DQIS-S — Distributed Quantum-Inspired Immune Surveillance (Surveillance Mode): A Multi-Channel Cell-Based Biosensor Framework for Pre-Symptomatic Cancer Detection with Autonomous Endogenous Chromogenic Urinary Reporter

Companion document to the DQIS Consolidated Framework v22.0 (DOI: 10.5281/zenodo.19855263). DQIS-S formalizes a Surveillance-only variant of the DQIS framework in which the distributed quorum logic (k≥3 of 5 orthogonal biophysical channels) activates a synthetic reporter signal rather than — or simultaneously with — cytotoxic effector function. The central result: a single administration produces three simultaneous outputs from the same quorum event: tumor cell killing (DQIS-A function), reporter signal activation (DQIS-S function), and autonomous chromogenic urinary output visible to the naked eye. Core innovation 1 — IS→Indigotin autonomous chromogenic reporter. Indoxyl Sulfate (IS) is naturally abundant in human urine (average 530 µM, produced endogenously from dietary tryptophan via gut microbiome). Enzymatic conversion IS→Indigotin (soluble blue, FDA/EMA-approved E132) produces visibly BLUE urine with no patient action required. Biological proof of concept: Purple Urine Bag Syndrome (PUBS) demonstrates this chemistry functions in real human urine in vivo. Systematic analysis of all 8 major endogenous urinary substrates confirms IS as the only candidate producing an unambiguous, fully autonomous color signal. Core innovation 2 — Decoupled hepatic amplification. Without amplification, visible blue requires ~10⁵–10⁶ tumor cells. With hepatic amplifier (engineered hepatocytes via AAV, Option A; or subcutaneous cellular depot, Option B; or engineered gut bacterium, Option C), N* ≈ 33–3,300 tumor cells suffice — a 600–3,000× advantage over OncoSCOUT (Carlson et al. bioRxiv 2026, threshold ~3×10⁶ cells). Quantitative analysis: 10⁶ hepatocytes activated by signal S produce 2.4×10¹⁷ E2 molecules/24h → 265 µM Indigotin → 53× above visibility threshold. Core innovation 3 — Unified differential equation model. DQIS-S and DQIS-A are one drug. Size-dependent behavior emerges automatically from the quorum term Q(N,M): below N*≈3,300 cells, active killing but no visible signal; above N*, blue urine + massive killing. No programming required — emergent from system physics. Version 2.0 updates (May 2026). Aligned to Consolidated Framework v22.0. New §3.5a documents convergence between the decoupled hepatic amplifier (this document) and the S_tm mechanism independently developed in Consolidated v22.0 §3.6bis (brain reporter resolution, O15) — the two formulations are architecturally identical; S_tm additionally resolves the renal filtration constraint since the T cell itself is the carrier. New §8.3 integrates the T-ζ-IPS module for PDAC: direct empirical measurement (GSE155698, Steele 2021, 11,448 EPCAM+ cells) shows θ=1.214 — PDAC is intrinsically cold (normal pancreas θ=1.107, GSE84133, Baron 2016). IPS penetrance signal: normal 0.5% → IPMN 5.0% (10.1×) → PDAC 7.7% (15.5×), P(false alarm, N=1,000 cells)=0.0003. The DQIS-S chromogenic pipeline is activatable by either k=3 standard quorum (hot tumors, GBM θ=0.199) or IPS penetrance signal (PDAC, IPMN). IPMN detection 5–10 years before invasive disease is the most clinically significant implication for the patient-facing DQIS-S design. Open items: CRISPRa toggle leakage rate λ in primary human CD8+ T cells (priority experiment: 4–8 weeks, €15,000–40,000 via CRO — single measurement determining minimum detectable tumor burden); long-term safety of hepatic amplifier; absence of in vivo experimental data. These are development pathway challenges, not conceptual barriers. Not a peer-reviewed publication. Prior art deposit — CC BY 4.0.Contact: dqis.research@proton.me Related documents: - DQIS Consolidated Framework (main document): https://zenodo.org/records/19877553 - Register of Scientific Objections v4.0: https://zenodo.org/records/19880166 - Addendum I — Temporal Stratification of Tail Dependence Risk: https://zenodo.org/records/19877810