chymotrypsin like elastase 3AGenealiases: ELA3 · ELA3A
Q-omics provides the consensus-scored CELA3A profile across patient tissues and cancer cell-line models. CELA3A expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, CELA3A is differentially expressed in 6, with the highest sampling consensus in COAD. Additionally, CELA3A RNA expression shows 7,270 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight ACC, COAD, and PDAC as cancer lineages where CELA3A 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 CELA3A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CELA3A survival associations across molecular data types. CELA3A RNA expression shows survival associations in the most cancer types (20), followed by mutation status (6) 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 CELA3A RNA expression–survival associations across cancer types. High CELA3A expression shows unfavorable associations in ACC, KIRC, SCLC, UVM, DLBC and MESO. The ACC 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 ACC as the clearest survival context for CELA3A RNA expression.
This table summarizes CELA3A tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 6, while mass-spec protein shows differences in 2. The strongest signals are observed in COAD for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for CELA3A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CELA3A shows lower tumor expression in COAD, BRCA, ESCA and STAD and higher tumor expression in LIHC and UCEC. The COAD box plot shows higher CELA3A RNA expression in normal versus tumor tissue (log2 FC = −0.389, t-test p < 0.001).
This table shows molecular features associated with CELA3A in patient tissues and cancer cell lines. In patient samples, CELA3A shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, CELA3A RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Leukemia, while CRISPR and shRNA rows add functional-dependency signals in LUNG_SCLC and LARGE_INTESTINE.
