Until now genetic aberrations have been seen as the main cause of almost all cancers. A new study says ovarian cancer cannot can solely occur as a result of protein imbalances within the cells. The study was published in the journal Oncogene.
"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 focused on two proteins; Plc1 (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," noted lead researcher Zahra Timsah from the University of Leeds.
"We found that in cells where Grb2 is depleted, FGFR2 was vulnerable to Plc1 binding and that this triggered uncontrolled proliferation," Timsah pointed out. The researchers looked at whether imbalance between Grb2 and Plc1 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 Plc1 and FGFR2 was associated with a significantly more favorable progress of treatment than patients with elevated levels of Plc1.
"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 Plc1 to ensure it does not overwhelm the cell," said Ladbury.
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