Novel Two MRT Cell Lines Established from Multiple Sites of a Synchronous MRT Patient.


Journal

Anticancer research
ISSN: 1791-7530
Titre abrégé: Anticancer Res
Pays: Greece
ID NLM: 8102988

Informations de publication

Date de publication:
Nov 2020
Historique:
received: 21 08 2020
revised: 15 09 2020
accepted: 16 09 2020
entrez: 28 10 2020
pubmed: 29 10 2020
medline: 5 11 2020
Statut: ppublish

Résumé

Malignant rhabdoid tumor (MRT) is a rare, aggressive neoplasm found in young children, caused by inactivation of a single gene, SNF5 (INI1, SMARCB1). MRT cases with multifocal tumors at diagnosis are categorized as synchronous MRT, often with a germline mutation of SNF5. The aim of this study was to establish new models useful in clarifying the biological basis of synchronous MRT. We established two novel MRT cell lines, designated as KP-MRT-KS and KP-MRT-KSa, derived from different lesions and at a different time from a synchronous multifocal 7-month-old female MRT patient. Both cells showed typical morphology of MRT, with a compound genomic mutation in exons 2 and 5 of the SNF5 gene. The exon 2 mutation was found in the germline. These cell lines could serve as powerful tools for unveiling the molecular mechanism of refractory synchronous MRT.

Sections du résumé

BACKGROUND/AIM OBJECTIVE
Malignant rhabdoid tumor (MRT) is a rare, aggressive neoplasm found in young children, caused by inactivation of a single gene, SNF5 (INI1, SMARCB1). MRT cases with multifocal tumors at diagnosis are categorized as synchronous MRT, often with a germline mutation of SNF5. The aim of this study was to establish new models useful in clarifying the biological basis of synchronous MRT.
MATERIALS AND METHODS METHODS
We established two novel MRT cell lines, designated as KP-MRT-KS and KP-MRT-KSa, derived from different lesions and at a different time from a synchronous multifocal 7-month-old female MRT patient.
RESULTS RESULTS
Both cells showed typical morphology of MRT, with a compound genomic mutation in exons 2 and 5 of the SNF5 gene. The exon 2 mutation was found in the germline.
CONCLUSION CONCLUSIONS
These cell lines could serve as powerful tools for unveiling the molecular mechanism of refractory synchronous MRT.

Identifiants

pubmed: 33109553
pii: 40/11/6159
doi: 10.21873/anticanres.14636
doi:

Substances chimiques

SMARCB1 Protein 0
SMARCB1 protein, human 0

Types de publication

Case Reports Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

6159-6170

Informations de copyright

Copyright© 2020, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.

Auteurs

Yasumichi Kuwahara (Y)

Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.

Tomoko Iehara (T)

Department of Pediatrics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.

Eisuke Ichise (E)

Department of Pediatrics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.

Yoshiki Katsumi (Y)

Department of Pediatrics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.

Kazutaka Ouchi (K)

Department of Pediatrics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.

Kunihiko Tsuchiya (K)

Department of Pediatrics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.

Mitsuru Miyachi (M)

Department of Pediatrics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.

Eiichi Konishi (E)

Department of Pathology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.

Hiroyasu Sasajima (H)

Department of Neurosurgery, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.

Satoaki Nakamura (S)

Department of Radiology, Kansai Medical University, Osaka, Japan.

Shigehisa Fumino (S)

Department of Pediatric Surgery, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.

Tatsuro Tajiri (T)

Department of Pediatric Surgery, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.

Pascal D Johann (PD)

Department of Pediatric Oncology, Hematology and Immunology, University Hospital Heidelberg, Heidelberg, Germany.

Michael C FrÜhwald (MC)

University Children's Hospital Augsburg, Swabian Children's Cancer Center, Augsburg, Germany.

Tatsushi Yoshida (T)

Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.

Tsukasa Okuda (T)

Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan okuda@koto.kpu-m.ac.jp hhosoi@koto.kpu-m.ac.jp.

Hajime Hosoi (H)

Department of Pediatrics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan okuda@koto.kpu-m.ac.jp hhosoi@koto.kpu-m.ac.jp.

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Classifications MeSH