Q-omics provides the consensus-scored TNS3 profile across patient tissues and cancer cell-line models. TNS3 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, TNS3 is differentially expressed in 10, with the highest sampling consensus in HNSC. Additionally, TNS3 protein abundance shows 23,988 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRC, HNSC, and LSCC as cancer lineages where TNS3 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 TNS3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TNS3 survival associations across molecular data types. TNS3 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (4) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TNS3 RNA expression–survival associations across cancer types. High TNS3 expression shows unfavorable associations in LAML, but favorable associations in KIRC, UCS, BRCA, HNSC and SCLC. 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 TNS3 RNA expression.
This table summarizes TNS3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 7. The strongest signals are observed in HNSC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for TNS3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TNS3 shows lower tumor expression in THCA, LUAD and LUSC and higher tumor expression in HNSC, STAD and LIHC. The HNSC box plot shows higher TNS3 RNA expression in tumor versus normal tissue (log2 FC = +1.695, t-test p < 0.001).
This table shows molecular features associated with TNS3 in patient tissues and cancer cell lines. In patient samples, TNS3 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, TNS3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Lymphoma, while CRISPR and shRNA rows add functional-dependency signals in SKIN and BONE.
