity to foretell malignant neoplastic disease ; telomerase activity is easy detected in many pre-malignant specimens ( lung and chest malignant neoplastic disease ) , while colon and pancreatic malignant neoplastic diseases can? t be detected until subsequently phase. The ability to utilize about any clinical specimen and to show telomerase may let the sensing of malignant neoplastic diseases at an earlier phase.

much advancement has been made in the development of more accurate molecular based malignant neoplastic disease trials to measure tissue specimen. unfortunately most of this method do non hold sufficient specificity ( ability to distinguish between normal, precancerous, and cancerous cells ) and sensitiveness ( truth in observing the presence of malignant neoplastic disease ) to place a broad assortment of malignant neoplastic disease types. Therefore, new clinical method, applicable to all malignant neoplastic disease types is needed.

presently research workers are working on that, though a merchandise called a PCR based telomerase method was produced in 1994, it still had a twosome of small set dorsums and didn? Ts live up to its outlook to the full.

Finally a inquiry, which must be of involvement to anyone interested in the development of telomerase, is how long before telomerase can hold a medical impact, such as malignant neoplastic disease screening/ telomerase therapy?

This is a statement I found in the cyberspace turn toing the inquiry, ? since telomerase is detected in about all tumours and in some instances early in the development of the malignant neoplastic disease, so early malignant neoplastic disease sensing utilizing telomerase may be a promising attack.

There are already a figure of state of affairss where cognition of the presence of telomerase may hold value in hazard stratifying patients into those that are likely to hold favourable results and those that are non. There is a major attempt at the national malignant neoplastic disease institute to set up a series of molecular markers for malignant neoplastic disease, and it is expected that within a few old ages we will hold possibly one hundred or more molecular markers that may bespeak the presence of malignant neoplastic disease. Its predictable that within the following 10 old ages, scientist will be able to take a few cells, do micro array analysis and determine non merely if a individual has malignant neoplastic disease, but besides the type of malignant neoplastic disease, the cistrons that are altered, and hopefully a curative

method that goes to work and destruct the malignant neoplastic disease instantly? .


While there is justifiable optimism sing telomerase activity, its of import to understand that their is still much to get about this enzyme, and extra proof surveies will be required before cognition of telomerase can be used to the fullest in medical pattern. Finally the public-service corporation of inhibitors of telomerase in the therapy of malignant neoplastic disease is awaited to with great expectancy.

Note- even though telomerase AIDSs malignant neoplastic disease cells in longetivity ( avoiding cell aging ) still telomerase as an enzyme has nil to make with the development of malignant neoplastic disease cells, its merely a assisting adjutant, so all incriminations should non be put on it.


Shay JW: Telomerase activity in human malignant neoplastic disease. 1996

Bacchetti S, counter CM: telomerase: a key to cell immortality. 1995

And a whole batch of notes taken from Internet site.

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TELOMERE AND TELOMERASE Research Paper An. (2017, Jul 22). Retrieved from