Q-omics provides the consensus-scored TINCR profile across patient tissues and cancer cell-line models. TINCR expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, TINCR is differentially expressed in 12, with the highest sampling consensus in COAD. Additionally, TINCR RNA expression shows 17,786 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRC, COAD, and UVM as cancer lineages where TINCR 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 TINCR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TINCR survival associations across molecular data types. TINCR RNA expression shows survival associations in the most cancer types (22). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TINCR RNA expression–survival associations across cancer types. High TINCR expression shows unfavorable associations in KIRC, KICH, ACC, KIRP, SKCM and UCEC. The KIRC 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 KIRC as the clearest survival context for TINCR RNA expression.
This table summarizes TINCR tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for TINCR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TINCR shows lower tumor expression in COAD, KIRC, KICH and LUAD and higher tumor expression in BLCA and THCA. The COAD box plot shows higher TINCR RNA expression in normal versus tumor tissue (log2 FC = −2.604, t-test p < 0.001).
This table shows molecular features associated with TINCR in patient tissues and cancer cell lines. In patient samples, TINCR shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, TINCR RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in BONE.
