Q-omics provides the consensus-scored KHDRBS2 profile across patient tissues and cancer cell-line models. KHDRBS2 expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in PAAD. Among the 18 cancer types available for tumor–normal comparison, KHDRBS2 is differentially expressed in 10, with the highest sampling consensus in COAD. Additionally, KHDRBS2 RNA expression shows 22,602 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight PAAD, COAD, and GBM as cancer lineages where KHDRBS2 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 KHDRBS2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes KHDRBS2 survival associations across molecular data types. KHDRBS2 RNA expression shows survival associations in the most cancer types (21), followed by mutation status (7) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible KHDRBS2 RNA expression–survival associations across cancer types. High KHDRBS2 expression shows favorable associations in PAAD, LGG, ESCA, SCLC, LUAD and HNSC. The PAAD Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify PAAD as the clearest survival context for KHDRBS2 RNA expression.
This table summarizes KHDRBS2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 5. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for KHDRBS2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. KHDRBS2 shows lower tumor expression in COAD, KIRC, THCA, LUSC, LUAD and READ. The COAD box plot shows higher KHDRBS2 RNA expression in normal versus tumor tissue (log2 FC = −0.931, t-test p < 0.001).
This table shows molecular features associated with KHDRBS2 in patient tissues and cancer cell lines. In patient samples, KHDRBS2 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, KHDRBS2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Lymphoma and LARGE_INTESTINE.
