Scientists Discover How Pancreatic Cancer Switches Off a 'Tumor Suppressor' Gene

An anonymous reader shared this report from the Guardian:

A team of researchers from the UK and US have found that pancreatic cancer is able to shut down molecules in one of the body's most important genes, helping the disease to grow and spread rapidly... Dr Maria Hatziapostolou, of Nottingham Trent University's John van Geest Cancer Research Centre, said: 'This work, which has provided new understanding and knowledge of how the cancer behaves, will hopefully help pave the way for potential new treatments in the future....'

For the study, published in the journal Gastro Hep Advances, the researchers analysed healthy as well as pancreatic cancer tissue samples. They found pancreatic cancers triggered a process known as DNA methylation, causing molecules in the normally beneficial HNF4A gene to switch off, allowing tumours to grow extremely quickly. The HNF4A gene is crucial to human health because it helps many of the body's organs to function properly. But the researchers discovered pancreatic cancer can covertly disable the gene's benefits. Hatziapostolou said: 'Loss of HNF4A drives pancreatic cancer development and aggressiveness and we now know correlates with poor patient survival.'
Scientists from the University of Nottingham, Stanford University and the University of California and Cedars-Sinai medical centre, Los Angeles, were also involved in the project.


The published study calls the targeted HNF4A gene is 'a novel tumor suppressor in pancreatic cancer, regulating cancer growth and aggressiveness.'

And ultimately, according to the Guardian, pancreatic cancer 'is the 12th most common cancer worldwide,' according to the Guardian, 'with more than half a million people diagnosed every year. It has the worst survival rates of all the most common forms of the disease.'

The researchers paper ends with this conclusion. 'HNF4A silencing... drives pancreatic cancer development and aggressiveness leading to poor patient survival.'

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