Q-omics provides the consensus-scored CSTF2 profile across patient tissues and cancer cell-line models. CSTF2 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in SCLC. Among the 18 cancer types available for tumor–normal comparison, CSTF2 is differentially expressed in 15, with the highest sampling consensus in LUAD. Additionally, CSTF2 protein abundance shows 28,311 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight SCLC, LUAD, and LSCC as cancer lineages where CSTF2 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 CSTF2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CSTF2 survival associations across molecular data types. CSTF2 RNA expression shows survival associations in the most cancer types (27), 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 CSTF2 RNA expression–survival associations across cancer types. High CSTF2 expression shows unfavorable associations in MESO, LIHC and KICH, but favorable associations in SCLC, OV and KIRC. The SCLC 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 SCLC as the clearest survival context for CSTF2 RNA expression.
This table summarizes CSTF2 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 9. The strongest signals are observed in LUAD for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for CSTF2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CSTF2 shows higher tumor expression in LUAD, COAD, BLCA, LIHC, LUSC and STAD. The LUAD box plot shows higher CSTF2 RNA expression in tumor versus normal tissue (log2 FC = +1.266, t-test p < 0.001).
This table shows molecular features associated with CSTF2 in patient tissues and cancer cell lines. In patient samples, CSTF2 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, CSTF2 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 BLOOD_Lymphoma and OVARY.
