protein tyrosine phosphatase receptor type JGenealiases: CD148 · DEP1 · HPTP eta · HPTPeta · R-PTP-ETA · R-PTP-J
Q-omics provides the consensus-scored PTPRJ profile across patient tissues and cancer cell-line models. PTPRJ expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, PTPRJ is differentially expressed in 12, with the highest sampling consensus in STAD. Additionally, PTPRJ protein abundance shows 23,973 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, STAD, and GBM as cancer lineages where PTPRJ 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 PTPRJ — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PTPRJ survival associations across molecular data types. PTPRJ RNA expression shows survival associations in the most cancer types (23), followed by mutation status (8) and 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 PTPRJ RNA expression–survival associations across cancer types. High PTPRJ expression shows unfavorable associations in UVM, MESO and ESCA, but favorable associations in KIRC, HNSC and UCS. The KIRC 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 KIRC as the clearest survival context for PTPRJ RNA expression.
This table summarizes PTPRJ 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 4. The strongest signals are observed in THCA for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for PTPRJ. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PTPRJ shows lower tumor expression in THCA and KIRC and higher tumor expression in STAD, LIHC, UCEC and BRCA. The STAD box plot shows higher PTPRJ RNA expression in tumor versus normal tissue (log2 FC = +1.279, t-test p < 0.001).
This table shows molecular features associated with PTPRJ in patient tissues and cancer cell lines. In patient samples, PTPRJ 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, PTPRJ 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 PANCREAS and BONE.
