Q-omics provides the consensus-scored SHPK profile across patient tissues and cancer cell-line models. SHPK expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in SCLC. Among the 18 cancer types available for tumor–normal comparison, SHPK is differentially expressed in 10, with the highest sampling consensus in BLCA. Additionally, SHPK RNA expression shows 16,821 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight SCLC, BLCA, and UVM as cancer lineages where SHPK 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 SHPK — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SHPK survival associations across molecular data types. SHPK RNA expression shows survival associations in the most cancer types (24), 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 SHPK RNA expression–survival associations across cancer types. High SHPK expression shows unfavorable associations in UVM, LGG, ACC and SKCM, but favorable associations in SCLC and KIRP. The SCLC 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 SCLC as the clearest survival context for SHPK RNA expression.
This table summarizes SHPK tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10. The strongest signals are observed in BLCA for RNA.
This table ranks reproducible tumor–normal expression differences for SHPK. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SHPK shows lower tumor expression in KICH and LIHC and higher tumor expression in BLCA, STAD, THCA and HNSC. The BLCA box plot shows higher SHPK RNA expression in tumor versus normal tissue (log2 FC = +0.602, t-test p < 0.001).
This table shows molecular features associated with SHPK in patient tissues and cancer cell lines. In patient samples, SHPK shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, SHPK RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in SKIN and BLOOD_Leukemia.
