Q-omics provides the consensus-scored THUMPD2 profile across patient tissues and cancer cell-line models. THUMPD2 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, THUMPD2 is differentially expressed in 14, with the highest sampling consensus in COAD. Additionally, THUMPD2 RNA expression shows 20,124 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight ACC, COAD, and UVM as cancer lineages where THUMPD2 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 THUMPD2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes THUMPD2 survival associations across molecular data types. THUMPD2 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (5) 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 THUMPD2 RNA expression–survival associations across cancer types. High THUMPD2 expression shows unfavorable associations in ACC, LIHC, UVM, KICH, HNSC and KIRP. The ACC 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 ACC as the clearest survival context for THUMPD2 RNA expression.
This table summarizes THUMPD2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 5. The strongest signals are observed in KIRC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for THUMPD2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. THUMPD2 shows lower tumor expression in KICH and higher tumor expression in COAD, KIRC, LUAD, BLCA and LIHC. The COAD box plot shows higher THUMPD2 RNA expression in tumor versus normal tissue (log2 FC = +1.053, t-test p < 0.001).
This table shows molecular features associated with THUMPD2 in patient tissues and cancer cell lines. In patient samples, THUMPD2 shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, THUMPD2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OESOPHAGUS, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and UPPER_AERODIGESTIVE_TRACT.
