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Published on: December 13, 2018
Minichromosome maintenance 2 (MCM2) is a new prognostic proliferative marker in Wilms tumour
Katarzyna Taran1, Anna Sitkiewicz, Ewa Andrzejewska
1Department of Pathology, Medical University of Lodz, Łódz, Poland dr.taran.patho@gmail.com
Objective:
We examined expression of minichromosome maintenance 2 (MCM2) by immunohistochemistry in nephrectomy specimens of children with nephroblastoma treated according to the Society International d'Oncologie Pediatrique (SIOP) scheme to determine its potential prognostic significance.
Material And Methods:
18 children with nephroblastoma, 9 females and 9 males, 2 months to 7 years of age, treated in the Department of Oncology and Paediatric Surgery, Medical University of Lodz, during the period 1994-2006 were analysed. Children were treated by neoadjuvant chemotherapy and subsequent nephrectomy according to SIOP protocols -93 and 2001 and followed up from 2 to 11 years. The tumour stage and classification in nephrectomy specimens were established according to the revised 2001 SIOP working classification of renal tumours of childhood.
Results:
In low risk nephroblastoma MCM2 expression was low, ranging from 0% in two cases of completely necrotic nephroblastoma to 5% in one child with cystic partially differentiated nephroblastoma. In mesoblastic nephroma, which is a distinct type of neoplasm with a low malignant potential and the most common congenital renal neoplasm, MCM2 expression was variable ranging from 2-5% in 2 children with stage I disease to 70% in one child with stage III disease In intermediate risk nephroblastoma MCM2 expression was low (10%) in one case of regressive type nephroblastoma and stage II disease and intermediate to high in children with epithelial type nephroblastoma, ranging from 40-50% in one case with stage I disease to 70% and 70-100% in 2 children with stage I and stage IV disease, respectively. In high risk nephroblastoma (7 children with nephroblastoma blastemal type) MCM2 expression was intermediate to high, ranging from 40 to 90%. MCM2 expression tends to be lower in children with less advanced stage of disease (stage II) and higher in more advanced disease (stage III and IV). Two children with blastemal type and high (> 60% MCM2) died of disease within 2-4 years from diagnosis and one child was lost to follow-up. Both children who died were older 8.5 yo M and 7 yo M and presented with advanced disease stage IV or III with anaplasia.
Conclusion:
MCM2 is a promising prognostic factor in WT treated according to the SIOP scheme.
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