Q-omics provides the consensus-scored SMR3A profile across patient tissues and cancer cell-line models. SMR3A expression is associated with patient survival in 11 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, SMR3A is differentially expressed in 6, with the highest sampling consensus in THCA. Additionally, SMR3A protein abundance shows 17,526 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight KIRP, THCA, and PDAC as cancer lineages where SMR3A 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 SMR3A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SMR3A survival associations across molecular data types. SMR3A RNA expression shows survival associations in the most cancer types (11), 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 SMR3A RNA expression–survival associations across cancer types. High SMR3A expression shows unfavorable associations in KIRP, BRCA, TGCT, THYM and BLCA, but favorable associations in LUSC. The KIRP 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 KIRP as the clearest survival context for SMR3A RNA expression.
This table summarizes SMR3A 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 3. The strongest signals are observed in THCA for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for SMR3A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SMR3A shows lower tumor expression in THCA, HNSC, PRAD and LUSC and higher tumor expression in UCEC and LIHC. The THCA box plot shows higher SMR3A RNA expression in normal versus tumor tissue (log2 FC = −1.175, t-test p < 0.001).
This table shows molecular features associated with SMR3A in patient tissues and cancer cell lines. In patient samples, SMR3A 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, SMR3A RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and UPPER_AERODIGESTIVE_TRACT.
