Q-omics provides the consensus-scored GLIPR1L2 profile across patient tissues and cancer cell-line models. GLIPR1L2 expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, GLIPR1L2 is differentially expressed in 13, with the highest sampling consensus in THCA. Additionally, GLIPR1L2 RNA expression shows 18,020 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRC, THCA, and UVM as cancer lineages where GLIPR1L2 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 GLIPR1L2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes GLIPR1L2 survival associations across molecular data types. GLIPR1L2 RNA expression shows survival associations in the most cancer types (22), followed by mutation status (3) 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 GLIPR1L2 RNA expression–survival associations across cancer types. High GLIPR1L2 expression shows favorable associations in KIRC, LUAD, UCS, MESO, ESCA and ACC. 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 GLIPR1L2 RNA expression.
This table summarizes GLIPR1L2 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 1. The strongest signals are observed in THCA for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for GLIPR1L2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. GLIPR1L2 shows lower tumor expression in THCA, LUAD, BLCA, KICH, LUSC and UCEC. The THCA box plot shows higher GLIPR1L2 RNA expression in normal versus tumor tissue (log2 FC = −1.214, t-test p < 0.001).
This table shows molecular features associated with GLIPR1L2 in patient tissues and cancer cell lines. In patient samples, GLIPR1L2 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, GLIPR1L2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and LARGE_INTESTINE.
