Q-omics provides the consensus-scored PTPRC profile across patient tissues and cancer cell-line models. PTPRC expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in SKCM. Among the 18 cancer types available for tumor–normal comparison, PTPRC is differentially expressed in 11, with the highest sampling consensus in KIRC. Additionally, PTPRC protein abundance shows 28,815 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight SKCM, KIRC, and LSCC as cancer lineages where PTPRC 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 PTPRC — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PTPRC survival associations across molecular data types. PTPRC RNA expression shows survival associations in the most cancer types (23), followed by mutation status (12) and mass-spec protein abundance (8). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PTPRC RNA expression–survival associations across cancer types. High PTPRC expression shows unfavorable associations in UVM and LGG, but favorable associations in SKCM, HNSC, LUAD and CESC. The SKCM 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 SKCM as the clearest survival context for PTPRC RNA expression.
This table summarizes PTPRC 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 3. The strongest signals are observed in KIRC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for PTPRC. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PTPRC shows lower tumor expression in COAD, LUSC and LUAD and higher tumor expression in KIRC, STAD and KIRP. The KIRC box plot shows higher PTPRC RNA expression in tumor versus normal tissue (log2 FC = +2.363, t-test p < 0.001).
This table shows molecular features associated with PTPRC in patient tissues and cancer cell lines. In patient samples, PTPRC 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, PTPRC 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 LUNG_NSCLC_LUAD and LARGE_INTESTINE.
