Q-omics provides the consensus-scored SHARPIN profile across patient tissues and cancer cell-line models. SHARPIN expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, SHARPIN is differentially expressed in 15, with the highest sampling consensus in HNSC. Additionally, SHARPIN protein abundance shows 18,130 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, HNSC, and GBM as cancer lineages where SHARPIN 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 SHARPIN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SHARPIN survival associations across molecular data types. SHARPIN RNA expression shows survival associations in the most cancer types (20), followed by mutation status (2) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible SHARPIN RNA expression–survival associations across cancer types. High SHARPIN expression shows unfavorable associations in KIRC, LIHC, UVM, CESC, UCS and HNSC. The KIRC Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRC as the clearest survival context for SHARPIN RNA expression.
This table summarizes SHARPIN tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 4. The strongest signals are observed in KIRC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for SHARPIN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SHARPIN shows higher tumor expression in HNSC, KIRC, COAD, KIRP, LIHC and LUAD. The HNSC box plot shows higher SHARPIN RNA expression in tumor versus normal tissue (log2 FC = +0.875, t-test p < 0.001).
This table shows molecular features associated with SHARPIN in patient tissues and cancer cell lines. In patient samples, SHARPIN 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, SHARPIN RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in BONE and BLOOD_Lymphoma.
