Q-omics provides the consensus-scored LIX1L profile across patient tissues and cancer cell-line models. LIX1L expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, LIX1L is differentially expressed in 14, with the highest sampling consensus in KIRC. Additionally, LIX1L protein abundance shows 27,530 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight UVM, KIRC, and LSCC as cancer lineages where LIX1L 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 LIX1L — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes LIX1L survival associations across molecular data types. LIX1L RNA expression shows survival associations in the most cancer types (20), 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 LIX1L RNA expression–survival associations across cancer types. High LIX1L expression shows unfavorable associations in UVM, ACC, BLCA, LIHC and KIRP, but favorable associations in LGG. The UVM 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 UVM as the clearest survival context for LIX1L RNA expression.
This table summarizes LIX1L tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 6. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for LIX1L. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. LIX1L shows lower tumor expression in THCA, BLCA and KICH and higher tumor expression in KIRC, KIRP and LIHC. The KIRC box plot shows higher LIX1L RNA expression in tumor versus normal tissue (log2 FC = +1.040, t-test p < 0.001).
This table shows molecular features associated with LIX1L in patient tissues and cancer cell lines. In patient samples, LIX1L 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, LIX1L RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Lymphoma, while CRISPR and shRNA rows add functional-dependency signals in URINARY_TRACT and BLOOD_Leukemia.
