Q-omics provides the consensus-scored CST7 profile across patient tissues and cancer cell-line models. CST7 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, CST7 is differentially expressed in 10, with the highest sampling consensus in KIRC. Additionally, CST7 RNA expression shows 20,854 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight HNSC, KIRC, and LSCC as cancer lineages where CST7 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 CST7 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CST7 survival associations across molecular data types. CST7 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (6) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CST7 RNA expression–survival associations across cancer types. High CST7 expression shows unfavorable associations in UVM, but favorable associations in HNSC, UCEC, CESC, SKCM and LIHC. The HNSC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify HNSC as the clearest survival context for CST7 RNA expression.
This table summarizes CST7 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 5. The strongest signals are observed in KIRC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for CST7. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CST7 shows lower tumor expression in LUSC and BLCA and higher tumor expression in KIRC, STAD, BRCA and ESCA. The KIRC box plot shows higher CST7 RNA expression in tumor versus normal tissue (log2 FC = +3.016, t-test p < 0.001).
This table shows molecular features associated with CST7 in patient tissues and cancer cell lines. In patient samples, CST7 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, CST7 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in STOMACH and BLOOD_Lymphoma.
