Q-omics provides the consensus-scored TSEN2 profile across patient tissues and cancer cell-line models. TSEN2 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in KICH. Among the 18 cancer types available for tumor–normal comparison, TSEN2 is differentially expressed in 12, with the highest sampling consensus in COAD. Additionally, TSEN2 RNA expression shows 21,131 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KICH, COAD, and ACC as cancer lineages where TSEN2 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 TSEN2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TSEN2 survival associations across molecular data types. TSEN2 RNA expression shows survival associations in the most cancer types (27), followed by mutation status (3) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TSEN2 RNA expression–survival associations across cancer types. High TSEN2 expression shows unfavorable associations in KICH, KIRC, LIHC and SCLC, but favorable associations in BLCA and UVM. The KICH Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .002). Together, the overview and detailed table identify KICH as the clearest survival context for TSEN2 RNA expression.
This table summarizes TSEN2 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 3. The strongest signals are observed in COAD for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for TSEN2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TSEN2 shows lower tumor expression in KIRC, THCA and KICH and higher tumor expression in COAD, LIHC and CHOL. The COAD box plot shows higher TSEN2 RNA expression in tumor versus normal tissue (log2 FC = +1.146, t-test p < 0.001).
This table shows molecular features associated with TSEN2 in patient tissues and cancer cell lines. In patient samples, TSEN2 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, TSEN2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Leukemia, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUAD and SOFT_TISSUE.
