Q-omics provides the consensus-scored SRRD profile across patient tissues and cancer cell-line models. SRRD expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in CESC. Among the 18 cancer types available for tumor–normal comparison, SRRD is differentially expressed in 13, with the highest sampling consensus in THCA. Additionally, SRRD RNA expression shows 20,071 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight CESC, THCA, and ACC as cancer lineages where SRRD 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 SRRD — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SRRD survival associations across molecular data types. SRRD RNA expression shows survival associations in the most cancer types (26), followed by mutation status (3) 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 SRRD RNA expression–survival associations across cancer types. High SRRD expression shows unfavorable associations in CESC, LIHC, ACC, PAAD and HNSC, but favorable associations in BRCA. The CESC 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 CESC as the clearest survival context for SRRD RNA expression.
This table summarizes SRRD tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 3. The strongest signals are observed in THCA for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for SRRD. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SRRD shows lower tumor expression in THCA and higher tumor expression in HNSC, LIHC, KIRC, LUSC and LUAD. The THCA box plot shows higher SRRD RNA expression in normal versus tumor tissue (log2 FC = −1.417, t-test p < 0.001).
This table shows molecular features associated with SRRD in patient tissues and cancer cell lines. In patient samples, SRRD 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, SRRD RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OESOPHAGUS, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Myeloma and BLOOD_Leukemia.
