Q-omics provides the consensus-scored SNX13 profile across patient tissues and cancer cell-line models. SNX13 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, SNX13 is differentially expressed in 7, with the highest sampling consensus in LIHC. Additionally, SNX13 protein abundance shows 29,800 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight KIRC, LIHC, and LUAD as cancer lineages where SNX13 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 SNX13 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SNX13 survival associations across molecular data types. SNX13 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (7) and mass-spec protein abundance (12). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible SNX13 RNA expression–survival associations across cancer types. High SNX13 expression shows unfavorable associations in CESC, UVM and LGG, but favorable associations in KIRC, UCS and LUSC. 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 SNX13 RNA expression.
This table summarizes SNX13 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 7, while mass-spec protein shows differences in 9. The strongest signals are observed in LIHC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for SNX13. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SNX13 shows lower tumor expression in THCA, UCEC and COAD and higher tumor expression in LIHC, HNSC and CHOL. The LIHC box plot shows higher SNX13 RNA expression in tumor versus normal tissue (log2 FC = +0.642, t-test p < 0.001).
This table shows molecular features associated with SNX13 in patient tissues and cancer cell lines. In patient samples, SNX13 shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, SNX13 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in URINARY_TRACT, while CRISPR and shRNA rows add functional-dependency signals in LIVER and UPPER_AERODIGESTIVE_TRACT.
