Q-omics provides the consensus-scored TSPAN2 profile across patient tissues and cancer cell-line models. TSPAN2 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, TSPAN2 is differentially expressed in 16, with the highest sampling consensus in KICH. Additionally, TSPAN2 protein abundance shows 30,956 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight KIRP, KICH, and LUAD as cancer lineages where TSPAN2 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 TSPAN2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TSPAN2 survival associations across molecular data types. TSPAN2 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (4) and mass-spec protein abundance (11). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TSPAN2 RNA expression–survival associations across cancer types. High TSPAN2 expression shows unfavorable associations in KIRP, UVM, LUSC, MESO, THCA and BLCA. 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 TSPAN2 RNA expression.
This table summarizes TSPAN2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 10. The strongest signals are observed in KICH for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for TSPAN2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TSPAN2 shows lower tumor expression in KICH, KIRP, LUSC, THCA, UCEC and BLCA. The KICH box plot shows higher TSPAN2 RNA expression in normal versus tumor tissue (log2 FC = −3.273, t-test p < 0.001).
This table shows molecular features associated with TSPAN2 in patient tissues and cancer cell lines. In patient samples, TSPAN2 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, TSPAN2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and BLOOD_Leukemia.
