Q-omics provides the consensus-scored XIRP2 profile across patient tissues and cancer cell-line models. XIRP2 expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in LIHC. Among the 18 cancer types available for tumor–normal comparison, XIRP2 is differentially expressed in 5, with the highest sampling consensus in HNSC. Additionally, XIRP2 protein abundance shows 13,723 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight LIHC, HNSC, and PDAC as cancer lineages where XIRP2 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 XIRP2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes XIRP2 survival associations across molecular data types. XIRP2 RNA expression shows survival associations in the most cancer types (21), followed by mutation status (11) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible XIRP2 RNA expression–survival associations across cancer types. High XIRP2 expression shows unfavorable associations in LIHC, THCA, READ, HNSC, SCLC and KIRP. The LIHC 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 LIHC as the clearest survival context for XIRP2 RNA expression.
This table summarizes XIRP2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 5, while mass-spec protein shows differences in 2. The strongest signals are observed in HNSC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for XIRP2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. XIRP2 shows lower tumor expression in HNSC, BLCA, LUSC, UCEC and KIRP. The HNSC box plot shows higher XIRP2 RNA expression in normal versus tumor tissue (log2 FC = −2.400, t-test p = .002).
This table shows molecular features associated with XIRP2 in patient tissues and cancer cell lines. In patient samples, XIRP2 shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, XIRP2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in UPPER_AERODIGESTIVE_TRACT, while CRISPR and shRNA rows add functional-dependency signals in BREAST and BLOOD_Leukemia.
