The science of aging and cancer treatment has started to cross paths. This article “Will Telomeres Transform The Way We Look At Aging And Cancer” looks at the relationship of telomeres, cancer and aging. There are additional links that will provide more information on the relationship of these topics.
Inside the core or nucleus of any cell, our genes are located on twisted, double-stranded molecules of DNA called chromosomes. Towards the ends of the chromosomes are usually sections of DNA called telomeres, which shield our genetic information, provide what is used for cells to divide, and hold some secrets to the way you age and get cancer.
Telomeres are already compared with the plastic tip covers on shoelaces since they prevent chromosome tips from fraying and sticking to one another, which might mix up an organism’s genetic information to lead to cancer, other illnesses or death.
Yet, whenever a cell divides, the telomeres get shorter. After they get too short, the cell will no longer be able to divide and ceases to be active or “senescent” or dies. The process is associated with aging, cancer and a higher risk of death. So telomeres also have been compared to a bomb fuse.
What exactly are telomeres?
Similar to the remainder of a chromosome as well as its genes, telomeres are chains of DNA – sequence of chemical information. Like other DNA, these are consist of four nucleic acid bases: G for guanine, A for adenine, T for thymine and C for cytosine.
Telomeres come from repeating chains of TTAGGG on a single strand of DNA attached to AATCCC on the other strand. Thus, one section of telomere is a “repeat” created from 6 “base sets.”
In cells within human blood, the duration of telomeres ranges from 8,000 base sets at birth to 3,000 base pairs as people age and as low as 1,500 in seniors. (A complete chromosome has about 150 million base sets.) Each time a cell divides, the average person loses between 30 and 200 base sets on the ends of the particular cell’s telomeres.
Cells usually can split no more than fifty to seventy times, with telomeres becoming progressively shorter till the cells become senescent, die or receive genetic damage that may cause cancer.
Telomeres don’t shorten as they age in tissues like heart muscle in which cells will not constantly divide.
So why do chromosomes have telomeres?
Without telomeres, the principle area of the chromosome – the portion containing genes required for life – would get shorter when a cell separates. So telomeres allow cells to separate without sacrificing genes. Cell splitting is necessary so you can grow completely new skin, blood, bone as well as other cells when needed.
Without telomeres, chromosome ends could fuse together and degrade the cell’s genetic blueprint, making the cell malfunction, become cancerous or die. Because broken DNA is dangerous, a cell contains the capability to sense and repair chromosome damage. With out telomeres, the ends of chromosomes would mimic broken DNA, and the cell would try to fix something which wasn’t broken. That also would make them stop dividing and eventually die.
Why do telomeres get shorter every time a cell splits?
Before a cell can separate , the chromosomes within it are duplicated to ensure that both of the two fresh cells contains identical genetic substance. A chromosome’s two strands of DNA must unwind and divide. An enzyme (DNA polymerase) then begins to make 2 fresh strands of DNA to fit each of the 2 unwound strands. It lets you do this along with the help involving short pieces of RNA. When each new matching string is finished, it’s a bit smaller compared to original strand as a result of room needed right at the end with this small part of RNA. It is just like somebody who paints themself into a corner and can’t paint the corner.
Will anything counteract telomere shortening?
An enzyme referred to as telomerase adds bases to the ends of telomeres. In fresh cells, telomerase keeps telomeres from breaking down too much. But as cells separate over and over again, there isn’t enough telomerase, so the telomeres grow shorter and the cells age.
Telomerase remains active in sperm and eggs, that are passed from one generation to the next. If reproductive cells did not include telomerase to keep the capacity of their telomeres, any organism with this kind of cells soon would go extinct.
What role do telomeres play in cancer?
As a cell actually starts to become dangerous, it divides more frequently, and its particular telomeres become much shorter. If its telomeres get short, the cell may die. It can escape this fate by becoming a cancer cell and activating an enzyme called telomerase, which in turn inhibits the telomeres from becoming even shorter.
Investigation has found shortened telomeres in lots of cancers, which includes pancreatic, bone, prostate, bladder, lung, kidney, and head and neck.
Measuring telomerase may be a brand new technique to discover cancer. If scientists can figure out how to stop telomerase, they may be in a position to combat cancer by causing cancer cells in order to age as well as perish . Within a experiment, researchers blocked telomerase activity in human breast and cancer of the prostate cells growing in the laboratory, prompting the tumor cells to die. But you will discover risks. Blocking telomerase could damage fertility, wound healing, and output of blood cells and immune system cells.
What about telomeres and aging?
Geneticist Richard Cawthon and colleagues at the University of Utah found shorter telomeres are associated with shorter lives. Among people older than 60, those with shorter telomeres were three times more likely to die from heart disease and eight times more likely to die from infectious disease.
While telomere shortening has been linked to the aging process, it is not yet known whether shorter telomeres are just a sign of aging – like gray hair – or actually contribute to aging.
If telomerase makes cancer cells immortal, could it prevent normal cells from aging? Could we extend lifespan by preserving or restoring the length of telomeres with telomerase? If so, does that raise a risk the telomerase also will cause cancer?
Scientists are not yet sure. But they have been able to use telomerase to make human cells keep dividing far beyond their normal limit in laboratory experiments, and the cells do not become cancerous.
If telomerase could be used routinely to “immortalize” human cells, it would be theoretically possible to mass produce any human cell for transplantation, including insulin-producing cells to cure diabetes patients, muscle cells for muscular dystrophy, cartilage cells for people with certain kinds of arthritis, and skin cells for people with severe burns and wounds. Efforts to test new drugs and gene therapies also would be helped by an unlimited supply of normal human cells grown in the laboratory.
How big a role do telomeres play in aging?
Some long-lived species like humans have telomeres that are much shorter than species like mice, which live only a few years. Nobody yet knows why. But it’s evidence that telomeres alone do not dictate lifespan.
Cawthon’s research found that whenever persons are split into two groups according to telomere extent, the 50 percent with longer telomeres lives five years more than those with shorter telomeres. That suggests lifespan could possibly be increased 5 years by increasing the length of telomeres in individuals with shorter ones.
People with longer telomeres continue to experience telomere shortening while they age. The number of years could possibly be added to our life-span by completely stopping telomere shortening? Cawthon believes a decade and perhaps thirty years.
When a person becomes older than 60, their risk of dying doubles with every eight years of age. So a 68-year-old has twice the potential risk of passing away inside a 12 month period in contrast to a sixty year old. Cawthon’s research found that differences in telomere length accounted for only 4 percent of the difference. And while intuition tells us the elderly have a greater risk of demise, only an additional six% is due solely to chronological age. When telomere length, chronological age and gender are combined (women live longer than men), those factors are the reason for thirty seven% in the variation in the probability of dying over age 60. Exactly what causes the additional 63 percent?
A significant cause of aging is “oxidative stress.” It’s the harm to DNA, proteins and lipids (fatty substances) due to oxidants, which are highly reactive substances containing oxygen. These types of oxidants are produced normally whenever we breathe, and in addition be a consequence of inflammation, infection and consumption of alcohol and cigarettes. In a single study, scientists exposed worms to two substances that reduce the effects of oxidants, and the worms’ lifespan increased almost 44 percent.
Another element in aging is “glycation.” It happens when glucose sugar from what we eat binds to some of your DNA, proteins and lipids, leaving them not able to do their jobs. The problem worsens when we get older, causing body tissues to malfunction, leading to illness and death. This might explain why studies in numerous laboratory animals indicate that restricting calorie consumption extends lifespan.
It’s possible oxidative stress, glycation, telomere shortening and chronological age – in addition to various genes – all work together to cause aging.
What are the prospects for human life extension?
Human lifespan has elevated considerably since the 1600s, when the average lifespan was 30 years. By 1998, the average U S life expectancy was seventy six. The reason why included sewers and also other sanitation measures, antibiotics, water that is clean, refrigeration, vaccines along with other medical efforts to prevent children and babies from dying, diet improvements and better health care.
A number of scientists feel average life expectancy will continue to rise, although many doubt the typical will grow past ninety. But a few predict vastly longer lifespans are possible.
Cawthon says should all processes of aging might be removed and oxidative stress damage might be mended, “one estimate is people could live one thousand years.”