Q-omics provides the consensus-scored TNNI3K profile across patient tissues and cancer cell-line models. TNNI3K expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in LUSC. Among the 18 cancer types available for tumor–normal comparison, TNNI3K is differentially expressed in 14, with the highest sampling consensus in KIRP. Additionally, TNNI3K protein abundance shows 35,646 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight LUSC, KIRP, and GBM as cancer lineages where TNNI3K 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 TNNI3K — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TNNI3K survival associations across molecular data types. TNNI3K RNA expression shows survival associations in the most cancer types (20), followed by mutation status (8) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TNNI3K RNA expression–survival associations across cancer types. High TNNI3K expression shows unfavorable associations in UVM, LIHC, READ and KIRC, but favorable associations in LUSC and MESO. The LUSC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .001). Together, the overview and detailed table identify LUSC as the clearest survival context for TNNI3K RNA expression.
This table summarizes TNNI3K tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 7. The strongest signals are observed in KIRP for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for TNNI3K. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TNNI3K shows lower tumor expression in KIRP, BLCA, KICH, UCEC, COAD and LUSC. The KIRP box plot shows higher TNNI3K RNA expression in normal versus tumor tissue (log2 FC = −0.423, t-test p < 0.001).
This table shows molecular features associated with TNNI3K in patient tissues and cancer cell lines. In patient samples, TNNI3K shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, TNNI3K RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in BREAST and CNS.
