Q-omics provides the consensus-scored CDKL3 profile across patient tissues and cancer cell-line models. CDKL3 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in SCLC. Among the 18 cancer types available for tumor–normal comparison, CDKL3 is differentially expressed in 10, with the highest sampling consensus in KIRC. Additionally, CDKL3 RNA expression shows 19,952 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight SCLC, KIRC, and UVM as cancer lineages where CDKL3 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 CDKL3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CDKL3 survival associations across molecular data types. CDKL3 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (5) and mass-spec protein abundance (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CDKL3 RNA expression–survival associations across cancer types. High CDKL3 expression shows unfavorable associations in SCLC, LIHC, UVM, ESCA and CESC, but favorable associations in PAAD. The SCLC 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 SCLC as the clearest survival context for CDKL3 RNA expression.
This table summarizes CDKL3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 5. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CDKL3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CDKL3 shows lower tumor expression in KICH and THCA and higher tumor expression in KIRC, LIHC, COAD and CHOL. The KIRC box plot shows higher CDKL3 RNA expression in tumor versus normal tissue (log2 FC = +0.382, t-test p < 0.001).
This table shows molecular features associated with CDKL3 in patient tissues and cancer cell lines. In patient samples, CDKL3 shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, CDKL3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in URINARY_TRACT, while CRISPR and shRNA rows add functional-dependency signals in PANCREAS and BLOOD_Leukemia.
