Q-omics provides the consensus-scored TSPAN13 profile across patient tissues and cancer cell-line models. TSPAN13 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, TSPAN13 is differentially expressed in 12, with the highest sampling consensus in LUAD. Additionally, TSPAN13 protein abundance shows 34,149 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight KIRP, LUAD, and PDAC as cancer lineages where TSPAN13 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 TSPAN13 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TSPAN13 survival associations across molecular data types. TSPAN13 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (1) and mass-spec protein abundance (10). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TSPAN13 RNA expression–survival associations across cancer types. High TSPAN13 expression shows unfavorable associations in KIRP, UVM, LIHC and GBM, but favorable associations in LUSC and SKCM. The KIRP 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 KIRP as the clearest survival context for TSPAN13 RNA expression.
This table summarizes TSPAN13 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 10. The strongest signals are observed in KIRC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for TSPAN13. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TSPAN13 shows lower tumor expression in LUAD and LUSC and higher tumor expression in KIRC, BRCA, BLCA and STAD. The LUAD box plot shows higher TSPAN13 RNA expression in normal versus tumor tissue (log2 FC = −0.987, t-test p < 0.001).
This table shows molecular features associated with TSPAN13 in patient tissues and cancer cell lines. In patient samples, TSPAN13 shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, TSPAN13 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in STOMACH and BLOOD_Leukemia.
