Metaplasia precursor step (Barrett's → EAC, gastric Correa cascade)

A metaplastic precursor — Barrett's oesophagus, gastric intestinal metaplasia — is the same R19 cell-fate switch with its stability scale lowered by injury, the g-reduction the §10 kernel uses for H. pylori. On the smaller barrier (Barrett's→EAC RR≈11, gastric IM RR≈3.6) the malignant crossing is rate-limited on the precursor; ablation restores the scale and collapses the next-step rate.

A metaplastic precursor (Barrett's oesophagus, gastric intestinal metaplasia) is the §7 R19 cell-fate switch with its stability SCALE reduced by sustained injury, g_meta = g − drop — the IDENTICAL g-reduction the §10 kernel already uses for chronic H. pylori, read here as a discrete compartment (vendored single-source as metaplastic_scale / metaplasia_barrier_drop in the substrate). The g-drop is locked to the cited precursor-vs-general RR by one bisection: Barrett's-vs-general EAC RR≈11 (Hvid-Jensen 2011), gastric intestinal-metaplasia RR≈3.6. Because the next-step crossing fold exceeds three, carcinoma arises ~only from the precursor — the metaplasia step is rate-limiting (why surveillance and ablation are the levers). A dysplasia ladder (deeper g-drop: NDBE→LGD→HGD) accelerates the crossing, reproducing the observed direction and convex acceleration; restoring g toward healthy collapses the rate monotonically to one (the treatment reading: anti-reflux for Barrett's, eradication for the gastric cascade). The precursor anchors are [L]; the rate-limiting step, the dysplasia-ladder shape, and the treatment direction are [V]; the absolute progression %/yr and the exact ladder ratios are [O] (the model's ratios are lower than clinical, needing external population calibration — the model fixes direction and rate-limiting, not the absolute hazard).

Some carcinomas do not arise directly from healthy tissue — they arise from a metaplastic precursor (Barrett's oesophagus before oesophageal adenocarcinoma; gastric intestinal metaplasia before intestinal-type gastric cancer, the Correa cascade). This is the one new reading the neoplastic extension adds, and like the gate and the reservoir it is not new dynamics: a metaplastic cell is the same §7 R19 cell-fate switch with its stability scale lowered by sustained injury, g_meta = g − drop — the identical g-reduction the §10 kernel already applies for chronic H. pylori, now read as a discrete compartment rather than a continuous background.

Sitting on the smaller barrier g_meta²/4 < g²/4, the metaplastic cell's next (malignant) crossing runs faster than a healthy cell's by the precursor-vs-general factor, locked to the cited anchor by a single bisection: Barrett's-vs-general EAC RR ≈ 11.0 (Hvid-Jensen 2011) and gastric intestinal-metaplasia RR ≈ 3.6. Because that fold exceeds three, carcinoma arises ~only from the precursor compartment — the metaplasia step is rate-limiting, which is exactly why Barrett's surveillance and metaplasia ablation are the clinical levers.

A dysplasia ladder — deeper injury, a further g-drop — accelerates the crossing (NDBE → low-grade → high-grade dysplasia), reproducing the observed direction and the convex acceleration of the progression hazard:

Treatment (model reading). The kernel makes prevention the lever: restoring the barrier scale g — ablating the metaplasia or removing the injury (anti-reflux for Barrett's, H. pylori eradication for the gastric cascade) — collapses the next-step crossing rate back toward the healthy baseline. Restoring g from g_meta toward healthy drops the malignant-crossing rate monotonically to one:

The precursor-vs-general RR anchors are cited [L]; the rate-limiting precursor step and the dysplasia-ladder shape (monotone, accelerating) and the treatment direction are verified [V]. What stays open [O], with its obstacle: the absolute progression rate (the model's ladder ratios, LGD/NDBE ≈ 1.8 and HGD/NDBE ≈ 3.1, are lower than the cited clinical ratios), because the absolute annual hazard — like absolute incidence and absolute organ size — needs external population calibration; the model fixes direction and rate-limiting, not the absolute %/yr.