Q-omics provides the consensus-scored TINF2 profile across patient tissues and cancer cell-line models. TINF2 expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in BRCA. Among the 18 cancer types available for tumor–normal comparison, TINF2 is differentially expressed in 11, with the highest sampling consensus in HNSC. Additionally, TINF2 protein abundance shows 24,129 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight BRCA, HNSC, and LUAD as cancer lineages where TINF2 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 TINF2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TINF2 survival associations across molecular data types. TINF2 RNA expression shows survival associations in the most cancer types (21), followed by mutation status (4) and mass-spec protein abundance (11). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TINF2 RNA expression–survival associations across cancer types. High TINF2 expression shows unfavorable associations in UVM, ACC and LAML, but favorable associations in BRCA, KIRC and SKCM. The BRCA 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 BRCA as the clearest survival context for TINF2 RNA expression.
This table summarizes TINF2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 6. The strongest signals are observed in HNSC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for TINF2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TINF2 shows lower tumor expression in LUAD, KICH, LUSC and THCA and higher tumor expression in HNSC and LIHC. The HNSC box plot shows higher TINF2 RNA expression in tumor versus normal tissue (log2 FC = +0.889, t-test p < 0.001).
This table shows molecular features associated with TINF2 in patient tissues and cancer cell lines. In patient samples, TINF2 shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, TINF2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and BLOOD_Leukemia.
