DQIS — Distributed Quorum-Based Independent Immune Surveillance (formerly: Quantum-Inspired): A Theoretical Framework for Multi-Channel Independent Immune Surveillance

DQIS — Distributed Quorum-Based Independent Immune Surveillance: Consolidated Framework v32. 0 This document presents DQIS — a theoretical framework proposing to augment natural immune surveillance with five engineered T-cell variants operating on orthogonal biophysical channels (metabolic, mechanical, bioelectric, chromosomal instability, topological), coordinated by a distributed consensus protocol. The core principle — borrowed from Byzantine Fault Tolerance in distributed computing — is that statistically independent verification channels reduce joint tumour escape probability multiplicatively via k-of-N quorum aggregation. Empirical foundations. Direct θ measurement on real scRNA-seq data (May 2026): GBM θ=0. 199 (GSE131928, 7, 911 cells) — reclassified from cold to hot; PDAC θ=1. 214 (GSE155698, 11, 448 cells) — confirmed cold, resolved via IPS module (15. 5× penetrance signal, P (false alarm) =0. 0003). Empirical pᵢ: T-γ* and T-δ v2. 0 already on target (0. 01–0. 03) ; T-β median pᵢ=0. 004 in AND-gate context (Monte Carlo, O1. 3). Inter-group correlation matrix corrected: T-α/T-δ θME=0. 40–0. 50 via ACLY→acetyl-CoA→HAT causal pathway (Shi et al. 2019, TCGA n=5, 726) — resolved by Design B (T-δ v2. 0 CIN sensor, θME reduced to ~0. 10). T-α/T-β τ=0. 31 (mTOR hub) identified as dominant system correlation. Operative efficacy claims (v30. 0 corrected). Phase 0 PoC (T-γ*+T-δ v2. 0, k=1/2, existing technology): 30–75× Pₑscape reduction (range depends on empirical pᵢ of T-δ v2. 0 CIN sensor). Design B k=2 (O29 resolved, Phase 2+): ~774×. Adaptive Quorum k=1/N + GateG (Phase 2+, see below): ~1, 286–1, 800× for Nₑff=3–4 tumors. Opt-B long-term vision (T-TRT telomerase sensor replacing T-β, Phase 3+): ~7, 500×. All claims stratified by tumour type and conditioned on ε (t). Theoretical ceiling (k=5, θ=0): ~4, 000, 000× — non-operative, preserved for completeness. Note: v30. 0 supersedes the progression ~75×→~500-1, 000×→~5, 000-30, 000× previously reported; Channel Paradox (O34) establishes that k=3 multi-channel expansion reduces security below Phase 0 until GateG and Design B conditions are met. Key architectural developments (v30. 0). Design B: T-δ redesigned as T-δ v2. 0 (Chromosomal Instability sensor, cGAS-STING pathway), eliminating the ACLY metabolic-epigenetic causal correlation. Adaptive Quorum Architecture: shifting from k=2/N (statistical security) to k=1/N + GateG (biological security via Ki-67 proliferation gate) resolves the Channel Paradox and upgrades ~91% of evaluated tumour types to Class A/A-B/B coverage — compared to ~68% with standard Design B k=2. GateG (O29, Ki-67 nanobody, Phase 2+) is the single most critical post-Phase 0 investment: its resolution unlocks the adaptive quorum for ~70+ tumour types across all histological categories. Adaptive tumour-type optimisation documented for all 104 evaluated types (§B. 15): Class A (~789×) via Design B k=2 for Nₑff=5 F=1 tumours; D→A/B via DQIS-CNS FUS module for all CNS tumours; C→A via k=1/3 for Nₑff=3 tumours with GateG. Self-audit. Companion Objections Register v30 documents 34 mapped objections: 12 RESOLVED, 2 LOW, 14 MEDIUM open with mitigation pathways, 4 HIGH open (O7 CHIP drift, O8 epigenetic silencing, O14 paediatric validation, O27 briquilimab non-standalone conditioning). O28 (Marsico 2025) maintained at MEDIUM-HIGH. O33 RESOLVED via Design B. O34 (Channel Paradox) MEDIUM OPEN — primary resolution via Adaptive k=1/N + GateG (Phase 2+). Companion Addendum I v16 provides Clayton copula formalism for tail dependence, IPS module derivation, TASE recalibration, Sequential Verification formalisation, Design B impact on tail dependence calculus (§16), and Adaptive Quorum Architecture integration into the formal threat model (§16. 5). Origin and intent. This framework was developed by an independent researcher without academic affiliation, using AI-assisted conceptual exploration and formalisation. It is explicitly theoretical — no wet-lab validation has been performed. The Phase 0 PoC (T-γ*+T-δ v2. 0, melanoma model, €2–5M, 24–30 months) is the single required experimental investment for framework credibility. GateG resolution (O29) is the recommended second investment. This document is structured as a foundation for academic discussion and a target for experimental falsification, not as a claim of completeness. Terminological note. From v22. 0, DQIS expands as "Distributed Quorum-Based Independent Immune Surveillance. " The architecture uses Byzantine Fault Tolerance k-of-N quorum logic. T-δ v2. 0 replaces the original epigenetic methylation sensor with a Chromosomal Instability sensor (cGAS-STING pathway) — mechanistically orthogonal to metabolic channels, resolving the dominant inter-group correlation identified in v30. 0. Contact: dqis. research@proton. me Related documents: - Register of Scientific Objections v4. 0: https: //zenodo. org/records/19880166 - Addendum I — Temporal Stratification of Tail Dependence Risk: https: //zenodo. org/records/19877810