Queensland researchers have identified three distinct molecular subtypes of oesophageal cancer that could signal an end to a one-size-fits-all approach to treatment.

The international team of researchers from the QIMR Berghofer Medical Research Institute, Cancer Research UK and the international Cancer Genome Consortium used whole genome sequencing to analyse changes to genes that drive the cancer at a molecular level.

They identified three etiologically distinct subgroups of the disease, the first of which was characterised by extensive DNA scaring and the inability of cells to repair damage.

“This sub-group accounts for 18 per cent of oesophageal cancer cases and is likely to respond to certain types of chemotherapy,” explained co-author Dr Nic Waddell from the Medical Genomics Group at QIMR Berghofer.

“About half of patients with oesophagael adenocarcinoma are in the second sub-group, which is characterised by a high rate of genetic mutations.

“This sub-group of patients could potentially be a target for immunotherapy treatments,” he said.

“The remainder of patients fall into the third category, but there is still a lot more work to be done to understand the best treatment options for these patients.”

Co-author Professor Andrew Barbour from UQ’s Surgical Oncology Group said the study reinforces the need for a more precise approach to diagnosing and treating oesophageal cancer.

“DNA sequence information could help streamline patients into the most appropriate treatment based on the genetic signature of their disease,” he said.

“It would mean we are giving the best treatment to the right patient, at the right time.

“We have uncovered possible reasons for the lack of efficacy in molecularly targeted trials and present a novel genomic classification that links etiology to patient stratification with potential therapeutic relevance,” concluded the research team in their paper published in Nature Genetics.

However, they noted that further research was needed for preclinical validation as well as to understand the extent to which the genomic distinctions were maintained downstream, at the level of the transcriptome, proteome and cellular phenotype.