Q-omics provides the consensus-scored TPX2 profile across patient tissues and cancer cell-line models. TPX2 expression is associated with patient survival in 29 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, TPX2 is differentially expressed in 18, with the highest sampling consensus in HNSC. Additionally, TPX2 protein abundance shows 32,272 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight KIRP, HNSC, and LUAD as cancer lineages where TPX2 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 TPX2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TPX2 survival associations across molecular data types. TPX2 RNA expression shows survival associations in the most cancer types (29), followed by mutation status (6) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TPX2 RNA expression–survival associations across cancer types. High TPX2 expression shows unfavorable associations in KIRP, MESO, ACC, LIHC, KICH and KIRC. 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 TPX2 RNA expression.
This table summarizes TPX2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 18, while mass-spec protein shows differences in 6. The strongest signals are observed in HNSC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for TPX2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TPX2 shows higher tumor expression in HNSC, LUAD, BLCA, KIRP, KIRC and COAD. The HNSC box plot shows higher TPX2 RNA expression in tumor versus normal tissue (log2 FC = +2.744, t-test p < 0.001).
This table shows molecular features associated with TPX2 in patient tissues and cancer cell lines. In patient samples, TPX2 shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, TPX2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in KIDNEY, while CRISPR and shRNA rows add functional-dependency signals in BREAST and BLOOD_Leukemia.
