Q-omics provides the consensus-scored PITHD1 profile across patient tissues and cancer cell-line models. PITHD1 expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in KICH. Among the 18 cancer types available for tumor–normal comparison, PITHD1 is differentially expressed in 9, with the highest sampling consensus in KICH. Additionally, PITHD1 protein abundance shows 34,931 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KICH, and GBM as cancer lineages where PITHD1 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 PITHD1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PITHD1 survival associations across molecular data types. PITHD1 RNA expression shows survival associations in the most cancer types (22), followed by mutation status (3) and mass-spec protein abundance (10). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PITHD1 RNA expression–survival associations across cancer types. High PITHD1 expression shows unfavorable associations in KICH, ACC, UCS, LIHC, SARC and KIRP. The KICH Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .001). Together, the overview and detailed table identify KICH as the clearest survival context for PITHD1 RNA expression.
This table summarizes PITHD1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9, while mass-spec protein shows differences in 11. The strongest signals are observed in LIHC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for PITHD1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PITHD1 shows lower tumor expression in KICH and higher tumor expression in LIHC, BLCA, LUSC, COAD and KIRC. The KICH box plot shows higher PITHD1 RNA expression in normal versus tumor tissue (log2 FC = −0.562, t-test p < 0.001).
This table shows molecular features associated with PITHD1 in patient tissues and cancer cell lines. In patient samples, PITHD1 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, PITHD1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and CNS.
