Q-omics provides the consensus-scored PTPRK profile across patient tissues and cancer cell-line models. PTPRK expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, PTPRK is differentially expressed in 9, with the highest sampling consensus in HNSC. Additionally, PTPRK RNA expression shows 19,964 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight KIRC, HNSC, and KIRP as cancer lineages where PTPRK 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 PTPRK — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PTPRK survival associations across molecular data types. PTPRK RNA expression shows survival associations in the most cancer types (25), followed by mutation status (4) 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 PTPRK RNA expression–survival associations across cancer types. High PTPRK expression shows unfavorable associations in MESO, PAAD and HNSC, but favorable associations in KIRC, PCPG 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 PTPRK RNA expression.
This table summarizes PTPRK tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9, while mass-spec protein shows differences in 3. The strongest signals are observed in HNSC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for PTPRK. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PTPRK shows lower tumor expression in KICH and higher tumor expression in HNSC, KIRP, KIRC, STAD and CHOL. The HNSC box plot shows higher PTPRK RNA expression in tumor versus normal tissue (log2 FC = +1.613, t-test p < 0.001).
This table shows molecular features associated with PTPRK in patient tissues and cancer cell lines. In patient samples, PTPRK shows the broadest associations at the RNA and protein expression levels, with KIRP recurring as the lineage with the largest associated feature set. In cancer cell lines, PTPRK RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SOFT_TISSUE, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and BLOOD_Lymphoma.
