Współczesna Onkologia

Abstract

1/2020 vol. 24
Original paper

Immunohistochemical evaluation of mismatch repair proteins and p53 expression in extrauterine carcinosarcoma/sarcomatoid carcinoma

  1. Department of Pathomorphology, Medical University of Gdansk, Gdansk, Poland
  2. Department of Paediatrics, Haematology and Oncology, Medical University of Gdansk, Gdansk, Poland
  3. Department of Pulmonology, Medical University of Gdansk, Gdansk, Poland
  4. Diagnostic and Research Center for Molecular BioMedicine, Institute of Pathology, Medical University of Graz, Austria
  5. Department of Pathology, Neuropathology and Molecular Pathology, Medical University of Innsbruck, Austria
  6. Department of Pathology, Medical Faculty, Otto-von-Guericke University Magdeburg, Germany
  7. Department of Pathology, Klinikum Dessau, Dessau, Germany
Contemp Oncol (Pozn) 2020; 24 (1): 1-4
Online publish date: 2020/03/30
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Introduction

Carcinosarcoma (CS) is a tumor with components: epithelial (carcinomatous) and mesenchymal (sarcomatous), developing in the mechanism of epithelial-mesenchymal transition. It is known that the p53 defect is a frequent finding in a carcinosarcoma in different anatomical locations, additionally, in a subgroup of uterine CS MMR defect plays a role in the pathogenesis. The aim of this paper was to investigate the frequency of MMR and p53 aberrations in extrauterine CS.

Material and methods

Twenty eight extrauterine CS from the lung (n = 8), breast (n = 6), head and neck (n = 5), ovary (n = 3), urinary bladder (n = 3), adrenal gland (n = 1), skin (n = 1), and stomach (n = 1) were stained for hMLH1, PMS2, hMSH2, hMSH6 and p53. The pattern of expression was evaluated separately in carcinomatous and sarcomatous component.

Results

Immunostainings for hMLH1, PMS2, hMSH2 and hMSH6 were positive in all tumors. p53 defect was observed in 19 out of 28 samples (67.85%). In all cases except one (96.42%) there was a concordance between sarcomatoid and carcinomatous components.

Conclusions

MMR deficiency does not seem to play a role in the pathogenesis of extrauterine CS. p53 aberrant expression is frequent and almost always consistent in carcinomatous and sarcomatous component.

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