Telomeres, Aging, and Cancer

Are the Genetics of Aging the Key to Cancer?

DNA double helix, artwork
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All cells have a programmed lifespan by which they are synthesized, multiply, and eventually undergo apoptosis (cell death) when they are no longer functional.

It often helps to think of cellular replication as old-fashioned photocopy machine: the more a cell copies itself, the more blurry and misaligned the image becomes. Over time, the genetic material of the cell (DNA) begins to fracture and the cell itself becomes a pale copy of the original.

When this happens, programmed cell death allows a new cell to take over and keep the systems running.

The number of times a cell can divide is bounded by a phenomenon known as the Hayflick limit. This describes the action by which the process of division (known as mitosis) progressively degrades the genetic material, specifically the part of DNA called a telomere.

The Hayflick limit dictates that the average cell will divide between 50 to 70 times before apoptosis.

Understanding Telomeres

Chromosomes are thread-like structures located inside the nucleus of a cell. Each chromosome is made of protein and a single molecule of DNA.

At each end of a chromosome is a telomere which people will often compare to the plastic tips at the ends of a shoelace. Telomeres are important because they prevent chromosomes from unraveling, sticking to each other, or fusing into a ring.

Each time a cell divides, the double-stranded DNA separates in order for the genetic information to be copied.

When this happens, the DNA coding is duplicated but not the telomere. When the copy is complete and mitosis begins, the place where the cell is snipped apart is at the telomere.

As such, with each cell generation, the telomere gets shorter and shorter until it can no longer maintain the integrity of the chromosome.

It is then that apoptosis occurs.

Telomeres' Relation to Aging and Cancer

Scientists can use the length of a telomere to determine the age of a cell and how many more replications it has left. As cellular division slows, it undergoes a progressive deterioration known as senescence, which we commonly refer to as aging. Cellular senescence explains why our organs and tissues begin to change as we grow older. In the end, all of our cells are "mortal" and subject to senescence.

All, that is, but one. Cancers cells are the one cell type that can truly be considered "immortal." Unlike normal cells, cancer cells do not undergo programmed cell death but can continue to multiply without end.

This, in and of itself, disrupts the balance of cellular replication in the body. If one type of cell is allowed to replicate unchecked, it can supplant all others and undermine key biological functions. This is what happens with cancer and why these "immortal" cells can cause disease and death.

It is believed that cancer occurs because a genetic mutation can trigger the production of an enzyme, known as telomerase, which prevents telomeres from shortening.

While every cell in the body has the genetic coding to produce telomerase, only certain cells actually need it.

Sperm cells, for example, need to the switch off telomere shortening in order to make more than 50 copies of themselves; otherwise, pregnancy could never occur.

If a genetic mishap inadvertently turns telomerase production on, it can cause abnormal cells to multiply and form tumors. It is believed that as life expectancy rates continue to grow, the chances of this occur will not only become greater but eventually become inevitable.

Source;

Arai, Y.; Martin-Ruiz, C.; Takayama, M. et al. "Inflammation, But Not Telomere Length, Predicts Successful Ageing at Extreme Old Age: A Longitudinal Study of Semi-supercentenarians." eBioMedicine. 2015; 2(10): 1549-48; DOI: 10.1016/j.ebiom.2015.07.029..

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