Q-omics provides the consensus-scored ATXN2L profile across patient tissues and cancer cell-line models. ATXN2L expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in LIHC. Among the 18 cancer types available for tumor–normal comparison, ATXN2L is differentially expressed in 16, with the highest sampling consensus in COAD. Additionally, ATXN2L protein abundance shows 27,391 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight LIHC, COAD, and LSCC as cancer lineages where ATXN2L 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 ATXN2L — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ATXN2L survival associations across molecular data types. ATXN2L RNA expression shows survival associations in the most cancer types (26), followed by mutation status (9) 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 ATXN2L RNA expression–survival associations across cancer types. High ATXN2L expression shows unfavorable associations in LIHC, KIRC, ACC, KIRP, COAD and BLCA. The LIHC 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 LIHC as the clearest survival context for ATXN2L RNA expression.
This table summarizes ATXN2L tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 6. The strongest signals are observed in COAD for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for ATXN2L. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ATXN2L shows higher tumor expression in COAD, KIRP, HNSC, BLCA, KIRC and LIHC. The COAD box plot shows higher ATXN2L RNA expression in tumor versus normal tissue (log2 FC = +1.122, t-test p < 0.001).
This table shows molecular features associated with ATXN2L in patient tissues and cancer cell lines. In patient samples, ATXN2L 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, ATXN2L 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 OESOPHAGUS and BLOOD_Leukemia.
