Q-omics provides the consensus-scored PSKH2 profile across patient tissues and cancer cell-line models. PSKH2 expression is associated with patient survival in 18 of 34 cancer types, with the highest sampling consensus in THYM. Among the 18 cancer types available for tumor–normal comparison, PSKH2 is differentially expressed in 8, with the highest sampling consensus in KIRC. Additionally, PSKH2 RNA expression shows 9,814 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight THYM, KIRC, and TGCT as cancer lineages where PSKH2 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 PSKH2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PSKH2 survival associations across molecular data types. PSKH2 RNA expression shows survival associations in the most cancer types (18), followed by mutation status (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PSKH2 RNA expression–survival associations across cancer types. High PSKH2 expression shows unfavorable associations in THYM, LUSC, CESC and READ, but favorable associations in UCS and BRCA. The THYM 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 THYM as the clearest survival context for PSKH2 RNA expression.
This table summarizes PSKH2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 8. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for PSKH2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PSKH2 shows lower tumor expression in KIRC, KIRP, LUAD and COAD and higher tumor expression in BRCA and HNSC. The KIRC box plot shows higher PSKH2 RNA expression in normal versus tumor tissue (log2 FC = −0.581, t-test p < 0.001).
This table shows molecular features associated with PSKH2 in patient tissues and cancer cell lines. In patient samples, PSKH2 shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, PSKH2 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 LARGE_INTESTINE and LUNG_NSCLC_LUAD.
