Q-omics provides the consensus-scored CSTB profile across patient tissues and cancer cell-line models. CSTB expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, CSTB is differentially expressed in 14, with the highest sampling consensus in KIRC. Additionally, CSTB RNA expression shows 18,892 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight UVM, KIRC, and GBM as cancer lineages where CSTB 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 CSTB — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CSTB survival associations across molecular data types. CSTB RNA expression shows survival associations in the most cancer types (25), followed by mutation status (1) 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 CSTB RNA expression–survival associations across cancer types. High CSTB expression shows unfavorable associations in UVM, ACC, LGG and LIHC, but favorable associations in DLBC and LUSC. The UVM 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 UVM as the clearest survival context for CSTB RNA expression.
This table summarizes CSTB 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 4. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CSTB. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CSTB shows lower tumor expression in HNSC and higher tumor expression in KIRC, KIRP, LIHC, THCA and COAD. The KIRC box plot shows higher CSTB RNA expression in tumor versus normal tissue (log2 FC = +0.728, t-test p < 0.001).
This table shows molecular features associated with CSTB in patient tissues and cancer cell lines. In patient samples, CSTB 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, CSTB 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 BREAST and BONE.
