Q-omics provides the consensus-scored THUMPD3 profile across patient tissues and cancer cell-line models. THUMPD3 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, THUMPD3 is differentially expressed in 15, with the highest sampling consensus in LIHC. Additionally, THUMPD3 protein abundance shows 27,271 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, LIHC, and GBM as cancer lineages where THUMPD3 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 THUMPD3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes THUMPD3 survival associations across molecular data types. THUMPD3 RNA expression shows survival associations in the most cancer types (22), followed by mutation status (5) and mass-spec protein abundance (10). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible THUMPD3 RNA expression–survival associations across cancer types. High THUMPD3 expression shows unfavorable associations in ACC, LIHC, MESO and KICH, but favorable associations in KIRC and READ. 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 THUMPD3 RNA expression.
This table summarizes THUMPD3 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 11. The strongest signals are observed in LIHC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for THUMPD3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. THUMPD3 shows lower tumor expression in KIRC and higher tumor expression in LIHC, LUAD, COAD, STAD and BLCA. The LIHC box plot shows higher THUMPD3 RNA expression in tumor versus normal tissue (log2 FC = +1.049, t-test p < 0.001).
This table shows molecular features associated with THUMPD3 in patient tissues and cancer cell lines. In patient samples, THUMPD3 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, THUMPD3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Lymphoma, while CRISPR and shRNA rows add functional-dependency signals in OESOPHAGUS and BLOOD_Leukemia.
