Q-omics provides the consensus-scored TNS2 profile across patient tissues and cancer cell-line models. TNS2 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, TNS2 is differentially expressed in 17, with the highest sampling consensus in BLCA. Additionally, TNS2 protein abundance shows 31,436 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight UVM, BLCA, and LSCC as cancer lineages where TNS2 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 TNS2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TNS2 survival associations across molecular data types. TNS2 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (8) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TNS2 RNA expression–survival associations across cancer types. High TNS2 expression shows unfavorable associations in UVM and BLCA, but favorable associations in HNSC, KIRC, PAAD and SARC. The UVM 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 UVM as the clearest survival context for TNS2 RNA expression.
This table summarizes TNS2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 17, while mass-spec protein shows differences in 8. The strongest signals are observed in BLCA for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for TNS2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TNS2 shows lower tumor expression in BLCA, LUAD, COAD, THCA, LUSC and KIRP. The BLCA box plot shows higher TNS2 RNA expression in normal versus tumor tissue (log2 FC = −3.152, t-test p < 0.001).
This table shows molecular features associated with TNS2 in patient tissues and cancer cell lines. In patient samples, TNS2 shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, TNS2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BONE, while CRISPR and shRNA rows add functional-dependency signals in KIDNEY and LARGE_INTESTINE.
