Examples

Analyses Inflexa actually produced

Real runs on published datasets. Every chart, table, and conclusion generated from the raw data, not mocked up for a website. Each one opens as a hosted report you can read without an account.

OncologyTCGA

How Genetic Ancestry Shapes Breast Cancer Biology

Multi-omics re-analysis of TCGA-BRCA (n = 1,084) and the RA-QA Arab cohort (n = 24), examining how genetic ancestry influences breast cancer across transcriptomic, immune, pathway, and genomic dimensions.

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InflammatoryGEO

IL-4, IL-13 & IL-33 Transcriptional Responses in Human Eosinophils and Mast Cells

Bulk RNA-seq re-analysis revealing cytokine-specific transcriptional programs and cell-type regulatory differences across type 2 inflammation.

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InflammatoryGEO

Genome-wide Dissection of IL-33 and IL-4Rα Blockade in HDM-driven Airway Inflammation

Transcriptomic analysis showing combination therapy produces a distinct molecular signature versus monotherapy in house dust mite–driven airway inflammation.

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InflammatoryGEO

Atopic Dermatitis Transcriptome Under Dupilumab and Cyclosporine

Comparative transcriptomic profiling of atopic dermatitis lesions treated with dupilumab versus cyclosporine, revealing divergent molecular responses to biologic and immunosuppressive therapy.

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NeurologyGEO

Pharmacogenomic Drug Screen in Mouse Cerebrocortical Cultures

Re-analysis of a pharmacogenomic screen uncovering analytical bias in the original methodology and revealing compound-specific transcriptional signatures in cortical neurons.

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NeurologyGEO

ATG7 Deficiency Reshapes Microglia Biology in Alzheimer’s Disease

Transcriptomic dissection of how ATG7 loss alters microglial identity, phagocytic programs, and neuroinflammatory signaling in an Alzheimer’s disease model.

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OncologyGEO

Fluoxetine in H460 Lung Cancer: SREBP-Driven Lipid Reprogramming Beyond the ATF4 Narrative

Re-analysis of fluoxetine-treated NSCLC cells revealing SREBF1/2-driven lipid biosynthesis and MYC post-translational suppression as the dominant mechanism, challenging the original ATF4-centric model.

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