ArticleDiscover oncology2026
A pan-cancer analysis of TMEM132A in human tumors.
Article in Discover oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Comprehensive pan-cancer analysis of MEX3A in human tumors.Discover oncology · 2026Article
- Comprehensive pan-cancer analysis of MEX3C in human tumors.Discover oncology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTMEM132A has recently been identified as a potential contributor to tumorigenesis. Nevertheless, a thorough examination of TMEM132A in human tumors across various cancer types has not been conducted to date.
methodsThe expression of TMEM132A was analyzed in 33 different types of human tumors by utilizing data from the TCGA and GTEx databases.
resultsTMEM132A was found to be significantly increased in 27 different types of cancer. High TMEM132A expression was linked to worse overall survival in KIRC, MESO, SARC and UVM, as well as unfavorable disease-free survival in KIRC and PRAD. The S530 locus of TMEM132A had lower phosphorylation in GBM but higher in HNSC, PAAD, LUAD and LUSC tumors. The S914 locus had higher phosphorylation in HNSC, KIRC, PAAD and LUSC tumors. TMEM132A genetic changes were thoroughly studied in different types of tumors using TCGA data. SKCM had the highest TMEM132A alteration frequency at 6.53%, predominantly characterized by “Mutation.” TMEM132A was significantly correlated with m1A, m5C and m6A genes in STAD, UCEC, GBM and DLBC tumors. TMEM132A was also associated with CAFs in various TCGA tumors. TMEM132A was positively correlated with immune genes in most cancers, but negatively correlated in CHOL and LIHC. We found a strong correlation between TMEM132A and TMB, MSI and HRD in various types of cancer. TMEM132A was positively correlated with APBA2, B4GALNT4, CDK5, CLSTN1 and PRPF19 genes. The heatmap confirms this correlation across different tumors. An analysis of the overlap between these groups identified ENOPH1 as a shared member. Finaly, GO enrichment and KEGG pathway were used to understand the functional role of TMEM132A in tumor development. GO enrichment highlighted terms like “endomembrane system” and “nervous system development” as important for TMEM132A’s impact. KEGG pathway analysis identified pathways such as “Axon guidance” and “Wnt signaling pathway” as relevant to TMEM132A’s influence on tumor pathogenesis.
conclusionThis is the first pan-cancer study to deeply understand the role of TMEM132A in tumor development across various types of cancers.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.