Q-omics provides the consensus-scored CST11 profile across patient tissues and cancer cell-line models. CST11 expression is associated with patient survival in 18 of 34 cancer types, with the highest sampling consensus in BLCA. Among the 18 cancer types available for tumor–normal comparison, CST11 is differentially expressed in 9, with the highest sampling consensus in KIRP. Additionally, CST11 protein abundance shows 19,531 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight BLCA, KIRP, and GBM as cancer lineages where CST11 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 CST11 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CST11 survival associations across molecular data types. CST11 RNA expression shows survival associations in the most cancer types (18), followed by mutation status (3) 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 CST11 RNA expression–survival associations across cancer types. High CST11 expression shows unfavorable associations in BLCA, KICH, ACC and LIHC, but favorable associations in BRCA and SARC. The BLCA Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .002). Together, the overview and detailed table identify BLCA as the clearest survival context for CST11 RNA expression.
This table summarizes CST11 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9, while mass-spec protein shows differences in 5. The strongest signals are observed in KIRP for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for CST11. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CST11 shows lower tumor expression in KIRP, KIRC, KICH and STAD and higher tumor expression in LUSC and LUAD. The KIRP box plot shows higher CST11 RNA expression in normal versus tumor tissue (log2 FC = −0.248, t-test p < 0.001).
This table shows molecular features associated with CST11 in patient tissues and cancer cell lines. In patient samples, CST11 shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, CST11 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in BREAST and STOMACH.
