Q-omics provides the consensus-scored GLIS2 profile across patient tissues and cancer cell-line models. GLIS2 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, GLIS2 is differentially expressed in 13, with the highest sampling consensus in KIRP. Additionally, GLIS2 RNA expression shows 18,379 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight UVM, KIRP, and THYM as cancer lineages where GLIS2 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 GLIS2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes GLIS2 survival associations across molecular data types. GLIS2 RNA expression shows survival associations in the most cancer types (27), followed by mutation status (4) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible GLIS2 RNA expression–survival associations across cancer types. High GLIS2 expression shows unfavorable associations in UVM, UCEC, BLCA and OV, but favorable associations in KICH and LGG. 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 GLIS2 RNA expression.
This table summarizes GLIS2 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 4. The strongest signals are observed in KIRP for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for GLIS2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. GLIS2 shows lower tumor expression in KICH, UCEC and LUSC and higher tumor expression in KIRP, HNSC and LIHC. The KIRP box plot shows higher GLIS2 RNA expression in tumor versus normal tissue (log2 FC = +1.058, t-test p < 0.001).
This table shows molecular features associated with GLIS2 in patient tissues and cancer cell lines. In patient samples, GLIS2 shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, GLIS2 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 LUNG_NSCLC_LUSC and UPPER_AERODIGESTIVE_TRACT.
