Q-omics provides the consensus-scored DSTN profile across patient tissues and cancer cell-line models. DSTN expression is associated with patient survival in 28 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, DSTN is differentially expressed in 16, with the highest sampling consensus in HNSC. Additionally, DSTN protein abundance shows 25,191 significant protein co-abundance associations, with the highest sampling consensus in HNSC. Together, these results highlight KIRC, and HNSC as cancer lineages where DSTN 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 DSTN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes DSTN survival associations across molecular data types. DSTN RNA expression shows survival associations in the most cancer types (28), 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 DSTN RNA expression–survival associations across cancer types. High DSTN expression shows unfavorable associations in CESC, BLCA, MESO, LIHC and HNSC, but favorable associations in KIRC. 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 DSTN RNA expression.
This table summarizes DSTN tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 7. The strongest signals are observed in HNSC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for DSTN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. DSTN shows lower tumor expression in THCA, BLCA, LUAD, KICH and LUSC and higher tumor expression in HNSC. The HNSC box plot shows higher DSTN RNA expression in tumor versus normal tissue (log2 FC = +0.513, t-test p < 0.001).
This table shows molecular features associated with DSTN in patient tissues and cancer cell lines. In patient samples, DSTN shows the broadest associations at the RNA and protein expression levels, with HNSC recurring as the lineage with the largest associated feature set. In cancer cell lines, DSTN RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SOFT_TISSUE, while CRISPR and shRNA rows add functional-dependency signals in CNS and BONE.
