Q-omics provides the consensus-scored TDRD3 profile across patient tissues and cancer cell-line models. TDRD3 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, TDRD3 is differentially expressed in 12, with the highest sampling consensus in KICH. Additionally, TDRD3 RNA expression shows 19,844 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRC, KICH, and ACC as cancer lineages where TDRD3 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 TDRD3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TDRD3 survival associations across molecular data types. TDRD3 RNA expression shows survival associations in the most cancer types (22), followed by mutation status (4) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TDRD3 RNA expression–survival associations across cancer types. High TDRD3 expression shows unfavorable associations in STAD and KICH, but favorable associations in KIRC, UCEC, KIRP and GBM. 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 TDRD3 RNA expression.
This table summarizes TDRD3 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 4. The strongest signals are observed in KIRC for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for TDRD3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TDRD3 shows lower tumor expression in KICH, LUSC, LUAD and THCA and higher tumor expression in KIRC and LIHC. The KICH box plot shows higher TDRD3 RNA expression in normal versus tumor tissue (log2 FC = −1.228, t-test p < 0.001).
This table shows molecular features associated with TDRD3 in patient tissues and cancer cell lines. In patient samples, TDRD3 shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, TDRD3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and BONE.
