Q-omics provides the consensus-scored IPMK profile across patient tissues and cancer cell-line models. IPMK expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in BLCA. Among the 18 cancer types available for tumor–normal comparison, IPMK is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, IPMK RNA expression shows 20,072 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight BLCA, KIRC, and ACC as cancer lineages where IPMK 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 IPMK — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes IPMK survival associations across molecular data types. IPMK RNA expression shows survival associations in the most cancer types (25), followed by mutation status (4) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible IPMK RNA expression–survival associations across cancer types. High IPMK expression shows unfavorable associations in BLCA, ACC, KIRP, THCA, KICH and LIHC. The BLCA 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 BLCA as the clearest survival context for IPMK RNA expression.
This table summarizes IPMK 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 3. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for IPMK. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. IPMK shows lower tumor expression in COAD and higher tumor expression in KIRC, KIRP, HNSC, STAD and LIHC. The KIRC box plot shows higher IPMK RNA expression in tumor versus normal tissue (log2 FC = +1.040, t-test p < 0.001).
This table shows molecular features associated with IPMK in patient tissues and cancer cell lines. In patient samples, IPMK shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, IPMK RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in BONE and BLOOD_Leukemia.
