Q-omics provides the consensus-scored TSPAN32 profile across patient tissues and cancer cell-line models. TSPAN32 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, TSPAN32 is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, TSPAN32 RNA expression shows 15,147 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight HNSC, KIRC, and UVM as cancer lineages where TSPAN32 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 TSPAN32 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TSPAN32 survival associations across molecular data types. TSPAN32 RNA expression shows survival associations in the most cancer types (27), followed by mutation status (4) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TSPAN32 RNA expression–survival associations across cancer types. High TSPAN32 expression shows favorable associations in HNSC, SKCM, LUAD, ESCA, CESC and LIHC. The HNSC 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 HNSC as the clearest survival context for TSPAN32 RNA expression.
This table summarizes TSPAN32 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for TSPAN32. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TSPAN32 shows lower tumor expression in LUAD, BLCA, LUSC, UCEC and BRCA and higher tumor expression in KIRC. The KIRC box plot shows higher TSPAN32 RNA expression in tumor versus normal tissue (log2 FC = +0.701, t-test p < 0.001).
This table shows molecular features associated with TSPAN32 in patient tissues and cancer cell lines. In patient samples, TSPAN32 shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, TSPAN32 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and SOFT_TISSUE.
