Q-omics provides the consensus-scored TDP2 profile across patient tissues and cancer cell-line models. TDP2 expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, TDP2 is differentially expressed in 12, with the highest sampling consensus in COAD. Additionally, TDP2 protein abundance shows 25,962 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight KIRC, COAD, and PDAC as cancer lineages where TDP2 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 TDP2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TDP2 survival associations across molecular data types. TDP2 RNA expression shows survival associations in the most cancer types (22), followed by mutation status (2) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TDP2 RNA expression–survival associations across cancer types. High TDP2 expression shows unfavorable associations in ESCA, HNSC and LIHC, but favorable associations in KIRC, BLCA and OV. The KIRC 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 KIRC as the clearest survival context for TDP2 RNA expression.
This table summarizes TDP2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 9. The strongest signals are observed in COAD for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for TDP2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TDP2 shows lower tumor expression in COAD, KICH, KIRP and READ and higher tumor expression in HNSC and LIHC. The COAD box plot shows higher TDP2 RNA expression in normal versus tumor tissue (log2 FC = −2.345, t-test p < 0.001).
This table shows molecular features associated with TDP2 in patient tissues and cancer cell lines. In patient samples, TDP2 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, TDP2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BONE, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and SKIN.
