Q-omics provides the consensus-scored GNL3L profile across patient tissues and cancer cell-line models. GNL3L expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, GNL3L is differentially expressed in 14, with the highest sampling consensus in COAD. Additionally, GNL3L RNA expression shows 19,720 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRC, COAD, and ACC as cancer lineages where GNL3L 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 GNL3L — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes GNL3L survival associations across molecular data types. GNL3L RNA expression shows survival associations in the most cancer types (26), followed by mutation status (9) 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 GNL3L RNA expression–survival associations across cancer types. High GNL3L expression shows unfavorable associations in THCA, MESO and PAAD, but favorable associations in KIRC, STAD and SCLC. 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 GNL3L RNA expression.
This table summarizes GNL3L tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 6. The strongest signals are observed in HNSC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for GNL3L. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. GNL3L shows lower tumor expression in THCA and higher tumor expression in COAD, BLCA, HNSC, STAD and LIHC. The COAD box plot shows higher GNL3L RNA expression in tumor versus normal tissue (log2 FC = +1.454, t-test p < 0.001).
This table shows molecular features associated with GNL3L in patient tissues and cancer cell lines. In patient samples, GNL3L 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, GNL3L 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 URINARY_TRACT and UPPER_AERODIGESTIVE_TRACT.
