Q-omics provides the consensus-scored HNRNPA1P52 profile across patient tissues and cancer cell-line models. HNRNPA1P52 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, HNRNPA1P52 is differentially expressed in 8, with the highest sampling consensus in COAD. Additionally, HNRNPA1P52 RNA expression shows 10,789 significant gene co-expression associations, with the highest sampling consensus in KICH. Together, these results highlight KIRP, COAD, and KICH as cancer lineages where HNRNPA1P52 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 HNRNPA1P52 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes HNRNPA1P52 survival associations across molecular data types. HNRNPA1P52 RNA expression shows survival associations in the most cancer types (24). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible HNRNPA1P52 RNA expression–survival associations across cancer types. High HNRNPA1P52 expression shows unfavorable associations in KIRP, PCPG, UVM and LIHC, but favorable associations in GBM and PRAD. 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 HNRNPA1P52 RNA expression.
This table summarizes HNRNPA1P52 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 8. The strongest signals are observed in COAD for RNA.
This table ranks reproducible tumor–normal expression differences for HNRNPA1P52. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. HNRNPA1P52 shows lower tumor expression in PAAD and higher tumor expression in COAD, LIHC, KIRC, KIRP and CHOL. The COAD box plot shows higher HNRNPA1P52 RNA expression in tumor versus normal tissue (log2 FC = +0.279, t-test p < 0.001).
This table shows molecular features associated with HNRNPA1P52 in patient tissues and cancer cell lines. In patient samples, HNRNPA1P52 shows the broadest associations at the RNA and protein expression levels, with KICH recurring as the lineage with the largest associated feature set.
