pre T cell antigen receptor alphaGenealiases: IMD126 · PT-ALPHA · PTA
Q-omics provides the consensus-scored PTCRA profile across patient tissues and cancer cell-line models. PTCRA expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, PTCRA is differentially expressed in 12, with the highest sampling consensus in LUAD. Additionally, PTCRA RNA expression shows 16,161 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight HNSC, LUAD, and GBM as cancer lineages where PTCRA 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 PTCRA — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PTCRA survival associations across molecular data types. PTCRA RNA expression shows survival associations in the most cancer types (23), followed by mutation status (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PTCRA RNA expression–survival associations across cancer types. High PTCRA expression shows unfavorable associations in LGG and ACC, but favorable associations in HNSC, CESC, KIRC and KIRP. The HNSC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .001). Together, the overview and detailed table identify HNSC as the clearest survival context for PTCRA RNA expression.
This table summarizes PTCRA tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for PTCRA. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PTCRA shows lower tumor expression in LUAD, LUSC and COAD and higher tumor expression in KIRC, KIRP and BRCA. The LUAD box plot shows higher PTCRA RNA expression in normal versus tumor tissue (log2 FC = −1.926, t-test p < 0.001).
This table shows molecular features associated with PTCRA in patient tissues and cancer cell lines. In patient samples, PTCRA shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, PTCRA RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LARGE_INTESTINE, while CRISPR and shRNA rows add functional-dependency signals in OESOPHAGUS and BLOOD_Lymphoma.
