Q-omics provides the consensus-scored HNRNPA0 profile across patient tissues and cancer cell-line models. HNRNPA0 expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, HNRNPA0 is differentially expressed in 12, with the highest sampling consensus in COAD. Additionally, HNRNPA0 protein abundance shows 24,894 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRP, COAD, and GBM as cancer lineages where HNRNPA0 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 HNRNPA0 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes HNRNPA0 survival associations across molecular data types. HNRNPA0 RNA expression shows survival associations in the most cancer types (22), followed by mutation status (3) 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 HNRNPA0 RNA expression–survival associations across cancer types. High HNRNPA0 expression shows unfavorable associations in KIRP, LUAD, LIHC and ACC, but favorable associations in KIRC and READ. The KIRP 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 KIRP as the clearest survival context for HNRNPA0 RNA expression.
This table summarizes HNRNPA0 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 6. The strongest signals are observed in COAD for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for HNRNPA0. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. HNRNPA0 shows higher tumor expression in COAD, LIHC, HNSC, KIRC, CHOL and STAD. The COAD box plot shows higher HNRNPA0 RNA expression in tumor versus normal tissue (log2 FC = +0.665, t-test p < 0.001).
This table shows molecular features associated with HNRNPA0 in patient tissues and cancer cell lines. In patient samples, HNRNPA0 shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, HNRNPA0 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Leukemia, while CRISPR and shRNA rows add functional-dependency signals in PANCREAS and LARGE_INTESTINE.
