Q-omics provides the consensus-scored TCL1A profile across patient tissues and cancer cell-line models. TCL1A expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, TCL1A is differentially expressed in 10, with the highest sampling consensus in COAD. Additionally, TCL1A RNA expression shows 12,858 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight HNSC, COAD, and LSCC as cancer lineages where TCL1A 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 TCL1A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TCL1A survival associations across molecular data types. TCL1A RNA expression shows survival associations in the most cancer types (21), followed by 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 TCL1A RNA expression–survival associations across cancer types. High TCL1A expression shows favorable associations in HNSC, SCLC, CESC, SKCM, ESCA and BRCA. The HNSC 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 HNSC as the clearest survival context for TCL1A RNA expression.
This table summarizes TCL1A tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 3. The strongest signals are observed in COAD for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for TCL1A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TCL1A shows lower tumor expression in COAD, KICH, BLCA and THCA and higher tumor expression in BRCA and STAD. The COAD box plot shows higher TCL1A RNA expression in normal versus tumor tissue (log2 FC = −1.554, t-test p < 0.001).
This table shows molecular features associated with TCL1A in patient tissues and cancer cell lines. In patient samples, TCL1A shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, TCL1A 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_Myeloma and BLOOD_Lymphoma.
