Q-omics provides the consensus-scored LRRC66 profile across patient tissues and cancer cell-line models. LRRC66 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in LUAD. Among the 18 cancer types available for tumor–normal comparison, LRRC66 is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, LRRC66 RNA expression shows 18,481 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight LUAD, KIRC, and UVM as cancer lineages where LRRC66 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 LRRC66 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes LRRC66 survival associations across molecular data types. LRRC66 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible LRRC66 RNA expression–survival associations across cancer types. High LRRC66 expression shows unfavorable associations in LUAD, UVM, LGG, CESC and ACC, but favorable associations in OV. 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 LRRC66 RNA expression.
This table summarizes LRRC66 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for LRRC66. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. LRRC66 shows lower tumor expression in COAD, KICH, READ, BLCA and BRCA and higher tumor expression in KIRC. The KIRC box plot shows higher LRRC66 RNA expression in tumor versus normal tissue (log2 FC = +0.687, t-test p < 0.001).
This table shows molecular features associated with LRRC66 in patient tissues and cancer cell lines. In patient samples, LRRC66 shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, LRRC66 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BONE, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Lymphoma and LARGE_INTESTINE.
