Q-omics provides the consensus-scored KRT16P3 profile across patient tissues and cancer cell-line models. KRT16P3 expression is associated with patient survival in 19 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, KRT16P3 is differentially expressed in 6, with the highest sampling consensus in LIHC. Additionally, KRT16P3 RNA expression shows 12,714 significant gene co-expression associations, with the highest sampling consensus in ESCA. Together, these results highlight UVM, LIHC, and ESCA as cancer lineages where KRT16P3 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 KRT16P3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes KRT16P3 survival associations across molecular data types. KRT16P3 RNA expression shows survival associations in the most cancer types (19), followed by mutation status (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible KRT16P3 RNA expression–survival associations across cancer types. High KRT16P3 expression shows unfavorable associations in UVM, PAAD, KICH and READ, but favorable associations in LIHC and ACC. The UVM Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .009). Together, the overview and detailed table identify UVM as the clearest survival context for KRT16P3 RNA expression.
This table summarizes KRT16P3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 6. The strongest signals are observed in LIHC for RNA.
This table ranks reproducible tumor–normal expression differences for KRT16P3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. KRT16P3 shows lower tumor expression in LIHC, BRCA, PRAD and KIRC and higher tumor expression in LUSC and LUAD. The LIHC box plot shows higher KRT16P3 RNA expression in normal versus tumor tissue (log2 FC = −0.028, t-test p = .001).
This table shows molecular features associated with KRT16P3 in patient tissues and cancer cell lines. In patient samples, KRT16P3 shows the broadest associations at the RNA and protein expression levels, with ESCA recurring as the lineage with the largest associated feature set.
