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Intercept cancer at the field stage

Whole regions of tissue carry cancer mutations long before a tumour exists. Detecting and treating the field, not the tumour, could prevent cancers rather than cure them.

Mutant clones in normal oesophagus, skin, and airway are pervasive; Barrett's surveillance and ablation, HPV vaccination, and Lynch aspirin already show interception works when the field is identifiable.

Hypothesis
Molecular field markers (e.g., TP53-mutant clone burden in Barrett's or bronchial brushings) identify individuals for whom ablation or chemoprevention reduces cancer incidence.
Rationale
Sanger normal-tissue sequencing; Cytosponge and nasal-brushing assays make field sampling minimally invasive.
What would test it
Randomised trial of field-marker-guided ablation versus standard surveillance in non-dysplastic Barrett's with high TP53 clone burden; endpoint progression to dysplasia/cancer.
Maturity
early clinical

Key papers

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basicScience 2015
Martincorena: normal sun-exposed skin is a patchwork of cancer-mutation clones

Carrying a cancer mutation is normal; most mutant clones never become cancer. This means blood or tissue tests that look for driver mutations alone will produce false positives, and that the question of what tips a mutant clone into cancer (tissue environment, further hits, immune surveillance) is as important as the mutation itself.

Connected

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Pages like this

not linked directly; found by shared links

cancers

3
Head and neck squamous cell carcinomaNon-small-cell lung cancerOesophageal cancer

technologies

3
Chemoprevention & risk-reducing surgeryEndoscopic resection (EMR / ESD)Thermal ablation and cryotherapy for cervical precancer

targets

1
TP53

institutions

2
Cancer Research UKThe Francis Crick Institute

pathways

2
Clonal evolution & minimal residual diseaseField cancerisation

terms

1
Barrett's oesophagus

key papers

1
Martincorena: normal sun-exposed skin is a patchwork of cancer-mutation clones