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FGFR-2 and Epithelial–Mesenchymal Transition in Endometrial Cancer
Background. At present, EC staging is based on the WHO conservative criteria, which only consider the percentage of gland formation. The molecular subgrouping of EC recently proposed by the Cancer Genome Atlas (TCGA) represents a milestone in precise molecular-based patient triage. The present study...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9504491/ https://www.ncbi.nlm.nih.gov/pubmed/36143062 http://dx.doi.org/10.3390/jcm11185416 |
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author | Adamczyk-Gruszka, Olga Horecka-Lewitowicz, Agata Gruszka, Jakub Wawszczak-Kasza, Monika Strzelecka, Agnieszka Lewitowicz, Piotr |
author_facet | Adamczyk-Gruszka, Olga Horecka-Lewitowicz, Agata Gruszka, Jakub Wawszczak-Kasza, Monika Strzelecka, Agnieszka Lewitowicz, Piotr |
author_sort | Adamczyk-Gruszka, Olga |
collection | PubMed |
description | Background. At present, EC staging is based on the WHO conservative criteria, which only consider the percentage of gland formation. The molecular subgrouping of EC recently proposed by the Cancer Genome Atlas (TCGA) represents a milestone in precise molecular-based patient triage. The present study aimed to investigate the influence of FGFR-2 on the epithelial–mesenchymal transition (EMT) and whether it can lead to endometrial cancer dedifferentiation. Methods. One hundred and three White female patients with confirmed EC were enrolled in our research. For the analysis, we performed next-generation sequencing and immunohistochemical analyses of E-cadherin, β-catenin, and vimentin. Results. Tumor grade progression was closely correlated with LVI (p = 0.0338), expression of vimentin (p = 0.000), tumor budding (p = 0.000), and lack of E-cadherin (p = 0.0028). Similar observations were noted with regard to TNM/FIGO stage progression. In terms of FGFR-2 mutation, we found the following correlation p-values: LVI (p = 0.069), expression of vimentin (p = 0.000), tumor budding (p = 0.000), and lack of E-cadherin (p = 0.000), RFS (p = 0.032), ECSS (p = 0.047). Conclusions. FGFR-2 is the important factor influencing on EMT. |
format | Online Article Text |
id | pubmed-9504491 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-95044912022-09-24 FGFR-2 and Epithelial–Mesenchymal Transition in Endometrial Cancer Adamczyk-Gruszka, Olga Horecka-Lewitowicz, Agata Gruszka, Jakub Wawszczak-Kasza, Monika Strzelecka, Agnieszka Lewitowicz, Piotr J Clin Med Article Background. At present, EC staging is based on the WHO conservative criteria, which only consider the percentage of gland formation. The molecular subgrouping of EC recently proposed by the Cancer Genome Atlas (TCGA) represents a milestone in precise molecular-based patient triage. The present study aimed to investigate the influence of FGFR-2 on the epithelial–mesenchymal transition (EMT) and whether it can lead to endometrial cancer dedifferentiation. Methods. One hundred and three White female patients with confirmed EC were enrolled in our research. For the analysis, we performed next-generation sequencing and immunohistochemical analyses of E-cadherin, β-catenin, and vimentin. Results. Tumor grade progression was closely correlated with LVI (p = 0.0338), expression of vimentin (p = 0.000), tumor budding (p = 0.000), and lack of E-cadherin (p = 0.0028). Similar observations were noted with regard to TNM/FIGO stage progression. In terms of FGFR-2 mutation, we found the following correlation p-values: LVI (p = 0.069), expression of vimentin (p = 0.000), tumor budding (p = 0.000), and lack of E-cadherin (p = 0.000), RFS (p = 0.032), ECSS (p = 0.047). Conclusions. FGFR-2 is the important factor influencing on EMT. MDPI 2022-09-15 /pmc/articles/PMC9504491/ /pubmed/36143062 http://dx.doi.org/10.3390/jcm11185416 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Adamczyk-Gruszka, Olga Horecka-Lewitowicz, Agata Gruszka, Jakub Wawszczak-Kasza, Monika Strzelecka, Agnieszka Lewitowicz, Piotr FGFR-2 and Epithelial–Mesenchymal Transition in Endometrial Cancer |
title | FGFR-2 and Epithelial–Mesenchymal Transition in Endometrial Cancer |
title_full | FGFR-2 and Epithelial–Mesenchymal Transition in Endometrial Cancer |
title_fullStr | FGFR-2 and Epithelial–Mesenchymal Transition in Endometrial Cancer |
title_full_unstemmed | FGFR-2 and Epithelial–Mesenchymal Transition in Endometrial Cancer |
title_short | FGFR-2 and Epithelial–Mesenchymal Transition in Endometrial Cancer |
title_sort | fgfr-2 and epithelial–mesenchymal transition in endometrial cancer |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9504491/ https://www.ncbi.nlm.nih.gov/pubmed/36143062 http://dx.doi.org/10.3390/jcm11185416 |
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