OnCo
ideasIdea

Group trials by broken mechanism, not by organ or single mutation

Rare cancers often share a broken cellular machine even when they arise in different organs. Grouping patients by that shared fault makes trials possible.

Tumour-agnostic approvals so far follow single alterations such as NTRK fusions or mismatch repair deficiency. Many rare cancers instead share mechanism classes — SWI/SNF complex loss including SMARCB1 and SMARCA4, chromatin regulator loss, fusion-driven transcription factor addiction, metabolic enzyme mutations — that could define baskets with dozens of contributing diagnoses and a common therapeutic hypothesis such as EZH2 or PRMT5 dependence.

Hypothesis
Mechanism-class baskets, for example SWI/SNF-deficient tumours treated with an EZH2 inhibitor, show consistent response across contributing histologies, justifying mechanism-level rather than mutation-level approvals.
Rationale
Tazemetostat activity in SMARCB1-deficient epithelioid sarcoma is proof that a chromatin mechanism class can be targeted, and synthetic lethal relationships in this space are well mapped in cell line dependency data. Mechanism classes are far more prevalent than any single alteration.
What would test it
A basket trial enrolling by mechanism class with pre-specified histology-level Bayesian borrowing; kill the class hypothesis if response is confined to one histology.
Maturity
early clinical
Who has to act
research
Cost to try
Medium ($1M to $50M)
Years to first evidence
6
Bottlenecks it attacks

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