Q-omics provides the consensus-scored ENPP3 profile across patient tissues and cancer cell-line models. ENPP3 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, ENPP3 is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, ENPP3 RNA expression shows 17,370 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRC, and UVM as cancer lineages where ENPP3 shows reproducible signals across survival, tumor–normal expression, and patient cross-omics analyses.
Every result is evaluated using two consensus scores. Sampling consensus measures how consistently a finding is reproduced within a cancer lineage across different conditions. Lineage consensus measures how broadly the result is shared across cancer types, distinguishing pan-cancer signals from lineage-specific patterns.
Premium analyses for ENPP3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ENPP3 survival associations across molecular data types. ENPP3 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (6) and mass-spec protein abundance (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ENPP3 RNA expression–survival associations across cancer types. High ENPP3 expression shows unfavorable associations in ACC, but favorable associations in KIRC, HNSC, UCEC, PAAD and MESO. The KIRC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRC as the clearest survival context for ENPP3 RNA expression.
This table summarizes ENPP3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 3. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for ENPP3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ENPP3 shows lower tumor expression in KICH, BLCA, LUSC, BRCA and HNSC and higher tumor expression in KIRC. The KIRC box plot shows higher ENPP3 RNA expression in tumor versus normal tissue (log2 FC = +5.312, t-test p < 0.001).
This table shows molecular features associated with ENPP3 in patient tissues and cancer cell lines. In patient samples, ENPP3 shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, ENPP3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SOFT_TISSUE, while CRISPR and shRNA rows add functional-dependency signals in CNS and BONE.
