A rare PALB2 germline variant causing G2/M cell cycle arrest is associated with isolated myelosarcoma in infancy.


Journal

Molecular genetics & genomic medicine
ISSN: 2324-9269
Titre abrégé: Mol Genet Genomic Med
Pays: United States
ID NLM: 101603758

Informations de publication

Date de publication:
09 2021
Historique:
revised: 12 05 2021
received: 18 02 2021
accepted: 01 07 2021
pubmed: 13 8 2021
medline: 17 3 2022
entrez: 12 8 2021
Statut: ppublish

Résumé

Isolated myelosarcoma of infancy is a rare presentation of acute myelogenous leukaemia (AML). Because of its rarity and early onset in infancy underlying genetic predisposition is potentially relevant in disease initiation. We report an oncologic emergency in an infant with thoracic and intraspinal aleukaemic myeloid sarcoma causing acute myelon compression and lower leg palsy. Whole-exome sequencing of the patient's germline DNA identified a rare PALB2 (OMIM 610355) variant (p.A1079S), which is located in a domain critical for the gene's proper function within the homology-directed repair pathway. In line with potential DNA damage repair defects mediated by the PALB2 deregulation, the patient's fibroblasts showed increased sensitivity towards radiation and DNA intercalating agents. Therefore, we suggest PALB2 p.A1079S as a pathogenic variant potentially contributing to the here observed patient phenotype.

Sections du résumé

BACKGROUND
Isolated myelosarcoma of infancy is a rare presentation of acute myelogenous leukaemia (AML). Because of its rarity and early onset in infancy underlying genetic predisposition is potentially relevant in disease initiation.
METHODS AND RESULTS
We report an oncologic emergency in an infant with thoracic and intraspinal aleukaemic myeloid sarcoma causing acute myelon compression and lower leg palsy. Whole-exome sequencing of the patient's germline DNA identified a rare PALB2 (OMIM 610355) variant (p.A1079S), which is located in a domain critical for the gene's proper function within the homology-directed repair pathway. In line with potential DNA damage repair defects mediated by the PALB2 deregulation, the patient's fibroblasts showed increased sensitivity towards radiation and DNA intercalating agents.
CONCLUSION
Therefore, we suggest PALB2 p.A1079S as a pathogenic variant potentially contributing to the here observed patient phenotype.

Identifiants

pubmed: 34382369
doi: 10.1002/mgg3.1746
pmc: PMC8457705
doi:

Substances chimiques

Fanconi Anemia Complementation Group N Protein 0
PALB2 protein, human 0

Types de publication

Case Reports Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e1746

Informations de copyright

© 2021 The Authors. Molecular Genetics & Genomic Medicine published by Wiley Periodicals LLC.

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Auteurs

Angelina Beer (A)

Neonatology and Pediatric Intensive Care, Department of Pediatrics, University Hospital Carl Gustav Carus, Dresden, Germany.

Ricardo Beck (R)

Department of Pediatric Surgery, University Hospital Carl Gustav Carus, Dresden, Germany.
Pediatric Oncology and Hematology, Department of Pediatrics, University Hospital Carl Gustav Carus, Dresden, Germany.

Anne Schedel (A)

Pediatric Oncology and Hematology, Department of Pediatrics, University Hospital Carl Gustav Carus, Dresden, Germany.

Malte von Bonin (M)

Medical Clinic I, University Hospital Carl Gustav Carus, Dresden, Germany.
German Cancer Consortium (DKTK, Dresden, Germany.
German Cancer Research Center (DKFZ, Heidelberg, Germany.

Jörn Meinel (J)

Institute of Pathology, University Hospital Carl Gustav Carus, Dresden, Germany.

Ulrike Anne Friedrich (UA)

Pediatric Oncology and Hematology, Department of Pediatrics, University Hospital Carl Gustav Carus, Dresden, Germany.

Maria Menzel (M)

Pediatric Oncology and Hematology, Department of Pediatrics, University Hospital Carl Gustav Carus, Dresden, Germany.

Meinolf Suttorp (M)

Medical Faculty, Pediatric Hematology & Oncology, Technical University, Dresden, Germany.

Sebastian Brenner (S)

Neonatology and Pediatric Intensive Care, Department of Pediatrics, University Hospital Carl Gustav Carus, Dresden, Germany.

Guido Fitze (G)

Department of Pediatric Surgery, University Hospital Carl Gustav Carus, Dresden, Germany.

Björn Lange (B)

Pediatric Oncology and Hematology, Department of Pediatrics, University Hospital Carl Gustav Carus, Dresden, Germany.

Ralf Knöfler (R)

Pediatric Oncology and Hematology, Department of Pediatrics, University Hospital Carl Gustav Carus, Dresden, Germany.

Julia Hauer (J)

Pediatric Oncology and Hematology, Department of Pediatrics, University Hospital Carl Gustav Carus, Dresden, Germany.
National Center for Tumor Diseases (NCT), Dresden, Germany.
German Cancer Research Center (DKFZ), Heidelberg, Germany.

Franziska Auer (F)

National Center for Tumor Diseases (NCT), Dresden, Germany.
German Cancer Research Center (DKFZ), Heidelberg, Germany.

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Classifications MeSH