lipase family member KGenealiases: LIPL2 · bA186O14.2
Q-omics provides the consensus-scored LIPK profile across patient tissues and cancer cell-line models. LIPK expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in DLBC. Among the 18 cancer types available for tumor–normal comparison, LIPK is differentially expressed in 7, with the highest sampling consensus in LUAD. Additionally, LIPK RNA expression shows 10,206 significant protein co-abundance associations, with the highest sampling consensus in HNSC. Together, these results highlight DLBC, LUAD, and HNSC as cancer lineages where LIPK 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 LIPK — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes LIPK survival associations across molecular data types. LIPK RNA expression shows survival associations in the most cancer types (20), followed by mutation status (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible LIPK RNA expression–survival associations across cancer types. High LIPK expression shows unfavorable associations in DLBC, KIRC, LUAD, OV, KIRP and LUSC. The DLBC 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 DLBC as the clearest survival context for LIPK RNA expression.
This table summarizes LIPK tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 7. The strongest signals are observed in LUAD for RNA.
This table ranks reproducible tumor–normal expression differences for LIPK. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. LIPK shows lower tumor expression in BRCA and KIRC and higher tumor expression in LUAD, BLCA, LUSC and COAD. The LUAD box plot shows higher LIPK RNA expression in tumor versus normal tissue (log2 FC = +0.982, t-test p < 0.001).
This table shows molecular features associated with LIPK in patient tissues and cancer cell lines. In patient samples, LIPK 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, LIPK RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LARGE_INTESTINE, while CRISPR and shRNA rows add functional-dependency signals in OESOPHAGUS and BREAST.
