Q-omics provides the consensus-scored TNNI1 profile across patient tissues and cancer cell-line models. TNNI1 expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, TNNI1 is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, TNNI1 RNA expression shows 17,547 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight HNSC, KIRC, and LSCC as cancer lineages where TNNI1 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 TNNI1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TNNI1 survival associations across molecular data types. TNNI1 RNA expression shows survival associations in the most cancer types (20), followed by mutation status (4) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TNNI1 RNA expression–survival associations across cancer types. High TNNI1 expression shows unfavorable associations in HNSC and LGG, but favorable associations in UCS, DLBC, KICH and SCLC. The HNSC 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 HNSC as the clearest survival context for TNNI1 RNA expression.
This table summarizes TNNI1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 2. The strongest signals are observed in KIRC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for TNNI1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TNNI1 shows lower tumor expression in KIRC, KICH and KIRP and higher tumor expression in LUAD, STAD and THCA. The KIRC box plot shows higher TNNI1 RNA expression in normal versus tumor tissue (log2 FC = −2.276, t-test p < 0.001).
This table shows molecular features associated with TNNI1 in patient tissues and cancer cell lines. In patient samples, TNNI1 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, TNNI1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Leukemia, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and LARGE_INTESTINE.
