Q-omics provides the consensus-scored GNPTG profile across patient tissues and cancer cell-line models. GNPTG expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, GNPTG is differentially expressed in 10, with the highest sampling consensus in KIRC. Additionally, GNPTG RNA expression shows 17,188 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight UVM, and KIRC as cancer lineages where GNPTG 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 GNPTG — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes GNPTG survival associations across molecular data types. GNPTG RNA expression shows survival associations in the most cancer types (27), 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 GNPTG RNA expression–survival associations across cancer types. High GNPTG expression shows unfavorable associations in UVM, UCS, KIRP, GBM and ESCA, but favorable associations in DLBC. 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 GNPTG RNA expression.
This table summarizes GNPTG 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 6. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for GNPTG. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. GNPTG shows lower tumor expression in LUSC and higher tumor expression in KIRC, KIRP, LIHC, HNSC and COAD. The KIRC box plot shows higher GNPTG RNA expression in tumor versus normal tissue (log2 FC = +0.640, t-test p < 0.001).
This table shows molecular features associated with GNPTG in patient tissues and cancer cell lines. In patient samples, GNPTG shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, GNPTG 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 URINARY_TRACT and BONE.
