Q-omics provides the consensus-scored TPD52 profile across patient tissues and cancer cell-line models. TPD52 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, TPD52 is differentially expressed in 15, with the highest sampling consensus in LUAD. Additionally, TPD52 protein abundance shows 25,889 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRP, LUAD, and GBM as cancer lineages where TPD52 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 TPD52 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TPD52 survival associations across molecular data types. TPD52 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (5) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TPD52 RNA expression–survival associations across cancer types. High TPD52 expression shows unfavorable associations in KIRP, UVM, UCEC, ESCA and LIHC, but favorable associations in BRCA. 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 TPD52 RNA expression.
This table summarizes TPD52 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 8. The strongest signals are observed in LUAD for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for TPD52. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TPD52 shows lower tumor expression in THCA, KIRP and KIRC and higher tumor expression in LUAD, LUSC and LIHC. The LUAD box plot shows higher TPD52 RNA expression in tumor versus normal tissue (log2 FC = +1.152, t-test p < 0.001).
This table shows molecular features associated with TPD52 in patient tissues and cancer cell lines. In patient samples, TPD52 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, TPD52 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in OESOPHAGUS and BLOOD_Lymphoma.
