Q-omics provides the consensus-scored LYPD3 profile across patient tissues and cancer cell-line models. LYPD3 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in LUAD. Among the 18 cancer types available for tumor–normal comparison, LYPD3 is differentially expressed in 11, with the highest sampling consensus in KIRC. Additionally, LYPD3 protein abundance shows 23,032 significant protein co-abundance associations, with the highest sampling consensus in HNSC. Together, these results highlight LUAD, KIRC, and HNSC as cancer lineages where LYPD3 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 LYPD3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes LYPD3 survival associations across molecular data types. LYPD3 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (6) and mass-spec protein abundance (10). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible LYPD3 RNA expression–survival associations across cancer types. High LYPD3 expression shows unfavorable associations in LUAD, KIRC, ACC, SKCM and LAML, but favorable associations in UVM. The LUAD 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 LUAD as the clearest survival context for LYPD3 RNA expression.
This table summarizes LYPD3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 9. The strongest signals are observed in KIRC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for LYPD3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. LYPD3 shows lower tumor expression in KIRC, KICH and KIRP and higher tumor expression in COAD, LUSC and LUAD. The KIRC box plot shows higher LYPD3 RNA expression in normal versus tumor tissue (log2 FC = −1.284, t-test p < 0.001).
This table shows molecular features associated with LYPD3 in patient tissues and cancer cell lines. In patient samples, LYPD3 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, LYPD3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in LUNG_SCLC and BLOOD_Leukemia.
