Q-omics provides the consensus-scored SCTR profile across patient tissues and cancer cell-line models. SCTR expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, SCTR is differentially expressed in 13, with the highest sampling consensus in KICH. Additionally, SCTR RNA expression shows 20,218 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRC, KICH, and LSCC as cancer lineages where SCTR 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 SCTR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SCTR survival associations across molecular data types. SCTR RNA expression shows survival associations in the most cancer types (21), followed by mutation status (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible SCTR RNA expression–survival associations across cancer types. High SCTR expression shows unfavorable associations in STAD, COAD, UVM and LUSC, but favorable associations in KIRC and MESO. 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 SCTR RNA expression.
This table summarizes SCTR 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 2. The strongest signals are observed in KIRC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for SCTR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SCTR shows lower tumor expression in KICH, KIRP, KIRC, COAD, LUAD and STAD. The KICH box plot shows higher SCTR RNA expression in normal versus tumor tissue (log2 FC = −3.730, t-test p < 0.001).
This table shows molecular features associated with SCTR in patient tissues and cancer cell lines. In patient samples, SCTR 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, SCTR 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 OVARY and LARGE_INTESTINE.
