Q-omics provides the consensus-scored SEPTIN7 profile across patient tissues and cancer cell-line models. SEPTIN7 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, SEPTIN7 is differentially expressed in 11, with the highest sampling consensus in HNSC. Additionally, SEPTIN7 protein abundance shows 36,458 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight MESO, HNSC, and PDAC as cancer lineages where SEPTIN7 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 SEPTIN7 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SEPTIN7 survival associations across molecular data types. SEPTIN7 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (5) 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 SEPTIN7 RNA expression–survival associations across cancer types. High SEPTIN7 expression shows unfavorable associations in MESO, CESC, ACC and UVM, but favorable associations in UCS and KIRC. The MESO 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 MESO as the clearest survival context for SEPTIN7 RNA expression.
This table summarizes SEPTIN7 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 6. The strongest signals are observed in KIRC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for SEPTIN7. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SEPTIN7 shows lower tumor expression in KICH and THCA and higher tumor expression in HNSC, KIRC, LIHC and KIRP. The HNSC box plot shows higher SEPTIN7 RNA expression in tumor versus normal tissue (log2 FC = +1.063, t-test p < 0.001).
This table shows molecular features associated with SEPTIN7 in patient tissues and cancer cell lines. In patient samples, SEPTIN7 shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, SEPTIN7 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 OVARY and BREAST.
