Q-omics provides the consensus-scored CTPS2 profile across patient tissues and cancer cell-line models. CTPS2 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, CTPS2 is differentially expressed in 15, with the highest sampling consensus in COAD. Additionally, CTPS2 RNA expression shows 20,530 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight KIRC, COAD, and KIRP as cancer lineages where CTPS2 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 CTPS2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CTPS2 survival associations across molecular data types. CTPS2 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (5) 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 CTPS2 RNA expression–survival associations across cancer types. High CTPS2 expression shows unfavorable associations in LIHC and STAD, but favorable associations in KIRC, OV, SCLC and GBM. The KIRC 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 KIRC as the clearest survival context for CTPS2 RNA expression.
This table summarizes CTPS2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 6. The strongest signals are observed in COAD for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CTPS2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CTPS2 shows lower tumor expression in KICH and higher tumor expression in COAD, LIHC, LUAD, STAD and BLCA. The COAD box plot shows higher CTPS2 RNA expression in tumor versus normal tissue (log2 FC = +0.859, t-test p < 0.001).
This table shows molecular features associated with CTPS2 in patient tissues and cancer cell lines. In patient samples, CTPS2 shows the broadest associations at the RNA and protein expression levels, with KIRP recurring as the lineage with the largest associated feature set. In cancer cell lines, CTPS2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in LIVER and UPPER_AERODIGESTIVE_TRACT.
