Q-omics provides the consensus-scored LCA5 profile across patient tissues and cancer cell-line models. LCA5 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, LCA5 is differentially expressed in 10, with the highest sampling consensus in KICH. Additionally, LCA5 RNA expression shows 20,542 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight KIRC, KICH, and KIRP as cancer lineages where LCA5 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 LCA5 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes LCA5 survival associations across molecular data types. LCA5 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (6) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible LCA5 RNA expression–survival associations across cancer types. High LCA5 expression shows unfavorable associations in COAD, BLCA, MESO and ESCA, but favorable associations in KIRC and LUAD. The KIRC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRC as the clearest survival context for LCA5 RNA expression.
This table summarizes LCA5 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 4. The strongest signals are observed in KICH for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for LCA5. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. LCA5 shows lower tumor expression in KICH, UCEC, LUAD, BRCA and LUSC and higher tumor expression in CHOL. The KICH box plot shows higher LCA5 RNA expression in normal versus tumor tissue (log2 FC = −1.648, t-test p < 0.001).
This table shows molecular features associated with LCA5 in patient tissues and cancer cell lines. In patient samples, LCA5 shows the broadest associations at the RNA and protein expression levels, with KIRP recurring as the lineage with the largest associated feature set. In cancer cell lines, LCA5 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SOFT_TISSUE, while CRISPR and shRNA rows add functional-dependency signals in URINARY_TRACT and UPPER_AERODIGESTIVE_TRACT.