Cybergenic
All findings

NRAS + RBM10

NRAS and RBM10 co-occurrence in thyroid cancer (MSK-IMPACT 50K)

Strengthened: held up under a stratified controlCo-occurrence · Evidence: pattern across patients, not yet tested within subtypes

DataMSK-IMPACT 50K (2026) · Thyroid cancer · 770 tumours · both altered in 9 (3.6 expected if independent)

Engine's conclusion

Strengthened. Significant, with a real effect in a consistent direction, and it still holds when tumours are compared only within the same tumour type (and within the same molecular subtype, wherever this cancer's subtypes are known in the data). No artifact check failed.

On the map: An early signal. Neither its statistical strength nor its expected value is high enough yet to count as a discovery.

Not called novel: a PubTator3 search finds 2 papers naming both NRAS and RBM10 in thyroid cancer in the title or abstract. See the PubTator3 search.

Statistical support48%Significance (FDR q)0.021Signal (x)5%Efficacy (y)0%

Signal (x) is the corrected significance on the map's scale, discounted from 11% to 5% because the cohort-composition confound is not yet controlled. Efficacy (y) is credibility times actionability.

Structure & site3D structure: AlphaFold

These genes are altered together more often than chance would predict.

Primary site

Thyroid

This finding's tumour type arises in the highlighted organ.

Drag to rotate. Dark marks the hotspot residues on the predicted fold. For a fuller read of this same model, open the interactive structure workbench for this protein on Nanoverse (a companion site we also run), which maps its binding pockets, per-region confidence, and the likely effect of a mutation.

NRASOncogeneIndirect

NRAS proto-oncogene GTPase

Oncogene: when altered it gets stuck ON and drives growth.

RAS isoform; no direct drug, targeted indirectly via MEK inhibitors.

Pathway
RTK to RAS to MAPK
Hotspots in 3D
G12 · G13 · Q61
Drives
Melanoma, AML, Thyroid
NRAS mutations in thyroid cancer →NRAS co-mutations by tumour type →Other findings with NRAS →

No structure profile is curated for this gene.

RBM10Gene

A human gene in this finding. Not in the curated driver set, so no structured profile is shown.

RBM10 co-mutations by tumour type →Other findings with RBM10 →

Anatomical figure from the EBI Expression Atlas anatomogram, and predicted structures from the AlphaFold Protein Structure Database (both CC-BY-4.0). A model shows the protein's healthy fold; a highlighted residue marks a recurrent cancer position, not a prediction of a specific mutation's effect.

Statistical evidence
Test p (raw)
0.00028
Effect (log₂ odds ratio)
1.9
Papers
115
Abstracts naming both
2
Trials
0
Contingency table: the source of the q770 tumours

The raw 2×2 the FDR q and log₂ odds ratio above were computed from. It is the immutable evidence the score re-derives from: every number on this page traces back to these four counts.

Gene stateRBM10 alteredRBM10 wild-type
NRAS altered995
NRAS wild-type18648

both 9 (expected 3.6 if independent) · NRAS-only 95 · RBM10-only 18 · neither 648

Sources
cBioPortal / MSK-IMPACT 50K (2026)Genome NexusOmniPath / Reactome / STRINGUCSC XenaOpen TargetsPubTator3NIH iCiteEurope PMCClinicalTrials.gov
Anytime-valid evidence (e-value)e = 3.4

Weak evidence. Below the α=0.05 reject threshold (e≥20). Unlike a single-look p, this stays valid under the engine's continuous re-testing.

Why it sits here on the map

Molecular-subtype certification is unresolved. Recorded lineage only. Within-lineage molecular subtype remains unresolved. The association remains visible, but does not qualify as a subtype-controlled discovery.

Opacity: novelty (display only)37%

The two axes are variables: signal (x) and efficacy (y = credibility × actionability). A point high on both lands in the frontier (top-right). A strong signal with low credibility sits low and to the right: statistically strong, not worth pursuing.

NRASOncogeneRBM10
HypothesisModel-generated hypothesis (not evidence)
Written by gpt-6-luna

A language model wrote this from the evidence listed below. It is annotation: the engine's verdict above comes only from the measured statistics, never from this text.

The NRAS–RBM10 co-occurrence across thyroid cancer patients is most likely driven by residual molecular-subtype or lineage composition: subgroups enriched for NRAS alterations may also be enriched for RBM10 alterations, without the two alterations necessarily occurring in the same tumour clone or cooperating.

Argument strength (model self-report)17%
After adversarial review17%
The argument
  1. 1The association is a credible population-level signal: it survives multiple-testing correction, and the reported lineage-stratified effect is positive. However, only 9 tumours carry both alterations, and the confidence interval is broad, so the effect estimate remains uncertain.E1E19
  2. 2Residual subtype composition is the leading explanation because lineage was recorded but molecular subtype remains unresolved. The absence of detected heterogeneity does not establish that the association is homogeneous across subtypes.E2
  3. 3The signal has not replicated across independent patient sources, making cohort-specific composition or a winner's-curse/data artifact an important competing explanation. Burden adjustment and FDR significance make a simple overall-mutation-burden explanation less compelling, but do not rule out other artifacts or confounding.E1E3E19
  4. 4The supplied thyroid-cancer paper abstracts discuss broader genomic progression or stage-specific drivers, but do not establish that NRAS and RBM10 were specifically studied as a pair. The reported co-mentions therefore do not support a pair-specific mechanism; that gap strengthens the claim that the relationship remains under-explored.E9E10E11
  5. 5This lead CONVERGES with the prior Cybergenic NRAS–RBM10 thyroid finding, which also favored residual subtype or lineage composition. It is also directionally consistent with the prior corpus's subtype/lineage explanations for other NRAS- or RBM10-containing pairs, but those findings are not independent replication of this thyroid association.E15E16E17E18
  6. 6There is no curated network edge linking the genes, and no supplied paper is shown to study their relationship. Thus the population co-occurrence does not earn a within-tumour cooperation or redundancy claim.E4E9E10E11
What would confirm or refute it

In an independent thyroid cancer cohort, obtain reliable molecular-subtype and lineage annotations and test the NRAS–RBM10 association within and across subtypes using a subtype-adjusted model; attenuation or disappearance after adjustment would support subtype composition as the explanation. To earn a within-tumour claim, additionally use single-cell or clonal genotyping to establish that both alterations occur in the same clone, followed by a functional co-dependency test.

Strongest competing explanation (model)

Ranked explanations: (1) residual molecular-subtype or lineage composition; (2) cohort-specific artifact or winner's curse, given the lack of cross-source replication; (3) a shared upstream driver; (4) deterministic co-amplification, for which no evidence of a shared amplicon is provided; (5) genuine within-tumour cooperation, which is unearned without pair-specific study and clonal or functional evidence. The significant adjusted association supports follow-up, but the small number of double-altered tumours and unresolved subtype confounding limit confidence. The supplied paper abstracts do not establish the NRAS–RBM10 relationship; this absence strengthens the under-explored interpretation rather than supplying a mechanism.

Adversarial review (second model pass)

Weakest link: The residual-subtype explanation is plausible but untested: subtype composition was not measured, and the observed within-lineage association could instead be cohort-specific or artifactual, with no independent replication.

Cross-cohort agreement (intra-snapshot)single source

Significant (after FDR correction) in one independent source of this tumour type so far. The engine records where a pattern is significant, not every source that could test it, so this calls for caution: a pattern selected from many tests tends to overstate its effect. It does not count against the pattern.

Evidence the argument cites

Model-written annotation, not a finding. The statistics it cites are real and are shown above; the argument connecting them is a hypothesis that needs wet-lab or clinical validation before it means anything.

Cite this finding
Permalink
https://cybergenic.im/findings/6829d849-9b35-4ebe-a4c3-7200b3c2249c
First seen
29 Sep 2026
Prediction registry
Locked 29 Sep 2026, row hash b254ba8d337e1516ee316d4a3219551d (not testable out of sample). How the registry works
BibTeX
@misc{cybergenic_6829d849,
  author       = {{Cybergenic}},
  title        = {{NRAS and RBM10 co-occurrence in thyroid cancer (MSK-IMPACT 50K)}},
  year         = {2026},
  howpublished = {\url{https://cybergenic.im/findings/6829d849-9b35-4ebe-a4c3-7200b3c2249c}},
  note         = {Research engine finding, first seen 2026-09-29; prediction locked 2026-09-29, registry row hash b254ba8d337e1516ee316d4a3219551d},
  month        = sep
}
See it on the live map Mutations in thyroid cancerNRAS and RBM10 in every cohort

Frontier alerts