{
  "title": "What this review means",
  "includeSubclaimIllustrations": false,
  "redteamReviewed": true,
  "accessNotice": "Source checking used complete abstracts/status records and selected original partial-body passages. No complete-paper audit or independent scientific peer review is claimed. Detailed access counts and limitations appear in the review.",
  "overview": "Chromatin changes can affect cancer initiation, persistence and treatment response. This review separates epigenetic first hits and state-dependent tumor behavior from the claim that autonomous chromatin disruption is the primary cause of human cancer.",
  "implications": "Scope-matched SC4 yields Γ for the registered mammalian-autonomy and general human-primacy claim. Transient fly initiation is Ε and its circuit perturbations provide Δ causal contribution, while mammalian epimutational and reprogramming causality is retained in defined engineered/predisposition settings. These positive settings do not establish representative autonomous chromatin-first human origin.",
  "limitations": "60 primary reports with 8 selected partial-body examinations; density, heterogeneous controls and incomplete access set the confidence, not correctness. The grade applies to the exact registered claim; stronger findings for narrower subclaims remain separate. No complete-paper audit or blinded calibration is claimed. This educational review does not establish an individual treatment recommendation."
}