Severe reaction to radiotherapy provoked by hypomorphic germline mutations in ATM (ataxia-telangiectasia mutated gene).


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:
10 2020
Historique:
received: 03 02 2020
accepted: 05 06 2020
pubmed: 5 8 2020
medline: 1 6 2021
entrez: 5 8 2020
Statut: ppublish

Résumé

A minority of breast cancer (BC) patients suffer from severe reaction to adjuvant radiotherapy (RT). Although deficient DNA double-strand break repair is considered the main basis for the reactions, pretreatment identification of high-risk patients has been challenging. To retrospectively determine the etiology of severe local reaction to RT in a 39-year-old woman with BC, we performed next-generation sequencing followed by further clinical and functional studies. We found a -4 intronic variant (c.2251-4A>G) in trans with a synonymous (c.3576G>A) variant affecting the ATM DNA-repair gene (NG_009830.1, NM_000051.3) which is linked to autosomal recessive ataxia-telangiectasia (A-T). We verified abnormal transcripts resulting from both variants, next to a minor wild-type transcript leading to a residual ATM kinase activity and genomic instability. Follow-up examination of the patient revealed no classic sign of A-T but previously unnoticed head dystonia and mild dysarthria, a family history of BC and late-onset ataxia segregating with the variants. Additionally, her serum level of alpha-fetoprotein (AFP) was elevated similar to A-T patients. Considering the variable presentations of A-T and devastating impact of severe reactions to RT, we suggest a routine measurement of AFP in RT-candidate BC patients followed by next-generation sequencing with special attention to non-canonical splice site and synonymous variants in ATM.

Sections du résumé

BACKGROUND
A minority of breast cancer (BC) patients suffer from severe reaction to adjuvant radiotherapy (RT). Although deficient DNA double-strand break repair is considered the main basis for the reactions, pretreatment identification of high-risk patients has been challenging.
METHODS
To retrospectively determine the etiology of severe local reaction to RT in a 39-year-old woman with BC, we performed next-generation sequencing followed by further clinical and functional studies.
RESULTS
We found a -4 intronic variant (c.2251-4A>G) in trans with a synonymous (c.3576G>A) variant affecting the ATM DNA-repair gene (NG_009830.1, NM_000051.3) which is linked to autosomal recessive ataxia-telangiectasia (A-T). We verified abnormal transcripts resulting from both variants, next to a minor wild-type transcript leading to a residual ATM kinase activity and genomic instability. Follow-up examination of the patient revealed no classic sign of A-T but previously unnoticed head dystonia and mild dysarthria, a family history of BC and late-onset ataxia segregating with the variants. Additionally, her serum level of alpha-fetoprotein (AFP) was elevated similar to A-T patients.
CONCLUSION
Considering the variable presentations of A-T and devastating impact of severe reactions to RT, we suggest a routine measurement of AFP in RT-candidate BC patients followed by next-generation sequencing with special attention to non-canonical splice site and synonymous variants in ATM.

Identifiants

pubmed: 32748564
doi: 10.1002/mgg3.1409
pmc: PMC7549565
doi:

Substances chimiques

alpha-Fetoproteins 0
ATM protein, human EC 2.7.11.1
Ataxia Telangiectasia Mutated Proteins EC 2.7.11.1

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

e1409

Informations de copyright

© 2020 The Authors. Molecular Genetics & Genomic Medicine published by Wiley Periodicals LLC.

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Auteurs

Reza Asadollahi (R)

Institute of Medical Genetics, University of Zurich, Schlieren-Zurich, Switzerland.

Christian Britschgi (C)

Department of Medical Oncology and Hematology, University Hospital Zurich, Comprehensive Cancer Center Zurich and University of Zurich, Zurich, Switzerland.

Pascal Joset (P)

Institute of Medical Genetics, University of Zurich, Schlieren-Zurich, Switzerland.

Beatrice Oneda (B)

Institute of Medical Genetics, University of Zurich, Schlieren-Zurich, Switzerland.

Detlev Schindler (D)

Institute of Human Genetics, University of Würzburg, Würzburg, Germany.

Urs R Meier (UR)

Department of Radiation Oncology, Kantonsspital Winterthur, Winterthur, Switzerland.

Anita Rauch (A)

Institute of Medical Genetics, University of Zurich, Schlieren-Zurich, Switzerland.
Zurich Center of Integrative Human Physiology, University of Zurich, Zurich, Switzerland.

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Classifications MeSH