Q-omics provides the consensus-scored SMPD4 profile across patient tissues and cancer cell-line models. SMPD4 expression is associated with patient survival in 28 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, SMPD4 is differentially expressed in 17, with the highest sampling consensus in HNSC. Additionally, SMPD4 protein abundance shows 28,995 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight MESO, HNSC, and LSCC as cancer lineages where SMPD4 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 SMPD4 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SMPD4 survival associations across molecular data types. SMPD4 RNA expression shows survival associations in the most cancer types (28), followed by mutation status (6) and mass-spec protein abundance (9). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible SMPD4 RNA expression–survival associations across cancer types. High SMPD4 expression shows unfavorable associations in MESO, ACC, LIHC, KIRP and KIRC, but favorable associations in BRCA. The MESO 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 MESO as the clearest survival context for SMPD4 RNA expression.
This table summarizes SMPD4 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 17, while mass-spec protein shows differences in 8. The strongest signals are observed in HNSC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for SMPD4. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SMPD4 shows lower tumor expression in THCA and higher tumor expression in HNSC, COAD, KIRP, STAD and BLCA. The HNSC box plot shows higher SMPD4 RNA expression in tumor versus normal tissue (log2 FC = +1.196, t-test p < 0.001).
This table shows molecular features associated with SMPD4 in patient tissues and cancer cell lines. In patient samples, SMPD4 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, SMPD4 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and LARGE_INTESTINE.
