Papillary renal neoplasm with reverse polarity has low frequency of alterations in chromosomes 7, 17, and Y.
Array-CGH
Chromosome
Fluorescence in situ hybridization
MET
Papillary renal neoplasm with reverse polarity
Journal
Virchows Archiv : an international journal of pathology
ISSN: 1432-2307
Titre abrégé: Virchows Arch
Pays: Germany
ID NLM: 9423843
Informations de publication
Date de publication:
14 Jun 2024
14 Jun 2024
Historique:
received:
01
08
2023
accepted:
30
05
2024
revised:
23
05
2024
medline:
15
6
2024
pubmed:
15
6
2024
entrez:
14
6
2024
Statut:
aheadofprint
Résumé
In papillary renal neoplasm with reverse polarity (PRNRP), the status of chromosomal copy number alterations, especially chromosomes 7/17 gain and chromosome Y loss, has remained controversial. In the literatures, there is a discrepancy among the results of chromosomal alteration in PRNRP depending on the analytical methods. Here, we comprehensively analyzed the status of chromosomal abnormalities in PRNRP. Nineteen PRNRP cases were analyzed by fluorescence in situ hybridization (FISH) and immunohistochemistry (IHC), five of which were additionally subjected to array-based comparative genomic hybridization (aCGH) analysis. Fifteen cases of PRCC were used as controls. From the aCGH results, no genome copy number abnormalities were found in the five PRNRP cases. By FISH, numbers of nuclei with abnormal chromosomal signals in PRNRP (centromere 7 gain: 11-21% of nuclei, centromere 17 gain: 11% of nuclei, centromere Y loss: 14-31% of nuclei) were similar to those in non-neoplastic tubular cells (centromere 7 gain: 11-15% of nuclei, centromere 17 gain: 12-15% of nuclei, centromere Y loss: 13-45% of nuclei). c-MET immunohistochemical overexpression, a substitute marker for chromosome 7 trisomy, was observed in 0 of 19 PRNRP cases, consistent with the analyses by aCGH and NGS regarding chromosome 7 gain. Taken together, the frequency of chromosomal alterations in PRNRP is similar to that in non-neoplastic tubular cells, and lower than that in PRCC. Our data suggest that PRNRP has a different tumorigenesis and is a distinct entity from PRCC.
Identifiants
pubmed: 38877360
doi: 10.1007/s00428-024-03840-6
pii: 10.1007/s00428-024-03840-6
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Japan Society for the Promotion of Science London
ID : 23K14479
Informations de copyright
© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.
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