short chain dehydrogenase/reductase family 16C member 5Genealiases: EPHD-2 · RDH#2 · RDH-E2 · RDHE2 · retSDR2
Q-omics provides the consensus-scored SDR16C5 profile across patient tissues and cancer cell-line models. SDR16C5 expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, SDR16C5 is differentially expressed in 10, with the highest sampling consensus in KIRC. Additionally, SDR16C5 RNA expression shows 18,574 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, and GBM as cancer lineages where SDR16C5 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 SDR16C5 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SDR16C5 survival associations across molecular data types. SDR16C5 RNA expression shows survival associations in the most cancer types (22), followed by mutation status (4) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible SDR16C5 RNA expression–survival associations across cancer types. High SDR16C5 expression shows unfavorable associations in KIRC, PAAD, LUSC and SKCM, but favorable associations in HNSC and LUAD. The KIRC 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 KIRC as the clearest survival context for SDR16C5 RNA expression.
This table summarizes SDR16C5 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 5. The strongest signals are observed in KIRC for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for SDR16C5. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SDR16C5 shows lower tumor expression in KIRC, LUAD, LUSC and KICH and higher tumor expression in THCA and PAAD. The KIRC box plot shows higher SDR16C5 RNA expression in normal versus tumor tissue (log2 FC = −0.143, t-test p < 0.001).
This table shows molecular features associated with SDR16C5 in patient tissues and cancer cell lines. In patient samples, SDR16C5 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, SDR16C5 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in UPPER_AERODIGESTIVE_TRACT, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and LUNG_NSCLC_LUAD.
