Development of mesothelioma in situ and its progression to invasive disease observed in a patient with uncontrolled pleural effusions for 15 years.
Aged
Biomarkers, Tumor
/ metabolism
Biopsy
Diagnosis, Differential
Disease Progression
Female
Humans
Immunohistochemistry
Mesothelioma
/ diagnosis
Mesothelioma, Malignant
/ diagnosis
Pleural Effusion
/ complications
Pleural Neoplasms
/ diagnosis
Prognosis
Retrospective Studies
Tumor Suppressor Proteins
/ metabolism
Ubiquitin Thiolesterase
/ metabolism
BAP1
MTAP
immunohistochemistry
mesothelioma in situ
Journal
Pathology international
ISSN: 1440-1827
Titre abrégé: Pathol Int
Pays: Australia
ID NLM: 9431380
Informations de publication
Date de publication:
Dec 2020
Dec 2020
Historique:
received:
01
07
2020
revised:
11
08
2020
accepted:
26
08
2020
pubmed:
22
9
2020
medline:
30
9
2021
entrez:
21
9
2020
Statut:
ppublish
Résumé
Mesothelioma in situ (MIS) has recently been investigated as a distinct phase of mesothelioma carcinogenesis. The diagnostic criteria proposed for MIS include a loss of BRCA1-associated protein 1 (BAP1) expression detected by immunohistochemistry (IHC). However, the length of time that MIS typically remains an in situ lesion before progression to invasive disease is still unclear. Herein, we report a case of a Japanese woman in her early seventies who had suffered from recurrent pleural effusions for 15 years, during which MIS developed and progressed to invasive mesothelioma. Retrospective diagnosis of partial MIS, fully developed MIS, and invasive disease was made using BAP1 IHC on three biopsy specimens and via clinical observations with radiological images. MIS and invasive lesions revealed BAP1 loss. The interval from partial or full MIS to invasive disease was 14 and 7 years, respectively. These results support a diagnostic strategy combining histomorphology with genomic-based assays including BAP1 IHC in biopsy tissues from a patient with recurrent pleural effusions.
Substances chimiques
BAP1 protein, human
0
Biomarkers, Tumor
0
Tumor Suppressor Proteins
0
Ubiquitin Thiolesterase
EC 3.4.19.12
Types de publication
Case Reports
Langues
eng
Sous-ensembles de citation
IM
Pagination
1009-1014Informations de copyright
© 2020 Japanese Society of Pathology and John Wiley & Sons Australia, Ltd.
Références
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