Q-omics provides the consensus-scored KHSRP profile across patient tissues and cancer cell-line models. KHSRP expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, KHSRP is differentially expressed in 14, with the highest sampling consensus in HNSC. Additionally, KHSRP protein abundance shows 25,633 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight ACC, HNSC, and GBM as cancer lineages where KHSRP 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 KHSRP — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes KHSRP survival associations across molecular data types. KHSRP RNA expression shows survival associations in the most cancer types (24), followed by mutation status (6) 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 KHSRP RNA expression–survival associations across cancer types. High KHSRP expression shows unfavorable associations in ACC, MESO, KIRP, LUAD and LIHC, but favorable associations in SCLC. The ACC 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 ACC as the clearest survival context for KHSRP RNA expression.
This table summarizes KHSRP tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 5. The strongest signals are observed in KIRC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for KHSRP. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. KHSRP shows higher tumor expression in HNSC, COAD, KIRC, STAD, KIRP and BLCA. The HNSC box plot shows higher KHSRP RNA expression in tumor versus normal tissue (log2 FC = +1.096, t-test p < 0.001).
This table shows molecular features associated with KHSRP in patient tissues and cancer cell lines. In patient samples, KHSRP 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, KHSRP RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and SOFT_TISSUE.
