Q-omics provides the consensus-scored HNRNPK profile across patient tissues and cancer cell-line models. HNRNPK expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, HNRNPK is differentially expressed in 16, with the highest sampling consensus in HNSC. Additionally, HNRNPK protein abundance shows 30,482 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight ACC, HNSC, and LSCC as cancer lineages where HNRNPK 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 HNRNPK — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes HNRNPK survival associations across molecular data types. HNRNPK RNA expression shows survival associations in the most cancer types (24), followed by mutation status (4) 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 HNRNPK RNA expression–survival associations across cancer types. High HNRNPK expression shows unfavorable associations in ACC, MESO, LIHC and UVM, but favorable associations in KIRC and BRCA. The ACC 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 ACC as the clearest survival context for HNRNPK RNA expression.
This table summarizes HNRNPK 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 5. The strongest signals are observed in HNSC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for HNRNPK. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. HNRNPK shows lower tumor expression in THCA and higher tumor expression in HNSC, BLCA, STAD, LIHC and BRCA. The HNSC box plot shows higher HNRNPK RNA expression in tumor versus normal tissue (log2 FC = +0.818, t-test p < 0.001).
This table shows molecular features associated with HNRNPK in patient tissues and cancer cell lines. In patient samples, HNRNPK 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, HNRNPK RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in SKIN and BLOOD_Leukemia.
