Contradiction Registry

Cross-page index of identified tensions, contradictions, and checked-but-clear paper pairs in the wiki. Each entry has a stable ID, links the two pages or sources in tension, states the overlap topic, the assessment, the resolution status, and cross-references to related tensions.

Resolution statuses:

  • resolved — the tension has a documented resolution in the concept page
  • flagged_unresolved — the tension is identified but not yet resolved; requires scholar attention
  • scholar_pending — the tension was identified by a bridge agent; awaiting human confirmation
  • not_applicable — no material conflict found; listed for coverage documentation

Assessment types:

  • contradiction — two sources make directly opposing claims on the same topic
  • conditional_difference — differences are explainable by context (methodology, resolution, tissue type, time period)
  • no_material_conflict — pair was checked, no tension found

Resolved or Conditionally Resolved

IDPaper/Source APaper/Source BOverlap TopicAssessmentResolutionCross-refs
CN-001Graham & Sottoriva (2017) — 1/f testBozic et al. (2016) — δ-generalized spectrum1/f as selection test vs. joint hypothesis (neutrality + pure birth)conditional_differenceResolved: Nested models. 1/f is the δ=0 special case of the Bozic 2016 spectrum. Two-step procedure: estimate δ independently, then test for selection against δ-calibrated null. Graham’s ~30% neutrality estimate is a lower bound.neutral-evolution, passenger-mutation
CN-002Nowell (1976) — sequential sweepsGreaves & Maley (2012) — clonal interferenceWhether clonal evolution proceeds via sequential sweeps or complex dynamics with interferenceconditional_differenceResolved: Resolution-dependent descriptions. Nowell’s karyotypic-resolution data shows major sweeps; Greaves’ nucleotide-resolution data shows coexistence. Not falsification — refinement.clonal-evolution
CN-003Nowell (1976) — continuous selectionTurajlic et al. (2019) — intermittent selectionWhether selection operates continuously or intermittently during tumor evolutionconditional_differenceResolved: Complementary timescale perspectives. Nowell describes net trajectory over decades; Turajlic describes microdynamics at any moment. Selection is episodic; neutral drift dominates between events.clonal-evolution, neutral-evolution
CN-004Nowell (1976) — acquired instability onlyPCAWG Consortium (2020) — germline contributionsWhether variation fueling clonal evolution is purely acquired somatic or also germline-shapedconditional_differenceResolved: Complementary sources. Germline variants set baseline mutational propensity; acquired instability accelerates above baseline. Both feed the evolutionary process.clonal-evolution
CN-005Gerstung et al. (2020) — ~40% spectrum shiftsGraham & Sottoriva (2017) — constant-rate clockConstancy of neutral mutation rate during tumor evolution; implications for molecular clock precisionconditional_differenceResolved: Constant-rate assumption holds in ~60% of samples. For the ~40% with shifts, clock precision is reduced, not invalidated. Rate changes can be calibrated over separate evolutionary epochs.molecular-clock
CN-006Graham & Sottoriva (2017) — ~30% no subclonal selectionGerstung et al. (2020) — fourfold driver diversification in late stagesPrevalence of detectable subclonal selection in cancer genomesconditional_differenceResolved: Scope difference. Graham’s 1/f test detects only SNV selection caught mid-expansion; Gerstung captures all mutation types across larger cohort. ~30% is a lower bound.neutral-evolution
CN-007Burns et al. (2013, 2015) — APOBEC3B primary mutatorPetljak et al. (2022) — APOBEC3A main driverWhich APOBEC3 paralog drives somatic mutagenesis in cancerconditional_differenceResolved: Stronger evidence supersedes weaker. Burns used correlative evidence (expression, in vitro activity); Petljak used causal evidence (CRISPR knockout, 251 clonal WGS lines). APOBEC3A is main driver; APOBEC3B is minor contributor that can restrain APOBEC3A. corpus_gap: true (Burns papers not in wiki)APOBEC-mutagenesis
CN-008Turajlic et al. (2019) — 1/f² neutral nullBozic et al. (2016) — δ-calibrated spectrumThe 1/f² distribution as the neutral null model in a growing populationconditional_differenceResolved: Turajlic’s null is correct for δ≈0 (fast growth). Bozic provides the δ-calibrated generalization. Both recommend same empirical approach: fit neutral expectation to low-frequency tail, test for excess at high frequencies.neutral-evolution
CN-009Sottoriva et al. (2015) — Big Bang (neutral-only colorectal)Turajlic et al. (2019) — four-mode taxonomy (neutral is one mode)Whether neutral dynamics account for entire observable tumor evolutionary historyconditional_differenceResolved: Domain-specific, not contradictory. Sottoriva’s finding is empirical (15/15 colorectal tumors, 349 glands). Turajlic’s taxonomy is pan-cancer generalization. Both can be true simultaneously.neutral-evolution

Checked — No Material Conflict

IDPaper/Source APaper/Source BOverlap TopicAssessment
CN-010Nik-Zainal et al. (2012) — APOBEC late in breast cancerGerstung et al. (2020) — ~40% spectrum shifts pan-cancerTemporal dynamics of mutational signature activityno_material_conflict — both find signatures change over time; Nik-Zainal specific to breast/APOBEC, Gerstung pan-cancer quantification
CN-011Tarabichi et al. (2021) — CCF detection floor ~0.05-0.10Gerstung et al. (2020) — subclonal architecture below ~0.1 CCF not capturedDetection limits for subclonal mutationsno_material_conflict — both converge on ~0.1 CCF as practical floor from different starting points (sequencing sensitivity vs. evolutionary dynamics)
CN-012Greaves & Maley (2012) — four-mode taxonomy (informal)Turajlic et al. (2019) — four-mode taxonomy (formal)Classification of evolutionary patterns in cancerno_material_conflict — Greaves acknowledges clonal interference, parallel expansions, stasis without formalizing taxonomy; Turajlic formalizes the same patterns
CN-013McGranahan & Swanton (2017) — truncal targetingPCAWG Consortium (2020) — pan-cancer driver landscapeClonal vs. subclonal driver therapeutic targetabilityno_material_conflict — McGranahan makes the therapeutic argument; PCAWG provides the pan-cancer empirical substrate (91% have ≥1 driver, chromothripsis clonal and driver-enriched)
CN-014Turajlic et al. (2019) — bulk sequencing time bias (~7 doublings)PCAWG Consortium (2020) — chromothripsis predominantly clonal (early)Whether early clonal events are genuinely early or artifacts of bulk sequencing detection biasno_material_conflict — Turajlic warns of the bias; PCAWG chromothripsis findings are consistent with genuinely early timing (22.3% pan-cancer, specific tissue patterns, driver enrichment). Both agree early events are disproportionately detected.

Flagged Unresolved

None yet. All tensions surfaced by bridge dispatches (2026-06-27) have been resolved or assessed as conditional differences with documented resolutions.

Scholar Pending

All CN-001 through CN-009 have scholar_confirmation: pending — the bridge synthesis agent identified and resolved these tensions, but the resolutions have not been independently confirmed by a human reader. Once confirmed, update resolution_status from scholar_pending to resolved and remove from this section.