Q-omics provides the consensus-scored CLIP2 profile across patient tissues and cancer cell-line models. CLIP2 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, CLIP2 is differentially expressed in 13, with the highest sampling consensus in KIRP. Additionally, CLIP2 protein abundance shows 20,809 significant protein co-abundance associations, with the highest sampling consensus in UCEC. Together, these results highlight MESO, KIRP, and UCEC as cancer lineages where CLIP2 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 CLIP2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CLIP2 survival associations across molecular data types. CLIP2 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (6) 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 CLIP2 RNA expression–survival associations across cancer types. High CLIP2 expression shows unfavorable associations in MESO, ACC, KICH, UVM and LUSC, but favorable associations in UCS. The MESO 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 MESO as the clearest survival context for CLIP2 RNA expression.
This table summarizes CLIP2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 7. The strongest signals are observed in KIRP for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for CLIP2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CLIP2 shows higher tumor expression in KIRP, LIHC, HNSC, THCA, KIRC and CHOL. The KIRP box plot shows higher CLIP2 RNA expression in tumor versus normal tissue (log2 FC = +1.276, t-test p < 0.001).
This table shows molecular features associated with CLIP2 in patient tissues and cancer cell lines. In patient samples, CLIP2 shows the broadest associations at the RNA and protein expression levels, with UCEC recurring as the lineage with the largest associated feature set. In cancer cell lines, CLIP2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in BONE and CNS.
