Q-omics provides the consensus-scored LPIN1 profile across patient tissues and cancer cell-line models. LPIN1 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, LPIN1 is differentially expressed in 9, with the highest sampling consensus in KIRC. Additionally, LPIN1 RNA expression shows 20,682 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight ACC, and KIRC as cancer lineages where LPIN1 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 LPIN1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes LPIN1 survival associations across molecular data types. LPIN1 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (5) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible LPIN1 RNA expression–survival associations across cancer types. High LPIN1 expression shows unfavorable associations in ACC and DLBC, but favorable associations in UVM, SCLC, CHOL and LUAD. The ACC 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 ACC as the clearest survival context for LPIN1 RNA expression.
This table summarizes LPIN1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9, while mass-spec protein shows differences in 5. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for LPIN1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. LPIN1 shows lower tumor expression in KIRC, HNSC, THCA, BRCA and KIRP and higher tumor expression in COAD. The KIRC box plot shows higher LPIN1 RNA expression in normal versus tumor tissue (log2 FC = −0.867, t-test p < 0.001).
This table shows molecular features associated with LPIN1 in patient tissues and cancer cell lines. In patient samples, LPIN1 shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, LPIN1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Leukemia, while CRISPR and shRNA rows add functional-dependency signals in BONE and UPPER_AERODIGESTIVE_TRACT.
