SINGAPORE - Researchers here have made two key findings about cancer from both ends of the process: working out one way that normal liver cells turn cancerous, and how mutations in cancer cells can interfere with drug or radiation treatment.
In the first study, scientists from the Cancer Science Institute (CSI) at the National University of Singapore compared healthy and cancerous tissue from over 180 patients with a type of liver cancer called hepatocellular carcinoma, and noticed that "edited" RNA (ribonucleic acid) was much higher in cancerous cells than in healthy ones.
DNA serves as the template to print out RNA sequences, which have various functions in all human cells. But the RNA molecule can get changed - or "edited" - by the action of enzymes after it is produced. The product of too much altered RNA encourages the growth of cancer cells. It is also linked to liver cirrhosis, tumour recurrence and a lower survival rate of liver cancer.
The scientists' work was published online in the journal Nature Medicine on Jan6, and is the first in the world to clearly link RNA editing with the development of liver cancer.
Lead author Polly Chen, of the CSI, said the link between RNA editing and cancer could apply to other tumours such as oesophageal and nasopharyngeal cancers.
The next step, the researchers said, is to work out if the edited RNA can be used as a biomarker, - an early warning sign of the disease - and whether halting or reversing the process can stop the spread of cancerous cells.
The other study, carried out by the National Cancer Centre Singapore (NCCS) using genetically modified mice, found that the same genetic mutations that fail to stop cancer developing, can also interfere with drug or radiation treatment. A gene called p53, which normally stops cells becoming cancerous, is mutated by a variety of factors and fails to work in up to half of all cancers.
Everyone has two copies of this gene, and in most cancer patients, only one copy is mutated. Cancer treatment should stop the growth of cancer cells, but when a patient with this mutation gets chemotherapy or radiation therapy, the mutant copy of the gene inhibits the normal copy from stopping cell growth.
This study, by Professor Kanaga Sabapathy and his team, was published in the journal Cancer Cell last month.
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