Abstract

The aim of the research was to study the expression of marker genes for the epithelial-mesenchymal transition in the ductal adenocarcinoma of the pancreas.Material and methods. Surgical material from 44 patients with ductal adenocarcinoma of the pancreas was subjected to morphological analysis with molecular genetic research. Total RNA was detected in the detected sections of the anaplastic component using the RNeasy Mini Kit (Qiagen, Germany). 5 marker genes were used for molecular genetic studies of the epithelial-mesenchymal transition (EMT): ZEB1, ZEB2, CDH1, VIM, SNAIL1 (SLUG). Gene expression was measured in triplicate using an EvaGreen intercalating dye. On serial paraffin sections using tissue microarrays technology, immunohistochemical detection of p63, smooth muscle actin, total cytokeratin, cytokeratin 7, vimentin, E-cadherin (Ventana) was performed.Results. As a result of the study, a positive reaction with mesenchymal markers (vimentin, p63, smooth muscle actin) was detected in the cells of the anaplastic component, in contrast to the glandular component. In a molecular study of the anaplastic component, changes in gene expression were characterized as EMT-positive.Conclusion. The heterogeneity of ductal cancer is manifested in the appearance of an anaplastic (sarcomalike) component, in which the ability of epithelial tumor cells to acquire the property of mesenchymal cells that do not require stroma and have aggressive malignant potential that affects the survival of patients is traced.

Highlights

  • The aim of the research was to study the expression of marker genes for the epithelial-mesenchymal transition in the ductal adenocarcinoma of the pancreas

  • Surgical material from 44 patients with ductal adenocarcinoma of the pancreas was subjected to morphological analysis with molecular genetic research

  • Total RNA was detected in the detected sections of the anaplastic component using the RNeasy Mini Kit (Qiagen, Germany). 5 marker genes were used for molecular genetic studies of the epithelial-mesenchymal transition (EMT): ZEB1, ZEB2, CDH1, VIM, SNAIL1 (SLUG)

Read more

Summary

Introduction

Операционный материал от 44 пациентов с протоковой аденокарциномой поджелудочной железы подвергался морфологическому анализу с молекулярно-генетическим исследованием. В обнаруженных участках анапластического компонента выявляли суммарную РНК с помощью набора RNeasy Mini Kit (Qiagen, Германия). Для молекулярно-генетического исследования эпителиальномезенхимального перехода (ЭМП) использовали 5 генов-маркеров: ZEB1, ZEB2, CDH1, VIM, SNAIL1 (SLUG). Измерение экспрессии генов проводили в 3 разовом повторении, используя интеркалирующий краситель EvaGreen. В результате проведенного исследования в клетках анапластического компонента выявлена положительная реакция с мезенхимальными маркерами (виментин, р63, гладкомышечный актин), в отличие от железистого компонента. При молекулярном исследовании анапластического компонента изменения экспрессии генов характеризовались как ЭМП-положительные. Гетерогенность протокового рака проявляется в появлении анапластического (саркомоподобного) компонента, в котором прослеживается способность эпителиальных опухолевых клеток приобретать свойство мезенхимальных клеток, не требующих стромы и обладающих агрессивным злокачественным потенциалом, влияющем на выживаемость больных. The aim of the research was to study the expression of marker genes for the epithelial-mesenchymal transition in the ductal adenocarcinoma of the pancreas

Objectives
Methods
Conclusion

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.