Q-omics provides the consensus-scored ESAM profile across patient tissues and cancer cell-line models. ESAM 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, ESAM is differentially expressed in 15, with the highest sampling consensus in LUAD. Additionally, ESAM protein abundance shows 23,056 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRC, LUAD, and LSCC as cancer lineages where ESAM 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 ESAM — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ESAM survival associations across molecular data types. ESAM RNA expression shows survival associations in the most cancer types (24), followed by mutation status (5) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ESAM RNA expression–survival associations across cancer types. High ESAM expression shows unfavorable associations in UVM, COAD, MESO, ACC and BLCA, 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 ESAM RNA expression.
This table summarizes ESAM tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 6. The strongest signals are observed in LUAD for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for ESAM. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ESAM shows lower tumor expression in LUAD, KICH, THCA, LUSC and KIRP and higher tumor expression in LIHC. The LUAD box plot shows higher ESAM RNA expression in normal versus tumor tissue (log2 FC = −2.241, t-test p < 0.001).
This table shows molecular features associated with ESAM in patient tissues and cancer cell lines. In patient samples, ESAM shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, ESAM 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 BONE and BLOOD_Leukemia.
