Q-omics provides the consensus-scored TNNI2 profile across patient tissues and cancer cell-line models. TNNI2 expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in LGG. Among the 18 cancer types available for tumor–normal comparison, TNNI2 is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, TNNI2 RNA expression shows 14,521 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight LGG, KIRC, and GBM as cancer lineages where TNNI2 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 TNNI2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TNNI2 survival associations across molecular data types. TNNI2 RNA expression shows survival associations in the most cancer types (22), followed by mutation status (3) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TNNI2 RNA expression–survival associations across cancer types. High TNNI2 expression shows unfavorable associations in LGG, LIHC and LAML, but favorable associations in SKCM, STAD and BLCA. The LGG 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 LGG as the clearest survival context for TNNI2 RNA expression.
This table summarizes TNNI2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 3. The strongest signals are observed in KIRC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for TNNI2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TNNI2 shows lower tumor expression in LUAD, HNSC and LUSC and higher tumor expression in KIRC, LIHC and KIRP. The KIRC box plot shows higher TNNI2 RNA expression in tumor versus normal tissue (log2 FC = +1.055, t-test p < 0.001).
This table shows molecular features associated with TNNI2 in patient tissues and cancer cell lines. In patient samples, TNNI2 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, TNNI2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in UPPER_AERODIGESTIVE_TRACT, while CRISPR and shRNA rows add functional-dependency signals in CNS and BLOOD_Leukemia.
