Q-omics provides the consensus-scored HNRNPA3 profile across patient tissues and cancer cell-line models. HNRNPA3 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, HNRNPA3 is differentially expressed in 13, with the highest sampling consensus in HNSC. Additionally, HNRNPA3 protein abundance shows 27,081 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRP, HNSC, and GBM as cancer lineages where HNRNPA3 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 HNRNPA3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes HNRNPA3 survival associations across molecular data types. HNRNPA3 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (5) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible HNRNPA3 RNA expression–survival associations across cancer types. High HNRNPA3 expression shows unfavorable associations in KIRP, ACC, LIHC and MESO, but favorable associations in KIRC and THYM. 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 HNRNPA3 RNA expression.
This table summarizes HNRNPA3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 6. The strongest signals are observed in HNSC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for HNRNPA3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. HNRNPA3 shows lower tumor expression in THCA and KICH and higher tumor expression in HNSC, LIHC, STAD and LUSC. The HNSC box plot shows higher HNRNPA3 RNA expression in tumor versus normal tissue (log2 FC = +0.989, t-test p < 0.001).
This table shows molecular features associated with HNRNPA3 in patient tissues and cancer cell lines. In patient samples, HNRNPA3 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, HNRNPA3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OESOPHAGUS, while CRISPR and shRNA rows add functional-dependency signals in SKIN and BLOOD_Leukemia.
