ArticleJournal of cancer research and clinical oncology2017
Prognostic relevance of high atonal homolog-1 expression in Merkel cell carcinoma.
Article in Journal of cancer research and clinical oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 28 citations in OpenAlex.
- An immunocompetent model of MCPyV-driven Merkel cell carcinoma reveals tumor evolution under immune selection.bioRxiv : the preprint server for biology · 2026Article
- Diagnostic Utility and Clinicopathologic Associations of Histone H3 Lysine 27 Trimethylation (H3K27me3) Immunohistochemistry for Merkel Cell Carcinoma.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2026Article
- A Polyomavirus-Positive Merkel Cell Carcinoma Mouse Model Supports a Unified Origin for Somatic and Germ Cell Cancers.Cancers · 2025Article
- Review
- Functional characterization of the ATOH1 molecular subtype indicates a pro-metastatic role in small cell lung cancer.Cell reports · 2025Article
- The role of pioneering transcription factors, chromatin accessibility and epigenetic reprogramming in oncogenic viruses.Frontiers in microbiology · 2025Review
- Functional Characterisation of the ATOH1 Molecular Subtype Indicates a Pro-Metastatic Role in Small Cell Lung Cancer.bioRxiv : the preprint server for biology · 2024Article
- ATOH1, TFAP2B, and CEACAM6 as Immunohistochemical Markers to Distinguish Merkel Cell Carcinoma and Small Cell Lung Cancer.Cancers · 2024Article
- Merkel cell carcinoma: updates in tumor biology, emerging therapies, and preclinical models.Frontiers in oncology · 2024Review
- Loss of ATOH1 in Pit Cell Drives Stemness and Progression of Gastric Adenocarcinoma by Activating AKT/mTOR Signaling through GAS1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- YAP1 and WWTR1 expression inversely correlates with neuroendocrine markers in Merkel cell carcinoma.The Journal of clinical investigation · 2023Article
- LRIG1 is a positive prognostic marker in Merkel cell carcinoma and Merkel cell carcinoma expresses epithelial stem cell markers.Virchows Archiv : an international journal of pathology · 2021Article
- Role of Virus-Induced Host Cell Epigenetic Changes in Cancer.International journal of molecular sciences · 2021Review
- Merkel Cell Carcinoma: An Immunotherapy Fairy-Tale?Frontiers in oncology · 2021Review
- Atonal bHLH transcription factor 1 is an important factor for maintaining the balance of cell proliferation and differentiation in tumorigenesis.Oncology letters · 2020Review
- Conversion of Sox2-dependent Merkel cell carcinoma to a differentiated neuron-like phenotype by T antigen inhibition.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Diagnostic accuracy of a panel of immunohistochemical and molecular markers to distinguish Merkel cell carcinoma from other neuroendocrine carcinomas.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2019Article
- Histogenesis of Merkel Cell Carcinoma: A Comprehensive Review.Frontiers in oncology · 2019Review
- Epidemiology, biology and therapy of Merkel cell carcinoma: conclusions from the EU project IMMOMEC.Cancer immunology, immunotherapy : CII · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIt has recently been reported that atonal homolog 1 (ATOH1) gene is down-regulated in Merkel cell carcinoma (MCC) and thus may represent a tumor suppressor gene.
objectivesWe aimed to test for ATOH1 gene mutations and expression levels in MCC tissues and cell lines.
methodsGenomic DNA isolation and amplification via PCR was successfully performed in 33 MCCs on formalin-fixed paraffin-embedded tissue and three MCC cell lines, followed by Sanger sequencing of the whole ATOH1 gene to detect genomic aberrations. ATOH1 mRNA levels were determined by RT-PCR. Immunohistochemistry of ATOH1 was performed to quantify protein expression in tumor samples and cell lines.
resultsNeither in any of the 33 MCC tissue samples nor in the three cell lines ATOH1 mutations were present. ATOH1 was expressed in all lesions, albeit at different expression levels. Univariate analysis revealed that the total immunohistology score significantly correlated with the occurrence of tumor relapse (r = 0.57; P = 0.0008). This notion was confirmed in multivariate analysis suggesting that ATOH1 expression is a potential independent predictor for tumor relapse in MCC patients (P = 0.028). MCC-related death also correlated with ATOH1 expression (r = 0.4; P = 0.025); however, ATOH1 expression did not retain its predictive value in the regression model.
conclusionsIn contrast to anecdotal reports ATOH1 expression is not lost by genetic alterations in MCC. However, protein expression of ATOH1 is increased in advanced MCC indicating that ATOH1 is involved in MCC progression.
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.