Q-omics provides the consensus-scored ITPKA profile across patient tissues and cancer cell-line models. ITPKA expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, ITPKA is differentially expressed in 17, with the highest sampling consensus in KICH. Additionally, ITPKA protein abundance shows 30,763 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, KICH, and GBM as cancer lineages where ITPKA 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 ITPKA — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ITPKA survival associations across molecular data types. ITPKA RNA expression shows survival associations in the most cancer types (24), followed by mutation status (3) and mass-spec protein abundance (9). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ITPKA RNA expression–survival associations across cancer types. High ITPKA expression shows unfavorable associations in KIRC, UVM, KICH, KIRP and HNSC, but favorable associations in LAML. 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 ITPKA RNA expression.
This table summarizes ITPKA tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 17, while mass-spec protein shows differences in 6. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for ITPKA. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ITPKA shows lower tumor expression in COAD and higher tumor expression in KICH, KIRC, THCA, LUAD and LIHC. The KICH box plot shows higher ITPKA RNA expression in tumor versus normal tissue (log2 FC = +3.215, t-test p < 0.001).
This table shows molecular features associated with ITPKA in patient tissues and cancer cell lines. In patient samples, ITPKA 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, ITPKA RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OESOPHAGUS, while CRISPR and shRNA rows add functional-dependency signals in SKIN and SOFT_TISSUE.
