Q-omics provides the consensus-scored TNNT3 profile across patient tissues and cancer cell-line models. TNNT3 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in SCLC. Among the 18 cancer types available for tumor–normal comparison, TNNT3 is differentially expressed in 13, with the highest sampling consensus in THCA. Additionally, TNNT3 protein abundance shows 20,805 significant protein co-abundance associations, with the highest sampling consensus in HNSC. Together, these results highlight SCLC, THCA, and HNSC as cancer lineages where TNNT3 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 TNNT3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TNNT3 survival associations across molecular data types. TNNT3 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (3) 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 TNNT3 RNA expression–survival associations across cancer types. High TNNT3 expression shows unfavorable associations in UCEC, LAML and THCA, but favorable associations in SCLC, CESC and LUAD. The SCLC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .011). Together, the overview and detailed table identify SCLC as the clearest survival context for TNNT3 RNA expression.
This table summarizes TNNT3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 9. The strongest signals are observed in THCA for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for TNNT3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TNNT3 shows lower tumor expression in THCA, COAD, LUAD, HNSC, UCEC and KICH. The THCA box plot shows higher TNNT3 RNA expression in normal versus tumor tissue (log2 FC = −2.040, t-test p < 0.001).
This table shows molecular features associated with TNNT3 in patient tissues and cancer cell lines. In patient samples, TNNT3 shows the broadest associations at the RNA and protein expression levels, with HNSC recurring as the lineage with the largest associated feature set. In cancer cell lines, TNNT3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OESOPHAGUS, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and SOFT_TISSUE.
