Q-omics provides the consensus-scored TENT2 profile across patient tissues and cancer cell-line models. TENT2 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, TENT2 is differentially expressed in 11, with the highest sampling consensus in KIRC. Additionally, TENT2 RNA expression shows 20,394 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRC, and UVM as cancer lineages where TENT2 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 TENT2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TENT2 survival associations across molecular data types. TENT2 RNA expression shows survival associations in the most cancer types (21), followed by mutation status (5) and mass-spec protein abundance (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TENT2 RNA expression–survival associations across cancer types. High TENT2 expression shows unfavorable associations in OV and LGG, but favorable associations in KIRC, SKCM, BLCA 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 TENT2 RNA expression.
This table summarizes TENT2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 1. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for TENT2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TENT2 shows lower tumor expression in LUSC and KICH and higher tumor expression in KIRC, LIHC, CHOL and KIRP. The KIRC box plot shows higher TENT2 RNA expression in tumor versus normal tissue (log2 FC = +0.543, t-test p < 0.001).
This table shows molecular features associated with TENT2 in patient tissues and cancer cell lines. In patient samples, TENT2 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, TENT2 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.
