Q-omics provides the consensus-scored NPRL3 profile across patient tissues and cancer cell-line models. NPRL3 expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in LIHC. Among the 18 cancer types available for tumor–normal comparison, NPRL3 is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, NPRL3 RNA expression shows 18,369 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight LIHC, KIRC, and ACC as cancer lineages where NPRL3 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 NPRL3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes NPRL3 survival associations across molecular data types. NPRL3 RNA expression shows survival associations in the most cancer types (21), followed by mutation status (3) and mass-spec protein abundance (8). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible NPRL3 RNA expression–survival associations across cancer types. High NPRL3 expression shows unfavorable associations in LIHC, LUAD, COAD, ACC and BLCA, but favorable associations in UVM. The LIHC Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p < 0.001). Together, the overview and detailed table identify LIHC as the clearest survival context for NPRL3 RNA expression.
This table summarizes NPRL3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 4. The strongest signals are observed in KIRC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for NPRL3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. NPRL3 shows higher tumor expression in KIRC, COAD, KIRP, STAD, LIHC and HNSC. The KIRC box plot shows higher NPRL3 RNA expression in tumor versus normal tissue (log2 FC = +0.615, t-test p < 0.001).
This table shows molecular features associated with NPRL3 in patient tissues and cancer cell lines. In patient samples, NPRL3 shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, NPRL3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in UPPER_AERODIGESTIVE_TRACT, while CRISPR and shRNA rows add functional-dependency signals in BONE and LARGE_INTESTINE.
