Q-omics provides the consensus-scored EMP3 profile across patient tissues and cancer cell-line models. EMP3 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, EMP3 is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, EMP3 RNA expression shows 23,532 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight MESO, KIRC, and LSCC as cancer lineages where EMP3 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 EMP3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes EMP3 survival associations across molecular data types. EMP3 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (2) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible EMP3 RNA expression–survival associations across cancer types. High EMP3 expression shows unfavorable associations in MESO, UVM, KIRC, LGG and LAML, but favorable associations in UCEC. The MESO 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 MESO as the clearest survival context for EMP3 RNA expression.
This table summarizes EMP3 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 3. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for EMP3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. EMP3 shows lower tumor expression in BLCA, LUSC and LUAD and higher tumor expression in KIRC, HNSC and KIRP. The KIRC box plot shows higher EMP3 RNA expression in tumor versus normal tissue (log2 FC = +1.993, t-test p < 0.001).
This table shows molecular features associated with EMP3 in patient tissues and cancer cell lines. In patient samples, EMP3 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, EMP3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and BLOOD_Lymphoma.
