A defective ageing gene may drive blood cancer by helping tumour cells become immortal, research has shown.

The discovery pinpointing the role of the TERC gene could lead to new treatments for myeloma, which affects around 4,700 UK patients each year.

Scientists identified four new gene variants linked to the disease, bringing the total number known to seven.

TERC regulates the length of telomeres, caps on the ends of chromosomes that play a major role in cellular ageing.

Telomeres have been compared to the plastic tips of shoe laces, because they prevent coiled double strands of DNA from fraying and sticking together.

Every time a cell divides, its telomeres shorten until a point of "senescence" is reached when no further division takes place.

Senescence is believed to contribute to ageing - but may also suppress cancer by halting the uncontrolled growth of tumours.

The new research suggests a problem with TERC may enable lymphoma cells to ignore the ageing trigger and keep on dividing.

Study co-author Professor Richard Houlston, from the Institute of Cancer Research in London, said: "Our study has taken an important step forward in understanding the genetics of myeloma, and suggested an intriguing potential link with a gene that acts as a cell's internal timer.

"We know cancer often seems to ignore the usual controls over ageing and cell death, and it will be fascinating to explore whether in blood cancers that is a result of a direct genetic link. Eventually, understanding the complex genetics of blood cancers should allow us to assess a person's risk or identify new avenues for treatment."

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