ArticlePathology oncology research : POR1997
Comparison of the morphology of renal cysts and cystic renal tumors.
Article in Pathology oncology research : POR, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed, 1 citations in OpenAlex.
- p53 mutation regulates PKD genes and results in co-occurrence of PKD and tumorigenesis.Cancer biology & medicine · 2019Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal tumors appear uncommonly with cystic changes. They may develop due to necrosis though well-formed real cysts are also known. Such lesions may present problems in distinguishing them from benign renal cysts. Conditions leading to cyst formation are not known, however cell proliferation, altered extracellular matrix production and oncoprotein expression have been reported in cystic renal disorders. In the present study, we analysed the morphological features of 23 cystic renal tumors in comparison with 16 benign cysts using immunohistochemical and lectin binding methods. By our knowledge there has not been any piblication on such studies. The cystic renal tumors were represented predominantly in males and the size of the cysts was slightly larger than that of benign cysts. Tumorous cysts shared similar morphological appearance to solitary and multilocular cysts. They all showed strong epithelial membrane antigen reactivity on the luminal surface of the cells indicating distal tubular origin. Cell proliferation and p53 expression proved to be low excluding their role in the formation of the cysts. The amount of extracellular matrix and basement membrane was increased with an elevated type IV collagen and reduced fibronectin content. Polycystic kidney disease is different from tumorous cysts as cell proliferation, p53 oncoprotein expression and the composiition of extracellular matrix proved to be the opposite. As renal cell tumors arise from proximal tubules, neoplastic or metaplastic differentiation toward distal tubular direction seems to be the key even in cyst formation. Altered cell-matrix or cell-cell contact can modulate this transformation providing a basis for further results.
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Registered trials
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