Q-omics provides the consensus-scored SEPTIN3 profile across patient tissues and cancer cell-line models. SEPTIN3 expression is associated with patient survival in 29 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, SEPTIN3 is differentially expressed in 15, with the highest sampling consensus in HNSC. Additionally, SEPTIN3 protein abundance shows 22,374 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight MESO, HNSC, and GBM as cancer lineages where SEPTIN3 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 SEPTIN3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SEPTIN3 survival associations across molecular data types. SEPTIN3 RNA expression shows survival associations in the most cancer types (29), followed by mutation status (4) 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 SEPTIN3 RNA expression–survival associations across cancer types. High SEPTIN3 expression shows unfavorable associations in MESO, ACC, UVM, UCEC and COAD, but favorable associations in LGG. The MESO Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .001). Together, the overview and detailed table identify MESO as the clearest survival context for SEPTIN3 RNA expression.
This table summarizes SEPTIN3 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 5. The strongest signals are observed in HNSC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for SEPTIN3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SEPTIN3 shows higher tumor expression in HNSC, KIRP, BLCA, THCA, LIHC and UCEC. The HNSC box plot shows higher SEPTIN3 RNA expression in tumor versus normal tissue (log2 FC = +0.796, t-test p < 0.001).
This table shows molecular features associated with SEPTIN3 in patient tissues and cancer cell lines. In patient samples, SEPTIN3 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, SEPTIN3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in LUNG_SCLC and LARGE_INTESTINE.
