Q-omics provides the consensus-scored TGFBR3 profile across patient tissues and cancer cell-line models. TGFBR3 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, TGFBR3 is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, TGFBR3 RNA expression shows 19,570 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRC, and UVM as cancer lineages where TGFBR3 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 TGFBR3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TGFBR3 survival associations across molecular data types. TGFBR3 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (7) 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 TGFBR3 RNA expression–survival associations across cancer types. High TGFBR3 expression shows unfavorable associations in SCLC, ESCA, COAD and THCA, but favorable associations in KIRC and HNSC. 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 TGFBR3 RNA expression.
This table summarizes TGFBR3 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 7. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for TGFBR3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TGFBR3 shows lower tumor expression in KIRC, KICH, BLCA, KIRP, THCA and LUAD. The KIRC box plot shows higher TGFBR3 RNA expression in normal versus tumor tissue (log2 FC = −1.338, t-test p < 0.001).
This table shows molecular features associated with TGFBR3 in patient tissues and cancer cell lines. In patient samples, TGFBR3 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, TGFBR3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Lymphoma and LARGE_INTESTINE.
