Q-omics provides the consensus-scored SENP1 profile across patient tissues and cancer cell-line models. SENP1 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, SENP1 is differentially expressed in 14, with the highest sampling consensus in HNSC. Additionally, SENP1 protein abundance shows 39,989 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight MESO, HNSC, and LSCC as cancer lineages where SENP1 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 SENP1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SENP1 survival associations across molecular data types. SENP1 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (4) and mass-spec protein abundance (11). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible SENP1 RNA expression–survival associations across cancer types. High SENP1 expression shows unfavorable associations in MESO, ACC, LIHC and KIRP, 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 SENP1 RNA expression.
This table summarizes SENP1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 11. The strongest signals are observed in HNSC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for SENP1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SENP1 shows higher tumor expression in HNSC, BLCA, COAD, LIHC, KIRP and KIRC. The HNSC box plot shows higher SENP1 RNA expression in tumor versus normal tissue (log2 FC = +1.096, t-test p < 0.001).
This table shows molecular features associated with SENP1 in patient tissues and cancer cell lines. In patient samples, SENP1 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, SENP1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in URINARY_TRACT and BLOOD_Leukemia.
