Cancerous growth can be induced by disruption of electrical coordination signals and reversed by re-establishing them, without genetic changes (Levin 2021a)

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• Suppression of cancer phenotypes despite strong oncogenic mutations via forced bioelectrical connections among cells, overriding single-cell goals with morphogenetic ones.finding0.841
  Empirical demonstration that bioelectric network topology, not genetic state, determines whether cellular optimization occurs at single-cell (cancer) vs. organ level.
• The cancer phenotype can be reverted by artificially managing the bioelectric connections between a cell and its neighbors.hypothesis0.833
  Predicts that restoring gap junctional coupling or appropriate Vmem can normalize oncogene-expressing cells.
• Cancer phenotypes can be suppressed by forcing bioelectrical connections among cells, overriding oncogenic mutations (Chernet & Levin 2013).finding0.822
  Shows that restoring bioelectric cohesion can override single-cell goals.
• Cancer can be normalized by reconnecting cells to the electrical network that harnesses them toward adaptive tissue homeostasis.claim0.815
  Proposes a non-toxic cancer treatment strategy.
• Disruptions in cells' ability to join into a cohesive information-processing network via oncogenes and other factors correlate with cancer developmentfinding0.805
  Empirical support for the cancer-as-cognitive-defect / cognitive light cone shrinkage hypothesis
• Disconnection from bioelectric tissue networks enables cancer progression; forced bioelectric coupling suppresses cancer phenotypes despite oncogenic mutations.finding0.801
• Cancer can be seen as a breakdown of the binding process that scales Selves, with cells reverting to unicellular goals.claim0.793
  Oncogene-induced gap junction closure shrinks the cognitive boundary of cells.
• If cancer represents a shrinkage of the cognitive light cone, then interventions that restore cellular participation in tissue-level information-processing networks should suppress cancer progression.hypothesis0.792
  Implicit predictive hypothesis from the cancer-as-cognitive-defect claim, with experimental implications for regenerative medicine