Q-omics provides the consensus-scored SNX3 profile across patient tissues and cancer cell-line models. SNX3 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, SNX3 is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, SNX3 protein abundance shows 24,736 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight HNSC, KIRC, and LSCC as cancer lineages where SNX3 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 SNX3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SNX3 survival associations across molecular data types. SNX3 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (1) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible SNX3 RNA expression–survival associations across cancer types. High SNX3 expression shows unfavorable associations in HNSC, KIRP, BRCA, ACC, LIHC and MESO. The HNSC 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 HNSC as the clearest survival context for SNX3 RNA expression.
This table summarizes SNX3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 7. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for SNX3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SNX3 shows lower tumor expression in THCA, KICH and LUAD and higher tumor expression in KIRC, LIHC and HNSC. The KIRC box plot shows higher SNX3 RNA expression in tumor versus normal tissue (log2 FC = +0.704, t-test p < 0.001).
This table shows molecular features associated with SNX3 in patient tissues and cancer cell lines. In patient samples, SNX3 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, SNX3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in STOMACH and BLOOD_Leukemia.
