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 pageflagged_unresolved— the tension is identified but not yet resolved; requires scholar attentionscholar_pending— the tension was identified by a bridge agent; awaiting human confirmationnot_applicable— no material conflict found; listed for coverage documentation
Assessment types:
contradiction— two sources make directly opposing claims on the same topicconditional_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
| ID | Paper/Source A | Paper/Source B | Overlap Topic | Assessment | Resolution | Cross-refs |
|---|---|---|---|---|---|---|
| CN-001 | Graham & Sottoriva (2017) — 1/f test | Bozic et al. (2016) — δ-generalized spectrum | 1/f as selection test vs. joint hypothesis (neutrality + pure birth) | conditional_difference | Resolved: 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-002 | Nowell (1976) — sequential sweeps | Greaves & Maley (2012) — clonal interference | Whether clonal evolution proceeds via sequential sweeps or complex dynamics with interference | conditional_difference | Resolved: Resolution-dependent descriptions. Nowell’s karyotypic-resolution data shows major sweeps; Greaves’ nucleotide-resolution data shows coexistence. Not falsification — refinement. | clonal-evolution |
| CN-003 | Nowell (1976) — continuous selection | Turajlic et al. (2019) — intermittent selection | Whether selection operates continuously or intermittently during tumor evolution | conditional_difference | Resolved: 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-004 | Nowell (1976) — acquired instability only | PCAWG Consortium (2020) — germline contributions | Whether variation fueling clonal evolution is purely acquired somatic or also germline-shaped | conditional_difference | Resolved: Complementary sources. Germline variants set baseline mutational propensity; acquired instability accelerates above baseline. Both feed the evolutionary process. | clonal-evolution |
| CN-005 | Gerstung et al. (2020) — ~40% spectrum shifts | Graham & Sottoriva (2017) — constant-rate clock | Constancy of neutral mutation rate during tumor evolution; implications for molecular clock precision | conditional_difference | Resolved: 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-006 | Graham & Sottoriva (2017) — ~30% no subclonal selection | Gerstung et al. (2020) — fourfold driver diversification in late stages | Prevalence of detectable subclonal selection in cancer genomes | conditional_difference | Resolved: 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-007 | Burns et al. (2013, 2015) — APOBEC3B primary mutator | Petljak et al. (2022) — APOBEC3A main driver | Which APOBEC3 paralog drives somatic mutagenesis in cancer | conditional_difference | Resolved: 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-008 | Turajlic et al. (2019) — 1/f² neutral null | Bozic et al. (2016) — δ-calibrated spectrum | The 1/f² distribution as the neutral null model in a growing population | conditional_difference | Resolved: 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-009 | Sottoriva 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 history | conditional_difference | Resolved: 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
| ID | Paper/Source A | Paper/Source B | Overlap Topic | Assessment |
|---|---|---|---|---|
| CN-010 | Nik-Zainal et al. (2012) — APOBEC late in breast cancer | Gerstung et al. (2020) — ~40% spectrum shifts pan-cancer | Temporal dynamics of mutational signature activity | no_material_conflict — both find signatures change over time; Nik-Zainal specific to breast/APOBEC, Gerstung pan-cancer quantification |
| CN-011 | Tarabichi et al. (2021) — CCF detection floor ~0.05-0.10 | Gerstung et al. (2020) — subclonal architecture below ~0.1 CCF not captured | Detection limits for subclonal mutations | no_material_conflict — both converge on ~0.1 CCF as practical floor from different starting points (sequencing sensitivity vs. evolutionary dynamics) |
| CN-012 | Greaves & Maley (2012) — four-mode taxonomy (informal) | Turajlic et al. (2019) — four-mode taxonomy (formal) | Classification of evolutionary patterns in cancer | no_material_conflict — Greaves acknowledges clonal interference, parallel expansions, stasis without formalizing taxonomy; Turajlic formalizes the same patterns |
| CN-013 | McGranahan & Swanton (2017) — truncal targeting | PCAWG Consortium (2020) — pan-cancer driver landscape | Clonal vs. subclonal driver therapeutic targetability | no_material_conflict — McGranahan makes the therapeutic argument; PCAWG provides the pan-cancer empirical substrate (91% have ≥1 driver, chromothripsis clonal and driver-enriched) |
| CN-014 | Turajlic 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 bias | no_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.