Scientists, including one of Indian-origin, have uncovered a survival mechanism that occurs in breast cells that have just turned premalignant - cells on the cusp between normalcy and cancers - which may lead to new methods of stopping or preventing tumours.
The Salk Institute researchers found that a protein known as transforming growth factor beta (TGF-beta), considered a tumour suppressor in early cancer development, can actually promote cancer once a cell drifts into a pre-cancerous state.
The surprising discovery raises the tantalising possibility that, with novel treatment, some cancers might be prevented before they even develop, researchers said.
"Our work suggests it might be possible to halt cancer development in premalignant cells-those that are just a few divisions away from being normal," said the study's lead author, Fernando Lopez-Diaz, a researcher in the Regulatory Biology Laboratory at Salk.
"This study offers both significant insights into early cancer development and a new direction to explore in cancer treatment. It would be fantastic if a single agent could shut down both advanced cancer and cancer that is primed to develop," said Beverly M Emerson, study's senior author.
The researchers conducted this study to learn exactly how p53, a known tumour suppressor, and TGF-beta interact in cancer development.
The team examined premalignant as well as cancer cells from breast and lung tumours and matched normal and premalignant breast cells from healthy women provided by scientists at the University of California San Francisco.
They found that TGF-beta can interfere with cells' damage responses in premalignant or cancer cells. They found that TGF-beta halts both the transcription of the p53 gene - the process by which cellular machinery reads the DNA code for a gene - and the subsequent process by which the corresponding p53 protein is produced, known as translation.
This could explain why, in about half of the breast tumours, including premalignant lesions, when TGF-beta1 signalling was highly activated, the levels of p53 were reduced, and vice versa if the TGF-beta1 pathway was reduced, there were high levels of p53.
The new findings shed light on how premalignant and early cancer cells are