Q-omics provides the consensus-scored PHLDA2 profile across patient tissues and cancer cell-line models. PHLDA2 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, PHLDA2 is differentially expressed in 15, with the highest sampling consensus in COAD. Additionally, PHLDA2 RNA expression shows 15,272 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight KIRC, COAD, and TGCT as cancer lineages where PHLDA2 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 PHLDA2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PHLDA2 survival associations across molecular data types. PHLDA2 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (1) 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 PHLDA2 RNA expression–survival associations across cancer types. High PHLDA2 expression shows unfavorable associations in KIRC, UVM, LUAD, LIHC, LGG and MESO. 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 PHLDA2 RNA expression.
This table summarizes PHLDA2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 5. The strongest signals are observed in COAD for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for PHLDA2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PHLDA2 shows lower tumor expression in KICH and higher tumor expression in COAD, THCA, LUAD, STAD and LIHC. The COAD box plot shows higher PHLDA2 RNA expression in tumor versus normal tissue (log2 FC = +1.865, t-test p < 0.001).
This table shows molecular features associated with PHLDA2 in patient tissues and cancer cell lines. In patient samples, PHLDA2 shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, PHLDA2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Lymphoma, while CRISPR and shRNA rows add functional-dependency signals in CNS and BONE.
