Q-omics provides the consensus-scored TMEM52B profile across patient tissues and cancer cell-line models. TMEM52B expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in SKCM. Among the 18 cancer types available for tumor–normal comparison, TMEM52B is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, TMEM52B RNA expression shows 17,971 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight SKCM, KIRC, and GBM as cancer lineages where TMEM52B 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 TMEM52B — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TMEM52B survival associations across molecular data types. TMEM52B RNA expression shows survival associations in the most cancer types (24), followed by mutation status (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TMEM52B RNA expression–survival associations across cancer types. High TMEM52B expression shows unfavorable associations in LGG, ACC, STAD and LIHC, but favorable associations in SKCM and KICH. The SKCM 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 SKCM as the clearest survival context for TMEM52B RNA expression.
This table summarizes TMEM52B tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for TMEM52B. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TMEM52B shows lower tumor expression in KIRC, KIRP and LUAD and higher tumor expression in HNSC, COAD and THCA. The KIRC box plot shows higher TMEM52B RNA expression in normal versus tumor tissue (log2 FC = −6.333, t-test p < 0.001).
This table shows molecular features associated with TMEM52B in patient tissues and cancer cell lines. In patient samples, TMEM52B 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, TMEM52B RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and UPPER_AERODIGESTIVE_TRACT.