Q-omics provides the consensus-scored TFR2 profile across patient tissues and cancer cell-line models. TFR2 expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, TFR2 is differentially expressed in 16, with the highest sampling consensus in COAD. Additionally, TFR2 RNA expression shows 17,230 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRC, COAD, and ACC as cancer lineages where TFR2 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 TFR2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TFR2 survival associations across molecular data types. TFR2 RNA expression shows survival associations in the most cancer types (21), followed by mutation status (3) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TFR2 RNA expression–survival associations across cancer types. High TFR2 expression shows unfavorable associations in KIRC, MESO, ACC, THCA and UVM, but favorable associations in HNSC. The KIRC 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 KIRC as the clearest survival context for TFR2 RNA expression.
This table summarizes TFR2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 5. The strongest signals are observed in COAD for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for TFR2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TFR2 shows higher tumor expression in COAD, BLCA, HNSC, LUAD, THCA and KIRC. The COAD box plot shows higher TFR2 RNA expression in tumor versus normal tissue (log2 FC = +1.732, t-test p < 0.001).
This table shows molecular features associated with TFR2 in patient tissues and cancer cell lines. In patient samples, TFR2 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, TFR2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Lymphoma and BLOOD_Leukemia.
