Replication-born double-strand break repair via sister chromatid exchange
associated omics data
GO:1990414Ontology (GO BP)GO biological process · ~7 member genes
Q-omics provides the Replication-born double-strand break repair via sister chromatid exchange (GO:1990414) pathway profile, scoring each patient from the combined activity of its roughly 7 member genes. Pathway activity is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, the pathway is differentially active in 11, with the highest sampling consensus in KIRC. Additionally, pathway RNA activity shows 35,669 significant cross-omics associations, again with the highest sampling consensus in STAD. Together, these results highlight KIRC, and STAD as cancer lineages where the pathway shows reproducible signals across outcome, tissue activity, and molecular association 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. Pathway-against-pathway and pathway-against-mutation comparisons are not available for ontology entities.
Survival associations
This table summarizes Replication-born double-strand break repair via sister chromatid exchange survival associations by molecular data type. RNA-level pathway activity shows survival associations in the most cancer types (25). The rightmost column indicates the cancer type with the highest sampling consensus for each layer.
This table ranks reproducible pathway activity–survival associations across cancer types. High Replication-born double-strand break repair via sister chromatid exchange activity shows favorable associations in CESC, LUSC and READ, but unfavorable associations in KIRC, OV and MESO. In the KIRC Kaplan–Meier curve the high-activity group declines faster, consistent with the unfavorable association (log-rank p < 0.001). KIRC ranks highest by sampling consensus for Replication-born double-strand break repair via sister chromatid exchange.
This table summarizes Replication-born double-strand break repair via sister chromatid exchange tumor–normal activity differences by data type. RNA-level activity shows significant tumor–normal differences in 11 cancer types, while mass-spec protein activity shows differences in 6. The strongest signals are in KIRC for RNA and COAD for protein.
This table ranks reproducible tumor–normal activity differences for the pathway. A positive fold-change indicates higher activity in tumor tissue. The pathway shows higher tumor activity across LUSC and LUAD and lower tumor activity in KIRC, THCA, KIRP and COAD. In the KIRC box plot, normal samples show higher pathway activity than tumor samples (log2 FC = −0.099, t-test p < 0.001).
This table shows molecular features associated with Replication-born double-strand break repair via sister chromatid exchange pathway activity in patient tissues and cancer cell lines. In patient samples, pathway activity is most strongly linked to RNA and protein features, with the largest associated set in STAD. In cancer cell lines, RNA-expression features and functional dependencies dominate, with the largest set in SKIN.
