Q-omics provides the consensus-scored CAMLG profile across patient tissues and cancer cell-line models. CAMLG 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, CAMLG is differentially expressed in 11, with the highest sampling consensus in KIRC. Additionally, CAMLG RNA expression shows 18,723 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRC, and ACC as cancer lineages where CAMLG 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 CAMLG — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CAMLG survival associations across molecular data types. CAMLG RNA expression shows survival associations in the most cancer types (24), followed by mutation status (1) 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 CAMLG RNA expression–survival associations across cancer types. High CAMLG expression shows unfavorable associations in SCLC, KIRP, KICH, HNSC and OV, but favorable associations in KIRC. 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 CAMLG RNA expression.
This table summarizes CAMLG tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 5. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for CAMLG. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CAMLG shows lower tumor expression in UCEC and BLCA and higher tumor expression in KIRC, LIHC, THCA and CHOL. The KIRC box plot shows higher CAMLG RNA expression in tumor versus normal tissue (log2 FC = +0.995, t-test p < 0.001).
This table shows molecular features associated with CAMLG in patient tissues and cancer cell lines. In patient samples, CAMLG shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, CAMLG RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LARGE_INTESTINE, while CRISPR and shRNA rows add functional-dependency signals in BONE and SOFT_TISSUE.
