Q-omics provides the consensus-scored CDKL5 profile across patient tissues and cancer cell-line models. CDKL5 expression is associated with patient survival in 18 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, CDKL5 is differentially expressed in 8, with the highest sampling consensus in LUAD. Additionally, CDKL5 protein abundance shows 24,534 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, LUAD, and GBM as cancer lineages where CDKL5 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 CDKL5 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CDKL5 survival associations across molecular data types. CDKL5 RNA expression shows survival associations in the most cancer types (18), followed by mutation status (8) 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 CDKL5 RNA expression–survival associations across cancer types. High CDKL5 expression shows unfavorable associations in STAD, SCLC, BLCA, UCEC and OV, but favorable associations in KIRC. The KIRC 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 KIRC as the clearest survival context for CDKL5 RNA expression.
This table summarizes CDKL5 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 8, while mass-spec protein shows differences in 6. The strongest signals are observed in THCA for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for CDKL5. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CDKL5 shows lower tumor expression in LUAD, THCA, KICH and LUSC and higher tumor expression in LIHC and CHOL. The LUAD box plot shows higher CDKL5 RNA expression in normal versus tumor tissue (log2 FC = −0.810, t-test p < 0.001).
This table shows molecular features associated with CDKL5 in patient tissues and cancer cell lines. In patient samples, CDKL5 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, CDKL5 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 OVARY and LARGE_INTESTINE.
