ideasIdea
Strip the platelet coat off travelling tumour cells in ctDNA-positive patients
Cancer cells in the blood wrap themselves in platelets as camouflage. Aspirin may remove that cloak, and it is cheapest to test in the patients at highest risk of relapse.
Platelet cloaking shields circulating tumour cells from natural killer cells and shear stress and supplies TGF-beta that drives epithelial-mesenchymal transition. Aspirin has adjuvant signals in PIK3CA-pathway-mutant colorectal cancer and is being tested at scale in unselected populations, but no trial has enriched for molecular residual disease, where the event rate is high and the biology is precisely platelet-tumour cell interaction.
Hypothesis
In patients who are ctDNA-positive after curative surgery, aspirin added to standard care produces higher ctDNA clearance at six months than standard care alone.
Rationale
An MRD-enriched design turns a small absolute effect in an unselected population into a testable large relative effect in a small trial, and gives a molecular endpoint that reads out in months rather than years.
What would test it
A 200-patient randomised trial inside an existing MRD platform in colorectal or breast cancer, with six-month ctDNA clearance as primary endpoint and platelet-CTC imaging as a mechanistic substudy.
Maturity
early clinical
Who has to act
research
Cost to try
Medium ($1M to $50M)
Years to first evidence
5
Bottlenecks it attacks
- Metastasis is understood least and studied last · Metastasis causes about nine in ten cancer deaths but gets a small fraction of research money and almost no trials of its own.
- Dormant cells and minimal residual disease · After a 'successful' treatment, cells can sleep for years then relapse. We can barely detect them and cannot target them.
- No incentive to repurpose cheap drugs · Old, cheap drugs with anti-cancer signals never get the trials they need because no one profits from the result.