Q-omics provides the consensus-scored TNNC2 profile across patient tissues and cancer cell-line models. TNNC2 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in LUAD. Among the 18 cancer types available for tumor–normal comparison, TNNC2 is differentially expressed in 13, with the highest sampling consensus in KIRP. Additionally, TNNC2 RNA expression shows 14,421 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight LUAD, KIRP, and TGCT as cancer lineages where TNNC2 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 TNNC2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TNNC2 survival associations across molecular data types. TNNC2 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (2) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TNNC2 RNA expression–survival associations across cancer types. High TNNC2 expression shows unfavorable associations in GBM, UVM and LAML, but favorable associations in LUAD, ACC and SKCM. The LUAD 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 LUAD as the clearest survival context for TNNC2 RNA expression.
This table summarizes TNNC2 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 4. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for TNNC2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TNNC2 shows lower tumor expression in KIRP, KIRC, HNSC, LUSC and BRCA and higher tumor expression in LIHC. The KIRP box plot shows higher TNNC2 RNA expression in normal versus tumor tissue (log2 FC = −0.739, t-test p < 0.001).
This table shows molecular features associated with TNNC2 in patient tissues and cancer cell lines. In patient samples, TNNC2 shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, TNNC2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and UPPER_AERODIGESTIVE_TRACT.
