Q-omics · data dictionary
Data Dictionary
What data Q-omics has, in what combinations, for which cancer types — and what it honestly doesn't have. Exact API parameter tokens for calling this data are in the Parameter Specification (Part II, below).
1Platform & data sources
Q-omics is a pre-computed, consensus-based cancer multi-omics platform — most results are validated across many sampling combinations before they're ever queried, not computed fresh per request (§4 explains why that matters).
| Domain | Source | Scale | Provides |
|---|---|---|---|
| Patient — tissue | TCGA + GENIE / GDC portal | 34 cancer types, ~11,000 patients | RNA, mutation, RPPA (TCGA only), clinical drug response, GO function scores |
| Patient — proteomics | CPTAC / PDC portal | 10 cancer types, ~1,067 patients | Mass-spec proteome + phosphoproteome. Largely overlaps TCGA — enables genomic↔proteomic integration |
| Patient — infiltrating cells | xCell | 33 lineages | Immune/stromal cell enrichment scores |
| Cell line | CCLE / DepMap | 20 lineages, ~1,000 cell lines | RNA, mutation, RPPA, mass-spec protein, CRISPR/shRNA dependency, GO scores |
| Cell line — drug response | GDSC / DepMap Sanger | ~561 compounds | Sensitivity (-log10 GI50) |
| Drug-induced expression | Connectivity Map (L1000) | 15 drugs | Expression change after drug treatment |
Two more domains sit outside this table because they use their own cohort system rather than TCGA/CCLE/CPTAC lineage codes: Pembrolizumab (6 clinical-trial cohorts, J-codes — §7) and DIG (NCI60 cell lines, 13 lineages — §5/§7).
2Data types
Patient / tissue domain
| Type | Meaning | Scale | Example entity |
|---|---|---|---|
| RNA expression | mRNA abundance in tumors | ~38K entities × 34 lineages | TP53, EGFR |
| Protein (RPPA) | Targeted protein/phosphoprotein via antibody panel | ~275 entities × 32 lineages | AKT_pT308 |
| Protein abundance (mass-spec) | Unbiased global proteome + phosphosites | >50K entities × 10 CPTAC lineages only | A2M_S1402 (phosphosite) |
| Somatic mutation | Whether a gene is mutated in a patient | ~21K entities × 34 lineages | KRAS, BRAF |
| Patient drug response | Responder/non-responder per RECIST | 31 drugs (30 + Pembrolizumab) | Cisplatin |
| Infiltrating cells | Immune/stromal enrichment (xCell) | 64 cell types × 33 lineages | CD8+ T-cells |
| GO function (RNA / Protein) | Pathway activity score, derived from RNA or mass-spec | ~7,200 processes | DNA repair |
Cell-line domain
| Type | Meaning | Scale | Example entity |
|---|---|---|---|
| RNA expression | mRNA abundance in cell lines | ~19K entities × 20 lineages | MYC |
| Protein (RPPA) | Antibody-panel protein/phospho | ~214 entities × 20 lineages | EGFR_pY1068 |
| Protein abundance (mass-spec) | Mass-spec, mapped to gene names | ~8.4K entities × 20 lineages | AKT1 |
| Somatic mutation | Mutation presence | ~19K entities | KRAS, PIK3CA |
| Drug response | -log10(GI50) — higher = more sensitive (less drug needed) | ~561 compounds | Erlotinib |
| CRISPR | Knockout dependency score — higher = stronger growth inhibition on disruption | ~18K genes | TP53 |
| shRNA | Knockdown dependency score, same scale sense as CRISPR | ~17K genes | MYC |
| Methylation cell-line only | DNA methylation β-value per genomic region, not per gene | ~19,867 features × 713 cell lines / 20 lineages | MGMT_10_129466683_129467683 |
| GO function (RNA / Protein) | Pathway activity score | — | — |
Methylation entities are genomic regions, not genes
Every other data type's entity is a gene symbol (TP53). Methylation's entity is a per-region feature named GENE_chr_start_end, and one gene maps to many features — a bare gene symbol resolves to nothing. Query methylation with the gene as the open axis (get the list of that gene's features), then pin a specific feature from the results for a plot. Also: methylation is cell-line domain only, and only inside Association/Correlation (§10 has the full limitation).
3RPPA vs. mass-spec protein
Two genuinely different protein data types exist side by side — mixing them up is the single most common protein-data mistake to guard against in client code.
| RPPA (Protein) | Mass-spec (Protein_ms) | |
|---|---|---|
| Technology | Antibody-based, targeted | Mass spectrometry, unbiased |
| Coverage | ~275–292 antibodies (curated panel) | >50K proteins + phosphosites |
| Tissue source | TCGA RPPA, 32 lineages | CPTAC, 10 lineages only |
| Cell source | CCLE RPPA, 20 lineages | CCLE MS, 20 lineages |
| Lineage codes | Same codes as everything else (LUAD, BRCA…) | Same codes — no "CP-" prefix |
| Best for | "Is AKT phosphorylated here?" (targeted, hypothesis-driven) | "Which proteins are differentially expressed?" (unbiased discovery) |
4The consensus mechanism
The single most distinctive thing about how Q-omics results differ from a raw statistical query.
Most results are pre-computed across many sampling combinations (stage, gender, sample split, time period — the exact factor set varies by analysis) before being stored. A result surfaces because it held up across many arbitrary re-splits of the data, not because it happened to be significant on one particular split.
Sampling consensus (technical) — S_Cscore
How consistently a result holds when the analytical conditions are perturbed. Count of sampling combinations where it stays significant.
Lineage consensus (biological) — L_Cscore
Whether a result is confined to one cancer type or reproduced across several. Count of cancer types with a consistent result.
High S_Cscore → not a statistical artifact of one arbitrary split. High L_Cscore → broad pan-cancer biology rather than a lineage-specific quirk. The two together let a consumer prioritize hits that are both reproducible and biologically general. Exception: Correlation and DIG rely on direct statistical metrics — no consensus sampling behind those two.
Two data-access tiers follow from this: pre-computed results (sampling-consensus validated, fast, what List/browse endpoints return) vs. on-the-fly computation (any valid entity × lineage pair the raw data supports, whether or not a significant pre-computed result exists — what Plot endpoints compute live). The only hard wall is whether the entity exists in the underlying data files at all.
5Analysis catalog
Nine analysis families. For each: what it answers, which domain, and the output-format rule — the single biggest thing to get right when building against this data, since List and Plot pull from genuinely different sources (§4).
1 — Survival
Whether a molecular feature associates with prognosis, measured as Kaplan-Meier AUC (1 = full survival, 0 = immediate non-survival) rather than a bare p-value. Tissue only. Up to 216 sampling combinations per gene. List shows pre-validated hits only — every row already cleared the significance bar.
2a — Normal vs. Tumor
Matched-pair differential expression, tissue only, 18 lineages with matched normal samples (BLCA, BRCA, CHOL, COAD, ESCA, HNSC, KICH, KIRC, KIRP, LIHC, LUAD, LUSC, PAAD, PRAD, READ, STAD, THCA, UCEC). Mutation and RPPA have no NT table — not available for this analysis at all.
2b — Drug response (Responder vs. non-responder)
RECIST-based responder classification against 30 patient drugs (§7 has the per-drug lineage table). Never confuse with Association — patient drug response is exclusively a Difference-analysis input; "mutations associated with Cisplatin resistance" routes through cell-domain Association using CCLE drug response instead, a different dataset entirely from the clinical RECIST one.
3a / 3b — Association & Correlation
Same infrastructure, different questions. Association tests both directions independently (X-score / Y-score, two p-values) and degrades gracefully to a hit table when an entity is left open. Correlation is always a scatter plot — both entities and a specific lineage are required, no open-axis table form exists. Both support tissue and cell domains with materially different valid-combination rules (§6).
4 — Pembrolizumab response
Same Responder/Non-responder structure as 2b, but its own clinical-trial cohort system (J0–J5, not TCGA/CCLE codes) and restricted to RNA expression / infiltrating cells as the paired data type. The only checkpoint inhibitor with cohort data in the platform (§10).
5a / 5b — Synthetic lethality
Gene pairs where joint disruption is more damaging to the cancer cell than either alone — the BRCA/PARP-inhibitor logic, generalized. Cell (5a): RNA × CRISPR/shRNA only. Patient (5b): D1/D2 must share the same type (RNA×RNA, MS×MS, or immune-cell×immune-cell) — but the List form only ever has RNA×RNA data (the pre-computed SL survival table stores RNA only); MS and immune-cell pairs only return something when both entities are pinned as a Plot.
6 — DIG (drug-induced gene expression)
Expression fold-change at 4 dose×time conditions (low/high × 6h/24h) for 15 specific drugs against NCI60 cell lines. Cell domain only. Only ~12–34% of genes have DIG data (2,800–8,500 of ~38,000, varying by drug) — worth flagging since it's easy to assume full gene coverage by analogy to RNA expression.
7 — Pan-cancer profile
One entity's distribution across every lineage at once, box-plot-per-cancer-type. Requires a specific entity — there's no pan-cancer profile without one. Not the same thing as an ALL-lineage List (which aggregates significant hits across lineages, a different question and a different output shape).
9 — Neoantigen analysis
More precisely: proteogenomic tumor-antigen discovery. Not strict neoantigen prediction (no mutation→MHC-binding→peptide pipeline) — instead, which mass-spec-quantified proteins are over-expressed in tumor-vs-normal or mutant-vs-wildtype, as candidate immunotherapy targets. Mass-spec protein abundance only, CPTAC tissue only, and lineage is ALL only — no per-lineage neoantigen queries in the current schema.
6Valid data-type combinations
Association and Correlation each have different valid-pair rules per domain — this is the table to check before assuming a combination exists.
Tissue Association (37 valid pairs)
| D1 \ D2 | RNA | Mut | MS | RPPA | IC | GO(R) | GO(P) |
|---|---|---|---|---|---|---|---|
| RNA | ✓ | ✓ | ✓ | ✓ | ✓ | ✓ | ✓ |
| Mutation | ✓ | – | ✓ | ✓ | ✓ | – | – |
| MS | ✓ | ✓ | ✓ | – | ✓ | ✓ | ✓ |
| RPPA | ✓ | ✓ | – | ✓ | ✓ | ✓ | – |
| IC | ✓ | ✓ | ✓ | ✓ | ✓ | ✓ | ✓ |
| GO(RNA) | ✓ | – | ✓ | ✓ | ✓ | – | – |
| GO(Protein) | ✓ | – | ✓ | ✓ | ✓ | – | – |
Excluded: Mutation×Mutation, RPPA×MS (either direction), RPPA×GO(Protein) as D1, GO×GO, Mutation×GO (either direction).
Cell Association
Wider than tissue — adds Drug response, CRISPR, shRNA, and cell-line-only Methylation. Rule of thumb: everything is valid except GO×GO (4 combinations) and Mutation×GO (4, either direction). Self-pairs allowed for every continuous type; Mutation×Mutation is allowed only as a Table (both entities null — a binary×binary box-plot has no meaning).
Tissue Correlation (29 valid pairs)
| D1 \ D2 | RNA | MS | RPPA | IC | GO(R) | GO(P) |
|---|---|---|---|---|---|---|
| RNA | ✓ | ✓ | ✓ | ✓ | ✓ | ✓ |
| MS | ✓ | ✓ | – | ✓ | ✓ | ✓ |
| RPPA | ✓ | – | ✓ | ✓ | ✓ | – |
| IC | ✓ | ✓ | ✓ | ✓ | ✓ | ✓ |
| GO(RNA) | ✓ | ✓ | ✓ | ✓ | – | – |
| GO(Protein) | ✓ | ✓ | ✓ | ✓ | – | – |
No Mutation (binary, not continuous — Correlation needs two continuous values). Excluded: RPPA×MS (either direction), RPPA×GO(Protein) as D1, GO×GO.
Cell Correlation
RNA, MS, RPPA, Drug response, CRISPR, shRNA, cell-line Methylation, GO(R), GO(P) — 9 types, everything valid except the 4 GO×GO pairs. Mutation excluded (binary); infiltrating cells absent from the cell domain entirely.
7Lineage coverage
Coverage is not uniform across lineages — it depends on the (data type, analysis) pair. This is the exhaustive set, not a suggestion list; there is no data outside it.
Tissue — by data type × analysis
| D1 | Paired with | Lineages |
|---|---|---|
| RNA | most tissue analyses | All 34 TCGA lineages |
| RNA / Mutation / Infiltrating cells / GO(RNA) | Normal vs Tumor | 18: BLCA, BRCA, CHOL, COAD, ESCA, HNSC, KICH, KIRC, KIRP, LIHC, LUAD, LUSC, PAAD, PRAD, READ, STAD, THCA, UCEC |
| RNA / Mutation / Infiltrating cells | Patient drug response | 21: ALL, BLCA, BRCA, CESC, COAD, ESCA, HNSC, LGG, LIHC, LUAD, LUSC, MESO, PAAD, PRAD, READ, SARC, SKCM, STAD, TGCT, UCEC, UCS |
| RNA / Mutation / IC / GO(RNA) | Protein (RPPA) | All TCGA except LAML |
| RNA / Mutation / IC / GO(RNA) | Mass-spec protein / GO(Protein) | 10 CPTAC: BRCA, CCRCC, COAD, GBM, HNSC, LSCC, LUAD, OV, PDAC, UCEC |
| Mass-spec protein / GO(Protein) | Survival | 9: CCRCC, COAD, GBM, HNSC, LSCC, LUAD, OV, PDAC, UCEC |
| Mass-spec protein / GO(Protein) | Normal vs Tumor | 7: CCRCC, COAD, HNSC, LSCC, LUAD, OV, PDAC |
| Patient drug response (30 drugs) | RNA / Infiltrating cells / Mutation only | Same 21-lineage pool as above (per-drug detail below) |
| Patient drug response (Pembrolizumab) | all valid combinations | J0–J5 cohort codes — not TCGA lineages at all |
Survival with RNA/Mutation/IC/RPPA/GO(RNA) — any of the 34 TCGA lineages, or ALL. Survival with mass-spec/GO(Protein) — the same 9-lineage CPTAC pool as above.
Cell line — by domain
| Context | Lineages |
|---|---|
| DIG (treated drug) | 10: ALL, BREAST, CNS, LARGE_INTESTINE, BLOOD_Leukemia, SKIN, LUNG_NSCLC_LUAD, LUNG_NSCLC_Others, OVARY, PROSTATE, KIDNEY |
| Everything else (cell domain) | 20: all CCLE lineages (ALL, BLOOD_Leukemia, LUNG_NSCLC_LUAD, CNS, LARGE_INTESTINE, SKIN, BREAST, OVARY, PANCREAS, OESOPHAGUS, STOMACH, BLOOD_Lymphoma, LUNG_SCLC, UPPER_AERODIGESTIVE_TRACT, URINARY_TRACT, SOFT_TISSUE, BONE, KIDNEY, BLOOD_Myeloma, LUNG_NSCLC_LUSC, LIVER) |
Per-drug lineage availability — patient drug response (30 drugs)
| Drug | Lineages | Drug | Lineages |
|---|---|---|---|
| 5-Fluorouracil | ALL, BRCA, COAD, PAAD, READ, STAD | Ipilimumab | SKCM |
| Anastrozole | BRCA | Irinotecan | COAD |
| Bevacizumab | ALL, COAD, LGG | Leucovorin | ALL, COAD, READ, STAD |
| Bicalutamide | PRAD | Leuprolide | PRAD |
| Bleomycin | ALL, TGCT | Lomustine | LGG |
| Capecitabine | ALL, COAD, ESCA, STAD | Oxaliplatin | ALL, COAD, READ, STAD |
| Carboplatin | ALL, BLCA, HNSC, LUAD, LUSC, UCEC, UCS | Paclitaxel | ALL, BRCA, CESC, HNSC, LUAD, UCEC, UCS |
| Cetuximab | ALL, HNSC | Pemetrexed | ALL, LUAD, MESO |
| Cisplatin | ALL, BLCA, CESC, ESCA, HNSC, LUAD, LUSC, MESO, STAD, TGCT | Sorafenib | LIHC |
| Cyclophosphamide | BRCA | Tamoxifen | BRCA |
| Dacarbazine | SKCM | Temozolomide | LGG |
| Docetaxel | ALL, BRCA, LUSC, SARC | Trastuzumab | BRCA |
| Doxorubicin | ALL, BLCA, BRCA, SARC | Vinorelbine | ALL, LUAD, LUSC |
| Epirubicin | ALL, BRCA, STAD | Etoposide | ALL, LUAD, STAD, TGCT |
| Gemcitabine | ALL, BLCA, LUSC, PAAD, SARC | Ifosfamide | SARC |
A lineage requested that isn't in a given drug's list has no data for that drug — the closest available lineage should be substituted rather than falling back to ALL, which understates specificity.
8Clinical-term mapping
Canonical stage/age bucketing (AJCC / WHO conventions) — useful reference for any client building a clinical-stratification UI on top of the API.
| Term | Mapping |
|---|---|
| Early stage | Stage I + II → [1, 2] |
| Late / advanced stage | Stage III + IV → [3, 4] |
| Young / younger patients | Age [0, 44] |
| Middle-aged | Age [45, 64] |
| Older / elderly / senior | Age [65, 200] |
| "Patients in their 60s" (and other decades) | Decade-specific, e.g. [60, 69] |
9Entity coverage at a glance
| Entity class | Count |
|---|---|
| Genes | ~38,000 (essentially all protein-coding genes) |
| Cell-line drugs | ~560 compounds |
| Patient drugs | 31 (30 chemo/targeted + Pembrolizumab) |
| DIG drugs | 15 |
| Immune cell types | 64 |
| Proteins (mass-spec) | ~141,000 |
| GO biological processes | ~7,200 |
10Known limitations
What Q-omics doesn't do, stated plainly — coverage gaps worth checking before assuming broader support than exists.
No patient lifestyle, comorbidity, or viral-infection-status data
Q-omics cannot stratify patients by smoking history, diet, BMI, prior treatment regimen, comorbid conditions (e.g. diabetes), or viral-infection status (HBV/HCV/HPV-positive) — this metadata isn't collected. The line is between a clinical attribute used to group patients (unsupported) and a molecular/pathway feature to measure (supported): a GO pathway like "cellular response to glucose starvation," or a viral gene's own expression (HPV E6), works fine; grouping patients by "diabetic" or "HPV-positive" doesn't.
Methylation: cell-line only, Association/Correlation only
No tissue methylation at all. No methylation survival, Normal-vs-Tumor, Difference, synthetic-lethality, DIG, or pan-cancer profile — only cell-line Association and Correlation. See §2 for the entity-naming gotcha (a methylation entity is a genomic region, not a gene).
Only Pembrolizumab has immunotherapy cohort data
Nivolumab, Atezolizumab, Durvalumab, Avelumab, Ipilimumab, Tremelimumab, Cemiplimab — none of these have clinical-trial cohort data in Q-omics. Immunotherapy-response analysis is Pembrolizumab-only (§5, analysis 4).
Drug coverage stops at the GDSC catalog (+ Pembrolizumab)
Common non-oncology drugs — aspirin, metformin, ibuprofen, acetaminophen, caffeine — have no response data; the catalog is the ~560-compound GDSC oncology set. Their well-established molecular targets are still queryable as genes (aspirin → PTGS1/PTGS2, metformin → PRKAA1/PRKAA2) — a target-biology question is answerable even when a response question isn't.
Network/ontology analysis and literature intelligence are separate products
NetCrafter (network/ontology) and OmixMind (literature intelligence) both exist on the Q-omics platform but aren't reachable through this data-mining API surface — independent entry points with their own access paths.