Q-omics provides the consensus-scored PSEN1 profile across patient tissues and cancer cell-line models. PSEN1 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, PSEN1 is differentially expressed in 13, with the highest sampling consensus in HNSC. Additionally, PSEN1 RNA expression shows 20,473 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight UVM, HNSC, and ACC as cancer lineages where PSEN1 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 PSEN1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PSEN1 survival associations across molecular data types. PSEN1 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (3) and mass-spec protein abundance (8). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PSEN1 RNA expression–survival associations across cancer types. High PSEN1 expression shows unfavorable associations in UVM, ACC, PAAD and LIHC, but favorable associations in KIRC and BRCA. The UVM 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 UVM as the clearest survival context for PSEN1 RNA expression.
This table summarizes PSEN1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 5. The strongest signals are observed in HNSC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for PSEN1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PSEN1 shows lower tumor expression in COAD and higher tumor expression in HNSC, BLCA, LIHC, STAD and KIRP. The HNSC box plot shows higher PSEN1 RNA expression in tumor versus normal tissue (log2 FC = +0.699, t-test p < 0.001).
This table shows molecular features associated with PSEN1 in patient tissues and cancer cell lines. In patient samples, PSEN1 shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, PSEN1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in CNS and BLOOD_Lymphoma.
