Q-omics provides the consensus-scored LCAT profile across patient tissues and cancer cell-line models. LCAT expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, LCAT is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, LCAT protein abundance shows 21,359 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight ACC, KIRC, and LSCC as cancer lineages where LCAT 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 LCAT — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes LCAT survival associations across molecular data types. LCAT RNA expression shows survival associations in the most cancer types (25), followed by mutation status (4) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible LCAT RNA expression–survival associations across cancer types. High LCAT expression shows unfavorable associations in ACC and KIRC, but favorable associations in THYM, SKCM, LGG and LIHC. 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 LCAT RNA expression.
This table summarizes LCAT tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 6. The strongest signals are observed in KIRC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for LCAT. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. LCAT shows lower tumor expression in LIHC, KICH, LUAD and THCA and higher tumor expression in KIRC and HNSC. The KIRC box plot shows higher LCAT RNA expression in tumor versus normal tissue (log2 FC = +0.978, t-test p < 0.001).
This table shows molecular features associated with LCAT in patient tissues and cancer cell lines. In patient samples, LCAT 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, LCAT RNA and mutation anchors are most strongly linked to RNA-expression features, especially in URINARY_TRACT, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and BONE.
