Q-omics provides the consensus-scored KLRG2 profile across patient tissues and cancer cell-line models. KLRG2 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in SKCM. Among the 18 cancer types available for tumor–normal comparison, KLRG2 is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, KLRG2 RNA expression shows 15,797 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight SKCM, KIRC, and THYM as cancer lineages where KLRG2 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 KLRG2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes KLRG2 survival associations across molecular data types. KLRG2 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (3) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible KLRG2 RNA expression–survival associations across cancer types. High KLRG2 expression shows unfavorable associations in SKCM, UCEC and MESO, but favorable associations in HNSC, LUAD and LUSC. The SKCM 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 SKCM as the clearest survival context for KLRG2 RNA expression.
This table summarizes KLRG2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 3. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for KLRG2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. KLRG2 shows lower tumor expression in KIRC, KICH, LUAD and THCA and higher tumor expression in COAD and BLCA. The KIRC box plot shows higher KLRG2 RNA expression in normal versus tumor tissue (log2 FC = −3.240, t-test p < 0.001).
This table shows molecular features associated with KLRG2 in patient tissues and cancer cell lines. In patient samples, KLRG2 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, KLRG2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in URINARY_TRACT and BREAST.
