Q-omics provides the consensus-scored LRIT3 profile across patient tissues and cancer cell-line models. LRIT3 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in LUAD. Among the 18 cancer types available for tumor–normal comparison, LRIT3 is differentially expressed in 9, with the highest sampling consensus in KIRC. Additionally, LRIT3 RNA expression shows 17,163 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight LUAD, KIRC, and UVM as cancer lineages where LRIT3 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 LRIT3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes LRIT3 survival associations across molecular data types. LRIT3 RNA expression shows survival associations in the most cancer types (23), 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 LRIT3 RNA expression–survival associations across cancer types. High LRIT3 expression shows unfavorable associations in LUAD and DLBC, but favorable associations in BLCA, ACC, HNSC and SKCM. The LUAD Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .013). Together, the overview and detailed table identify LUAD as the clearest survival context for LRIT3 RNA expression.
This table summarizes LRIT3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for LRIT3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. LRIT3 shows lower tumor expression in KIRC, KIRP and THCA and higher tumor expression in COAD, CHOL and LIHC. The KIRC box plot shows higher LRIT3 RNA expression in normal versus tumor tissue (log2 FC = −0.968, t-test p < 0.001).
This table shows molecular features associated with LRIT3 in patient tissues and cancer cell lines. In patient samples, LRIT3 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, LRIT3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in CNS and LARGE_INTESTINE.
