Q-omics provides the consensus-scored SEPTIN12 profile across patient tissues and cancer cell-line models. SEPTIN12 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, SEPTIN12 is differentially expressed in 12, with the highest sampling consensus in HNSC. Additionally, SEPTIN12 protein abundance shows 25,956 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRP, HNSC, and LSCC as cancer lineages where SEPTIN12 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 SEPTIN12 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SEPTIN12 survival associations across molecular data types. SEPTIN12 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (3) 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 SEPTIN12 RNA expression–survival associations across cancer types. High SEPTIN12 expression shows unfavorable associations in KIRP, KIRC, LIHC, ACC and DLBC, but favorable associations in BRCA. The KIRP 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 KIRP as the clearest survival context for SEPTIN12 RNA expression.
This table summarizes SEPTIN12 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 6. The strongest signals are observed in HNSC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for SEPTIN12. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SEPTIN12 shows lower tumor expression in COAD and KICH and higher tumor expression in HNSC, BRCA, LUAD and LUSC. The HNSC box plot shows higher SEPTIN12 RNA expression in tumor versus normal tissue (log2 FC = +0.069, t-test p = .008).
This table shows molecular features associated with SEPTIN12 in patient tissues and cancer cell lines. In patient samples, SEPTIN12 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, SEPTIN12 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SOFT_TISSUE, while CRISPR and shRNA rows add functional-dependency signals in URINARY_TRACT and LARGE_INTESTINE.
