Q-omics provides the consensus-scored TIPIN profile across patient tissues and cancer cell-line models. TIPIN expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KICH. Among the 18 cancer types available for tumor–normal comparison, TIPIN is differentially expressed in 17, with the highest sampling consensus in HNSC. Additionally, TIPIN protein abundance shows 23,432 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KICH, HNSC, and LSCC as cancer lineages where TIPIN 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 TIPIN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TIPIN survival associations across molecular data types. TIPIN RNA expression shows survival associations in the most cancer types (26), followed by mutation status (4) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TIPIN RNA expression–survival associations across cancer types. High TIPIN expression shows unfavorable associations in KICH, LIHC, UVM, BLCA and ACC, but favorable associations in KIRC. The KICH Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .001). Together, the overview and detailed table identify KICH as the clearest survival context for TIPIN RNA expression.
This table summarizes TIPIN tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 17, 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 TIPIN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TIPIN shows higher tumor expression in HNSC, BLCA, STAD, COAD, LIHC and LUSC. The HNSC box plot shows higher TIPIN RNA expression in tumor versus normal tissue (log2 FC = +1.074, t-test p < 0.001).
This table shows molecular features associated with TIPIN in patient tissues and cancer cell lines. In patient samples, TIPIN 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, TIPIN RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and BLOOD_Lymphoma.
