AI-Orchestrated Analysis

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CORTEX+SYNAPSE

From raw data to defensible results. Cortex executes rigorous, multi-method analysis with full traceability. Synapse connects every finding to scored evidence from the literature and 20+ public databases.

Agentic Analysis

From question to insight: autonomous, multi-step, fully traceable

Upload your data, ask a question, and Cortex deploys a team of specialized AI agents, each an expert in a different analytical domain. They design a multi-step plan, execute each step with the right statistical method, and cross-validate findings against Synapse's evidence from hundreds of thousands of papers and 20+ public databases.

Every method is justified. Every finding is traceable. You stay in control at every checkpoint.

CORTEX+SYNAPSE
Identifying Research Gaps for Novel Insights

Read the paper and identify gaps in the authors' analysis. What can we focus on to uncover novel insights?

Used 22 tools

I now have a thorough picture of the paper and its analytical pipeline. Let me update working memory and compile the gap analysis.

Gap Analysis: Roelands et al. 2021 — What Was Left on the Table

Paper Summary

Roelands et al. characterized ancestry-associated transcriptomic differences in breast cancer across TCGA-BRCA (n=1,051; EA/AA/AsA) and a Qatar cohort (n=24; Arab/Asian). The central finding: African-American (AA) patients in the BasalMyo subtype have worse overall survival, lower immune cytolytic response (ICR), higher AMPK signaling, and reduced immunoediting — suggesting metabolic reprogramming as a driver of immune evasion. The analysis pipeline spans 87 R scripts covering ICR clustering, IMS subtyping, ssGSEA, survival analysis, mutational load, and an XGBoost prediction model.

Gap 1 — Survival Analysis Is Unadjusted

What they did: Kaplan-Meier curves and univariate Cox regression stratified by ancestry × IMS subtype. Stage-stratified forest plots were generated (C41), but the hardcoded HR values (HR=2.39 for all BasalMyo AA vs EA, p=0.020) come from a univariate model only.

What's missing: No multivariate Cox model adjusting simultaneously for tumor stage, age at diagnosis, and ICR cluster. The cBioPortal data contains AJCC stage, age, and mutation count for all BRCA samples. The stage distribution difference between AA and EA in BasalMyo (C54 script) is acknowledged but never statistically controlled. The survival disparity could be partially or fully explained by stage imbalance — this is unresolved.

What to do: Fit a multivariate Cox model: OS ~ ancestry + stage + age + ICR_cluster within BasalMyo. Test the ancestry × ICR interaction term. This directly tests whether the immune microenvironment mediates the ancestry–survival relationship.

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Interactive Reports

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Chat with Cortex to build interactive reports from your analysis results. Describe the story you want to tell: survival curves, feature importance, mediation diagrams, and the AI assembles a polished, navigable report in minutes.

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CORTEX
Summary
Study Design
Arab Cohort
Differential Expression
Pathways
Dose-Response
Immune
TF Activity
Pathway Networks
Genomics
Survival
Synthesis
Limitations

Generated by Inflexa on February 20, 2026 at 9:00 PM

Survival & Prognosis

HR=1.05p=0.84
Total Effect (Null)
1.2%(2/167)
Signature Overlap
0.652
EA C-index
37–48%
TF SHAP Share
HR=1.05p = 0.837

Total ancestry effect on survival is null

After adjusting for subtype, age, and stage, African ancestry does not confer a survival advantage or disadvantage (OS endpoint, n=957, 137 events). Breast cancer survival disparities are largely explained by clinical factors, not ancestry-specific molecular features.

SHAP Feature Importance: Ancestry-Specific Survival Models

Top 20 features by mean |SHAP| value for each ancestry-specific CoxPH model. Colors indicate feature group.

TF activity
Pathway
Immune
Checkpoint
Genomic

EA Model (C-index = 0.652)

NT5E
0.234
PAX7
0.173
Macrophages
0.146
(HM) Estrogen resp.
0.134
EHF
0.113
FOXA2
0.106
PTF1A
0.102
MSX2
0.101
LAG3
0.099
(HM) KRAS sig. down
0.098
GFI1
0.092
(HM) UV resp. up
0.083
Neutrophils
0.082
HDAC5
0.081

Mean |SHAP|

AA Model (C-index = 0.408)

(HM) PI3K Akt mTOR
0.510
Th2 cells
0.364
LAG3
0.290
KDM5C
0.252
GRHL2
0.215
HEY1
0.154
FOXP1
0.154
(IPA) ERK MAPK Sig.
0.151
(HM) Angiogenesis
0.133
(HM) KRAS sig. down
0.130
iDC
0.130
(HM) Reactive O₂
0.129
ADORA2A
0.127
KCNIP3
0.121

Mean |SHAP|

AA model is dominated by PI3K-Akt-mTOR (SHAP=0.510), while EA model spreads importance across TF and checkpoint features. NT5E (CD73) is the top EA feature — consistent with the adenosine immunosuppression pathway identified in the checkpoint analysis.

Feature Group SHAP Contributions

TF activity
Checkpoint
Immune
Pathway
Genomic
Combined
EA
AA
BasalMyo

TF activity contributes 37\u201348% of SHAP importance across all models, peaking in BasalMyo (47.6%). This layer was entirely absent from the original paper.

Causal Mediation: Ancestry → Survival

TReg *
-0.089
PD-1 (PDCD1)
-0.083
OX40 (TNFRSF4)
-0.063
B cells
-0.061
DNA repair
-0.039
ICR genes
-0.031
Mast cells
0.018
PI3K-Akt-mTOR
0.017
Th2 cells
0.006
Wnt beta-catenin
-0.006
AMPK Signaling
-0.005
Th17 cells
0.002

Indirect Effect (Δ log-HR)

TReg is the sole significant mediator (indirect = −0.089, p=0.030) via suppression. Green = p<0.05, Yellow = p<0.10.

Target Intelligence

Everything known about your target. One dossier.

Synapse reads thousands of papers and cross-references 20+ public databases to build comprehensive target dossiers. Druggability scores, disease associations, drug interactions, safety signals, clinical trial landscapes, all structured, scored, and continuously updated.

Every data point traced to its source. Every claim scored for evidence strength.

SYNAPSE
GLP1Rgene
Decision
Executive Summary
Drug Interactions
Indications
Clinical Development
Safety Profile
Reference
Disease Associations
Molecular Interactions
Biomarker Potential
Genetic Alterations
Resistance Landscape
Pathway Context
Interaction Network
Key Papers
Analytics
Contradicted Evidence
Evidence Timeline
Translational Chain
Additional Evidence
Possibly Related Trials
Executive Summary

GLP1R Target Assessment

Target

GLP1R

HGNC:4324 · gene

Top indications: Hypertension, Coronary Artery Disease, Obesity +17 more

Modality

Unknown

Precedent: DULAGLUTIDE, LIRAGLUTIDE, EXENATIDE

+14 more

Safety Signal

2 Class Liabilities

0/0 tissues > 1000 TPM

Key Findings
2 class liabilities (cns, gi)
251Papers
1301Evidence Items
317Clinical Trials
ClinicalHighest Tier
317 trialshuman dataEvidence
Evidence Distribution by Category
Biomarkers
0.48
Genetic
0.52
Biology
0.59
Drugs
1
Diseases
1
00.20.40.60.81
Drug Interactions

Drug Interactions (309)

CSV
DrugScorePredicatesSourcesPap.HC
EXENATIDE
1.00
bindingcausal negativecausal positiveincreased in
chembldgidbpharmgkbliterature
29×
TIRZEPATIDE
1.00
bindingcausal negativecausal positiveresistance
chembldgidbliterature
24
SEMAGLUTIDE
1.00
bindingcausal positivemetabolicresistance
chembldgidbliterature
9
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Runs multi-track, multi-step analysis on your omics, cheminformatics, and imaging data with full provenance. Every finding traced to source.

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Synthesizes scored evidence from 20+ databases and the full scientific literature into target dossiers, disease landscapes, and safety profiles.

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Your storage, your data (BYOS)
Full provenance for every result
Literature-grounded methods
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