New clues to telomeres and cancer

Researchers in the UK have uncovered important clues about how
cells age that could be used to develop treatments that counteract
the ability of cancers to grow and spread.

Researchers in the UK have uncovered important clues about how cells age that could be used to develop treatments that counteract the ability of cancers to grow and spread.

A report published on-line in the journal Nature​ today reveals the molecular events that take place when a cell becomes old and stops dividing.

Scientists from Cancer Research UK, The Wellcome Trust and The Institute of Ageing and Health at the University of Newcastle upon Tyne claim to have uncovered a mechanism for repairing damaged DNA that can also stop ageing cells from dividing by sending them into senescence.

At the heart of the new research is the understanding that when cells age, structures called telomeres are worn away from the ends of chromosomes. Telomeres protect chromosomes from becoming tangled or degraded, so they can be faithfully copied when cells divide. However, as cells age, and as telomeres get shorter - this system begins to fail.

In the new study, the scientists found that DNA repair molecules recognise worn telomeres as genetic damage. It has already been established that these molecules activate a response to damaged DNA to repair it and prevent the cell from dividing before this process has taken place. Now the UK scientists have found the repair molecules initiate this mechanism when telomeres are truncated, driving the ageing cell into senescence.

The DNA repair molecules form structures at the end of telomeres, which theresearchers have called SDFs (senescence-associated DNA damage foci). They found that SDFs are only present in senescent cells and not young cells, and also that blocking the response from the DNA repair molecules could cause senescent cells to activate and begin dividing again.

While normal cells only divide a certain number of times before they senesce, this process goes wrong in cancer cells and they continue to multiply well beyond their allotted lifespan. The hope is that the new research will lead to ways to age cancer cells and halt their rapid growth and division.

Since the work has uncovered a structure that is only present in senescentcells, we have a diagnostic marker for cell ageing, it could be used to distinguish between healthy cells and cancer cells. This could lead to a test to detect cancer at a very early stage.

Prof Steve Jackson of Cancer Research UK said: "While we are not yet able to fully reverse the process of cell ageing our study gives us an insight into what happens when a cell grows old.

"Now we know how healthy cells age, we can work out how cancer cells ignore this process, which could lead to new treatments for the disease."

Related topics Clinical trials & development

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