Reference: January 2026 | Issue 1 | Vol 12 | Page 7
Dr Iseult Browne, Royal Marsden Hospital, London, UK, delivered a presentation titled ‘Integrating circulating tumour DNA into treatment decision-making in breast cancer’.
“Cell-free DNA is present in the circulation of all… individuals as a result of apoptosis, necrosis, and secretion. A proportion of that in patients with cancer is termed ctDNA and that is a direct result of tumour bulk and tumour cell turnover.”
She discussed how various types of tumour assays are used in her clinic. Some of these are ultra-sensitive, but the sophistication of the assays is still evolving, she explained. Dr Browne also presented data from various clinical trials on how tumour mutations are assessed and dealt with.
She outlined some of the exploratory research she and colleagues have conducted in ctDNA testing in different types of breast cancer. “Potentially, low baseline ctDNA levels can be associated with a less aggressive tumour phenotype with higher response rates,” said Dr Browne. “High baseline ctDNA levels may become both selection and stratification factors for future targeted trials.”
Dr Browne also emphasised: “ctDNA assessment may differ between therapies with different mechanisms of action, and this is really important, because implementing dynamics in clinical trials and in practice may require distinct analyses for different therapies,” she told the attendees.
She also discussed the Fulvestrant, Ipatasertib and CDK4/6 Inhibition in Metastatic ER+/HER2- Breast Cancer Patients Without ctDNA Suppression (FAIM) trial, which she is conducting with colleagues. The trial is studying the effect of fulvestrant, ipatasertib, and CDK4/6 inhibition in metastatic ER+/HER2- breast cancer patients without ctDNA suppression.
FAIM is using ctDNA analysis and imaging techniques to determine whether the addition of the experimental drug ipatasertib to a standard combination of fulvestrant and palbociclib increases progression free survival for these patients.
“ctDNA can guide treatment for breast cancer,” Dr Browne concluded. “Undetectable on-treatment ctDNA is associated with good outcomes across treatments. Incorporating early mutation and methylation-based dynamics into treatment pathways in advanced breast cancer offers patients the potential to personalise therapy and, by assessing response early, clinicians may be able to tailor treatments, optimise outcomes, and guide treatment approaches.”
