Q-omics provides the consensus-scored SYN3 profile across patient tissues and cancer cell-line models. SYN3 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, SYN3 is differentially expressed in 11, with the highest sampling consensus in KIRP. Additionally, SYN3 RNA expression shows 17,708 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, KIRP, and GBM as cancer lineages where SYN3 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 SYN3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SYN3 survival associations across molecular data types. SYN3 RNA expression shows survival associations in the most cancer types (27), followed by mutation status (8) 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 SYN3 RNA expression–survival associations across cancer types. High SYN3 expression shows unfavorable associations in MESO and LUSC, but favorable associations in KIRC, UVM, LGG and GBM. 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 SYN3 RNA expression.
This table summarizes SYN3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 1. The strongest signals are observed in KIRP for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for SYN3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SYN3 shows lower tumor expression in KIRP, KIRC, KICH, LUSC and THCA and higher tumor expression in LIHC. The KIRP box plot shows higher SYN3 RNA expression in normal versus tumor tissue (log2 FC = −0.593, t-test p < 0.001).
This table shows molecular features associated with SYN3 in patient tissues and cancer cell lines. In patient samples, SYN3 shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, SYN3 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 LIVER and LARGE_INTESTINE.
