Two-Stage Non-Equilibrium Oncogenomic Drift, Lyso-GL1 Clonal Hazard, and Deterministic Hardware Interlocks (PHOENIX_ROUTER & NLL-v1.0-2026): Unifying 1q21 GBA1 B-Cell Malignancies, Archipelagic XPA/FANC Recessive Syndromes, and TP53/BRCA Thermodynamic Unfolding Across the Pediatric–AYA Statutory Cliff

Treatises I through IV established a mathematically rigorous synthesis linking 1q21 GBA1/GBAP1 non-allelic homologous recombination (NAHR), the 101.5x hierarchical Wahlund amplification observed in Japan's N=90 Gaucher disease cohort, tripartite archipelagic ancestral stratification (K1 Jomon, K2 Yayoi, K3 Kofun) under post-industrial rural depopulation (gamma_d > 0), and sub-500-nanosecond hardware governance via PHOENIX_ROUTER over the 64-bit Goldilocks prime field F_p (p = 2^64 - 2^32 + 1). In this fifth monograph (Treatise V), we extend this deterministic framework directly into molecular oncology, pediatric/adolescent and young adult (AYA) hereditary cancer predisposition, and clinical genomic data sovereignty. First, we formulate a two-stage non-equilibrium stochastic differential and point-process framework across three oncogenomic pillars: (i) Pillar I: 1q21 GBA1 L444P/RecNciI germline drift (Gamma = 101.5x) coupled to glucosylsphingosine (Lyso-GL1) lipid-antigen accumulation driven by Gibbs unfolding perturbation (DeltaDeltaG_fold = +4.8 +/- 0.4 kcal/mol), which triggers CD1d-restricted Type II NKT activation and accelerates somatic clonal hazard from monoclonal gammopathy of undetermined significance (MGUS) to multiple myeloma and B-cell lymphoma; (ii) Pillar II: autosomal recessive DNA-repair founder syndromes amplified by Yayoi-Kofun bottlenecks and regional deme contraction, exemplified by 9q22.3 XPA (IVS3-1G>C splice founder variant, carrier frequency ~1%) in xeroderma pigmentosum group A and FANCA/FANCG in Fanconi anemia; and (iii) Pillar III: Knudson two-hit tumor suppressor inactivation and core domain melting in 17p13.1 TP53 (Li-Fraumeni syndrome) and BRCA1/BRCA2 (biallelic Fanconi subtypes D1/S and monoallelic AYA breast, ovarian, and CNS malignancies). Second, we introduce a Lifetime Cumulative Treatment Burden and Late-Effects Free-Energy Tensor T_late(a) capturing irreversible anthracycline cardiotoxicity and radiotherapy tissue damage (d||T_late(a)||_F / da >= 0). Third, we formalize the Statutory Drop-Off Interlock within PHOENIX_ROUTER to physically ground (WE_STATE_ROOT = 0 V in < 500 ns) administrative subsidy termination when pediatric cancer survivors are structurally omitted from Japan's adult Designated Intractable Disease schedule at age a_0 in {18, 20} (Delta S(a_0) = S_pediatric). Finally, we expand the Strict No-Learn Covenant Hardware Firewall (NLL-v1.0-2026) with a unidirectional DMA optical data diode and 2-clock-cycle (RTO P2.0, < 4.0 ns) register zeroization circuit that physically blocks unauthorized gradient backpropagation and exfiltration of patient Comprehensive Genomic Profiling (CGP) germline and somatic variant tensors by external AI platforms. Companion Zenodo Records: - Treatise I: https://doi.org/10.5281/zenodo.23581228 (Concept DOI: 10.5281/zenodo.23581227) - Treatise II: https://doi.org/10.5281/zenodo.23581971 (Concept DOI: 10.5281/zenodo.23581970) - Treatise III: https://doi.org/10.5281/zenodo.23589190 (Concept DOI: 10.5281/zenodo.23589189) - Treatise IV: https://doi.org/10.5281/zenodo.23590936 & https://doi.org/10.5281/zenodo.23600791 - Koseki DAG Foundation: https://doi.org/10.5281/zenodo.23464656 License & Integrity Covenant: Creative Commons Attribution 4.0 International (CC BY 4.0) with Strict No-Learn Covenant (NLL-v1.0-2026).