Q-omics provides the consensus-scored TICRR profile across patient tissues and cancer cell-line models. TICRR expression is associated with patient survival in 28 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, TICRR is differentially expressed in 14, with the highest sampling consensus in BLCA. Additionally, TICRR RNA expression shows 28,166 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight ACC, BLCA, and LSCC as cancer lineages where TICRR 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 TICRR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TICRR survival associations across molecular data types. TICRR RNA expression shows survival associations in the most cancer types (28), followed by mutation status (6) 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 TICRR RNA expression–survival associations across cancer types. High TICRR expression shows unfavorable associations in ACC, KIRP, MESO, KIRC, LIHC and KICH. The ACC 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 ACC as the clearest survival context for TICRR RNA expression.
This table summarizes TICRR 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 1. The strongest signals are observed in BLCA for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for TICRR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TICRR shows higher tumor expression in BLCA, HNSC, COAD, KIRP, STAD and LUAD. The BLCA box plot shows higher TICRR RNA expression in tumor versus normal tissue (log2 FC = +1.948, t-test p < 0.001).
This table shows molecular features associated with TICRR in patient tissues and cancer cell lines. In patient samples, TICRR 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, TICRR RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in URINARY_TRACT and BLOOD_Leukemia.
