Q-omics provides the consensus-scored TSR2 profile across patient tissues and cancer cell-line models. TSR2 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, TSR2 is differentially expressed in 12, with the highest sampling consensus in HNSC. Additionally, TSR2 protein abundance shows 24,382 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight ACC, HNSC, and PDAC as cancer lineages where TSR2 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 TSR2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TSR2 survival associations across molecular data types. TSR2 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (1) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TSR2 RNA expression–survival associations across cancer types. High TSR2 expression shows unfavorable associations in COAD, LIHC and LAML, but favorable associations in ACC, KIRC and SCLC. The ACC 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 ACC as the clearest survival context for TSR2 RNA expression.
This table summarizes TSR2 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 5. The strongest signals are observed in HNSC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for TSR2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TSR2 shows lower tumor expression in THCA and KIRP and higher tumor expression in HNSC, LIHC, COAD and BRCA. The HNSC box plot shows higher TSR2 RNA expression in tumor versus normal tissue (log2 FC = +0.710, t-test p < 0.001).
This table shows molecular features associated with TSR2 in patient tissues and cancer cell lines. In patient samples, TSR2 shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, TSR2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in LUNG_SCLC and BLOOD_Leukemia.
