The expression of 52 genes can accurately predict the survival of individual idiopathic pulmonary fibrosis (IPF) patients, a new study confirms. This could improve treatment approaches and aid in management decisions such as prioritizing patients for lung transplants.
The study, “Validation of a 52-gene risk profile for outcome prediction in patients with idiopathic pulmonary fibrosis: an international, multicentre, cohort study,” led by Dr. José Herazo-Maya and Dr. Naftali Kaminski of the Yale School of Medicine, appeared in The Lancet Respiratory Medicine.
A previous study, led by the same Yale research team, discovered that the 52-gene panel gave a good prediction of survival in IPF patients.
In normal circumstances, pieces of DNA in human genes are copied to be used as codes to make the different proteins that compose and regulate a cell’s stability. The number of copies a gene has in a certain situation offers a certain expression profile, for example.
The expression of genes from the DNA changes in different situations. In case of disease, the expression of these genes can be fewer or more copies. Researchers had previously analyzed the blood of IPF patients for more than 17,000 genes and identified 52 that were the most relevant for predicting survival. At that time, only four of these 52 genes were confirmed to be involved.
To get confirmation that these 52 genes were sufficient for a good patient survival prediction, researchers needed a larger group study.
The latest trial involved more than 400 IPF patients recruited in six groups from U.S. universities (Yale, Chicago, Pittsburgh and Harvard Medical School), and well as two universities in Germany and Great Britain. These patients were followed for more than 10 years.
Researchers were able to confirm that the 52 genes gave an accurate and reliable prediction of survival in IPF patients at an individual level, where they could predict which patients were at higher or lower risk of survival.
“IPF is known to have a variable and unpredictable course, and therefore we were so impressed that the results were validated in all six cohorts,” Heraza-Maya said in a press release.
Added Kaminski: “Shifts in the 52-gene risk profile could eventually be used to indicate response to therapy, and allow more efficient drug trial designs and disease management plans.”
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