ITU and Cancer Biology: A Single-Axiom View of Cellular Breakdown, Metabolism, Immunology, and the 2026-2040 Treatment Roadmap

We apply the Information-Theoretic Unification (ITU) framework (Terada 2026, DOI 10. 5281/zenodo. 20109210) to cancer biology. Cancer is re-expressed as the breakdown of the ITU axiom dS = d at cellular and tissue levels. This is Tier 1 paper #5, the first ITU paper in the medicine domain, opening the medicine vector after completing the engineering rectangle (Tier 1 #1-#4). Phase 59: ITU foundation. Healthy cells are biological QECCs with regulatory K (p53, RB1, DNA repair, apoptosis). Cancer cells exhibit dS >> d (entropy runaway) or corrupted K (driver mutations). The 10 Hallmarks of Cancer (Hanahan-Weinberg) are reframed as 10 K-component failures (mean K-control loss ~75% in cancer cells). The Knudson two-hit hypothesis is reinterpreted as redundant QECC; BRCA1 carrier risk at age 80 reaches 72% in our model, matching epidemiology. The Armitage-Doll multi-hit model (n=5-7) emerges from critical-mass K failure. Phase 60: The Warburg effect (1924) is reframed as deliberate degradation of Kₘetabolic. Cancer cells choose glycolysis even with O2 present to maximise entropy production rate (~7x normal), supplying the physical fuel for dS runaway. PI3K/AKT/mTOR constitutive activation is shown as K-circuit corruption. Tumor microenvironment pH ~6. 5 is reproduced from lactate accumulation. Single-axis metabolic drugs (2-DG, metformin, DCA) achieve 15-56% ATP reduction; combination of three drugs reaches 74%, illustrating the ITU prediction that single-K therapies fail due to K-redundancy. Phase 61: Cancer immunology under ITU. The Chen-Mellman Cancer-Immunity Cycle (2013) is decomposed into 7 Kᵢmmune sub-components. Cancer attacks all 7 simultaneously: PD-L1 over-expression, CTLA-4 abuse, MHC-I downregulation, TGF-beta, Treg, MDSC, IDO. Immune checkpoint inhibitors (Keytruda, Yervoy) restore K (response 20-50%). The TMB-response sigmoid matches Rizvi 2015; the PD-L1 x TMB sweet spot predicts 60% response in dual-positive patients. CAR-T (Kymriah, Yescarta) is K-augmentation; TIL therapy (Amtagvi 2024) is K-amplification. Phase 62: 2026-2040 treatment roadmap. Multi-K simultaneous restoration (3-4 axes: cellular + metabolic + immune + microbiome) is shown to be ITU-necessary. Response rates: 1-axis 25%, 2-axis 45%, 3-axis 65%, 4-axis 75% (saturation). 5-year survival projections: melanoma 50% -> 80%, NSCLC 25% -> 60%, pancreatic 10% -> 50%, glioblastoma 5% -> 30% (all 2024 -> 2040). Cancer market grows 240B -> 500B by 2040. Per-patient cost rises 50K -> 150K, creating access-inequity concerns. Ten falsifiable predictions are issued for 2026-2040 validation. Central thesis: cancer is a multi-component K-breakdown; therapy must restore multiple K-components simultaneously to overcome biological redundancy. The ITU framework provides a unified language across cellular regulation, metabolism, immunology, and drug response. Honest framing: this is a Pass-1 interpretive paper that reframes known cancer biology (Hallmarks, Warburg, ICI, CAR-T) and reproduces established clinical data (BRCA1 72%, tumor pH 6. 5, TMB response, ICI combo 50%) but does not produce ITU-unique cancer-biology predictions. Pass-2 follow-up work would derive an ITU-specific therapeutic figure-of-merit validated against patient outcome data. This paper opens the medicine vector of the ITU programme. Tier 1 #6 (Aging) and #7 (Psychiatry) will form a medicine triangle, paralleling the engineering rectangle (Quantum Computing 10. 5281/zenodo. 20139391 + Machine Consciousness 10. 5281/zenodo. 20150501 + Cryptography 10. 5281/zenodo. 20151059 + Semiconductors 10. 5281/zenodo. 20174036). Includes 4 theory documents, 4 Python numerical experiments, 4 figures, 4 JSON summaries. Total runtime ~20 seconds.