Non-genetic cancer mechanism identified

London (IANS) Calling in question the effectiveness of genetic screening alone in preventing cancer, a new study of ovarian cancer has found that the deadly disease can be caused solely by protein imbalances within cells.

The discovery is a major breakthrough because, until now, genetic aberrations have been seen as the main cause of almost all cancers.

The findings suggest that measuring and preventing dangerous imbalances in cells can lead to new cancer therapies.

“There has been huge investment in sequencing the human genome with the idea that if we get all the relevant genetic information we can predict whether you have a predisposition to cancer and, ultimately, use a precision medicine-based approach to develop a therapeutic approach,” said lead author John Ladbury, professor at the University of Leeds in Britain.

“Our study demonstrates that genetic screening alone is not enough,” Ladbury noted.

The research focussed on two proteins; Plc?1 (pronounced “plc-gamma-1”) and Grb2 (pronounced “grab-2”).

These proteins compete for binding to a cell wall-bound receptor FGFR2.

“This competition for binding to the receptor represents an unexpected way in which cancer can occur,” lead researcher Zahra Timsah from the University of Leeds noted.

“We found that in cells where Grb2 is depleted, FGFR2 was vulnerable to Plc?1 binding and that this triggered uncontrolled proliferation,” Timsah pointed out.

The researchers looked at whether imbalance between Grb2 and Plc?1 was predictive of the progress of ovarian cancers in patients.

Measuring the levels of the proteins in patient tissues followed by database analysis of clinical information revealed that a high level of Grb2 relative to Plc?1 and FGFR2 was associated with a significantly more favourable progress of treatment than patients with elevated levels of Plc?1.

“From the patient’s point of view, the key findings are that these proteins are biomarkers. They could offer information to clinicians on who is going to benefit from therapy and, just as importantly, who is not,” Ladbury explained.

“On the treatment side, the proteins’ interaction could be a valid therapeutic target: you could, for instance, target Plc?1 to ensure it does not overwhelm the cell,” Ladbury said.

The study was published in the journal Oncogene.

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