DNA differences in telomeres may explain how different types of cancer cells divide unchecked
Understanding how cancer cells can multiply indefinitely is a key challenge for scientists. For the first time, researchers at the Children’s Medical Research Institute have identified differences in the DNA of cancer cells which may help to pinpoint how they can divide unchecked.
Using state-of-the-art whole genome sequencing, researchers in the laboratory of Dr Hilda Pickett investigated the DNA of telomeres – short DNA stretches located at the end of chromosomes. In normal cells, telomeres are cut shorter every time a cell divides. In cancer the opposite can occur – telomere length is maintained, allowing for uncontrolled cell division and tumour growth.
Dr Pickett and her team discovered critical differences in particular telomere DNA sequences, called variant repeats. Cancer cells use one of two possible mechanisms for telomere maintenance, and importantly, Dr Pickett observed different patterns and types of variant repeats between cancer cells that use each mechanism.
This novel finding by CMRI researchers suggests that generation of variant repeats differs at a molecular level. Further investigation into the effects of these variants on cell division will reveal their potential role in finding novel anti-cancer therapeutic targets. As new drugs designed to block telomere maintenance are currently in clinical development, these results have exciting implications for cancer-specific therapeutic strategies.
The full article, published by the journal Nucleic Acids research, is available here: Lee M et al. Telomere extension by telomerase and ALT generates variant repeats by mechanistically distinct processes. Nucleic Acids Res. 2014 Feb;42(3):1733-46.