Q-omics provides the consensus-scored RANBP3L profile across patient tissues and cancer cell-line models. RANBP3L expression is associated with patient survival in 29 of 34 cancer types, with the highest sampling consensus in LUAD. Among the 18 cancer types available for tumor–normal comparison, RANBP3L is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, RANBP3L RNA expression shows 18,559 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight LUAD, KIRC, and THYM as cancer lineages where RANBP3L 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 RANBP3L — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes RANBP3L survival associations across molecular data types. RANBP3L RNA expression shows survival associations in the most cancer types (29), followed by mutation status (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible RANBP3L RNA expression–survival associations across cancer types. High RANBP3L expression shows unfavorable associations in KIRP, but favorable associations in LUAD, LIHC, SKCM, UCS and LAML. The LUAD 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 LUAD as the clearest survival context for RANBP3L RNA expression.
This table summarizes RANBP3L tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for RANBP3L. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. RANBP3L shows lower tumor expression in KIRC, KIRP, THCA, BLCA, LUAD and KICH. The KIRC box plot shows higher RANBP3L RNA expression in normal versus tumor tissue (log2 FC = −4.668, t-test p < 0.001).
This table shows molecular features associated with RANBP3L in patient tissues and cancer cell lines. In patient samples, RANBP3L shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, RANBP3L RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in LUNG_SCLC and CNS.
