Q-omics provides the consensus-scored PSEN2 profile across patient tissues and cancer cell-line models. PSEN2 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, PSEN2 is differentially expressed in 10, with the highest sampling consensus in LIHC. Additionally, PSEN2 RNA expression shows 18,732 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRP, LIHC, and ACC as cancer lineages where PSEN2 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 PSEN2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PSEN2 survival associations across molecular data types. PSEN2 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (5) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PSEN2 RNA expression–survival associations across cancer types. High PSEN2 expression shows unfavorable associations in KIRP, ACC, LGG, LIHC, CESC and SKCM. 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 PSEN2 RNA expression.
This table summarizes PSEN2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 3. The strongest signals are observed in LIHC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for PSEN2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PSEN2 shows lower tumor expression in LUSC and higher tumor expression in LIHC, STAD, BRCA, CHOL and ESCA. The LIHC box plot shows higher PSEN2 RNA expression in tumor versus normal tissue (log2 FC = +1.251, t-test p < 0.001).
This table shows molecular features associated with PSEN2 in patient tissues and cancer cell lines. In patient samples, PSEN2 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, PSEN2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Lymphoma and LARGE_INTESTINE.
