Q-omics provides the consensus-scored CSH2 profile across patient tissues and cancer cell-line models. CSH2 expression is associated with patient survival in 15 of 34 cancer types, with the highest sampling consensus in COAD. Among the 18 cancer types available for tumor–normal comparison, CSH2 is differentially expressed in 5, with the highest sampling consensus in KIRC. Additionally, CSH2 RNA expression shows 8,132 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight COAD, KIRC, and TGCT as cancer lineages where CSH2 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 CSH2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CSH2 survival associations across molecular data types. CSH2 RNA expression shows survival associations in the most cancer types (15), followed by mutation status (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CSH2 RNA expression–survival associations across cancer types. High CSH2 expression shows unfavorable associations in COAD, UCEC, BRCA, ESCA and DLBC, but favorable associations in HNSC. The COAD 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 COAD as the clearest survival context for CSH2 RNA expression.
This table summarizes CSH2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 5. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for CSH2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CSH2 shows lower tumor expression in KIRC and higher tumor expression in BRCA, LUSC, LUAD and HNSC. The KIRC box plot shows higher CSH2 RNA expression in normal versus tumor tissue (log2 FC = −0.008, t-test p = .008).
This table shows molecular features associated with CSH2 in patient tissues and cancer cell lines. In patient samples, CSH2 shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, CSH2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Leukemia, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and LUNG_SCLC.
