Q-omics provides the consensus-scored GPKOW profile across patient tissues and cancer cell-line models. GPKOW expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, GPKOW is differentially expressed in 16, with the highest sampling consensus in COAD. Additionally, GPKOW protein abundance shows 25,361 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, COAD, and GBM as cancer lineages where GPKOW 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 GPKOW — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes GPKOW survival associations across molecular data types. GPKOW RNA expression shows survival associations in the most cancer types (24), followed by mutation status (7) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible GPKOW RNA expression–survival associations across cancer types. High GPKOW expression shows unfavorable associations in LUAD, UVM and LIHC, but favorable associations in KIRC, SCLC and SKCM. The KIRC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRC as the clearest survival context for GPKOW RNA expression.
This table summarizes GPKOW tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 7. The strongest signals are observed in HNSC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for GPKOW. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. GPKOW shows lower tumor expression in KICH and higher tumor expression in COAD, HNSC, LIHC, CHOL and STAD. The COAD box plot shows higher GPKOW RNA expression in tumor versus normal tissue (log2 FC = +0.645, t-test p < 0.001).
This table shows molecular features associated with GPKOW in patient tissues and cancer cell lines. In patient samples, GPKOW shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, GPKOW RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Myeloma, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and UPPER_AERODIGESTIVE_TRACT.
