A novel variant in the SPTB gene underlying hereditary spherocytosis and a literature review of previous variants.


Journal

BMC medical genomics
ISSN: 1755-8794
Titre abrégé: BMC Med Genomics
Pays: England
ID NLM: 101319628

Informations de publication

Date de publication:
12 Aug 2024
Historique:
received: 26 01 2024
accepted: 29 07 2024
medline: 13 8 2024
pubmed: 13 8 2024
entrez: 12 8 2024
Statut: epublish

Résumé

Hereditary spherocytosis (HS, MIM#612641) is one of the most common hereditary hemolytic disorders. This study aimed to confirm a novel variant's pathogenicity and reveal a patient's genetic etiology. The clinical data of a patient with HS who underwent genetic sequencing at the Children's Hospital of Chongqing Medical University were reviewed retrospectively. In silico prediction and in vitro minigene splicing reporter system were then conducted on the detected variant to analyze its intramolecular impact. A summary of the literature related to HS due to SPTB gene variants was also presented. A novel variant (c.301-2 A > G) in the SPTB gene (NM_001024858.4) was identified in the proband. Using Sanger sequencing, we conclusively confirmed that the inheritance of the variant could not be traced to the biological parents. The in vitro minigene assay revealed three different transcripts derived from the c.301-2 A > G variant: r.301_474del, r.301_306delCCAAAG, and r.301-1_301-57ins. Through a literature review, patients with HS who had been genotypically validated were summarized and the SPTB gene variant profile was mapped. We identified a splicing variant of the SPTB gene, thus confirming its aberrant translation. The novel variant was the probable genetic etiology of the proband with HS. Our findings expanded the variant spectrum of the SPTB gene, thus improving the understanding of the associated hereditary hemolytic disorders from a clinical and molecular perspective and contributing to the foundation of genetic counseling and diagnosis.

Sections du résumé

BACKGROUND BACKGROUND
Hereditary spherocytosis (HS, MIM#612641) is one of the most common hereditary hemolytic disorders. This study aimed to confirm a novel variant's pathogenicity and reveal a patient's genetic etiology.
METHODS METHODS
The clinical data of a patient with HS who underwent genetic sequencing at the Children's Hospital of Chongqing Medical University were reviewed retrospectively. In silico prediction and in vitro minigene splicing reporter system were then conducted on the detected variant to analyze its intramolecular impact. A summary of the literature related to HS due to SPTB gene variants was also presented.
RESULTS RESULTS
A novel variant (c.301-2 A > G) in the SPTB gene (NM_001024858.4) was identified in the proband. Using Sanger sequencing, we conclusively confirmed that the inheritance of the variant could not be traced to the biological parents. The in vitro minigene assay revealed three different transcripts derived from the c.301-2 A > G variant: r.301_474del, r.301_306delCCAAAG, and r.301-1_301-57ins. Through a literature review, patients with HS who had been genotypically validated were summarized and the SPTB gene variant profile was mapped.
CONCLUSION CONCLUSIONS
We identified a splicing variant of the SPTB gene, thus confirming its aberrant translation. The novel variant was the probable genetic etiology of the proband with HS. Our findings expanded the variant spectrum of the SPTB gene, thus improving the understanding of the associated hereditary hemolytic disorders from a clinical and molecular perspective and contributing to the foundation of genetic counseling and diagnosis.

Identifiants

pubmed: 39135028
doi: 10.1186/s12920-024-01973-w
pii: 10.1186/s12920-024-01973-w
doi:

Substances chimiques

SPTB protein, human 0
Spectrin 12634-43-4

Types de publication

Journal Article Case Reports Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

206

Subventions

Organisme : Public Welfare Project for Rare Blood Disorders in the field of Hematology in China
ID : xyxthjb-2023-006
Organisme : Public Welfare Project for Rare Blood Disorders in the field of Hematology in China
ID : xyxthjb-2023-006
Organisme : Public Welfare Project for Rare Blood Disorders in the field of Hematology in China
ID : xyxthjb-2023-006
Organisme : Public Welfare Project for Rare Blood Disorders in the field of Hematology in China
ID : xyxthjb-2023-006
Organisme : Public Welfare Project for Rare Blood Disorders in the field of Hematology in China
ID : xyxthjb-2023-006
Organisme : Public Welfare Project for Rare Blood Disorders in the field of Hematology in China
ID : xyxthjb-2023-006
Organisme : Public Welfare Project for Rare Blood Disorders in the field of Hematology in China
ID : xyxthjb-2023-006
Organisme : Public Welfare Project for Rare Blood Disorders in the field of Hematology in China
ID : xyxthjb-2023-006
Organisme : Public Welfare Project for Rare Blood Disorders in the field of Hematology in China
ID : xyxthjb-2023-006

Informations de copyright

© 2024. The Author(s).

Références

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Auteurs

Yang Wang (Y)

Department of Hematology and Oncology, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Pediatric Metabolismand Inflammatory Diseases, Children's Hospital of Chongqing Medical University, 136 Zhongshanerlu, Yu Zhong district, Chongqing, 400014, China.

Tao Liu (T)

Department of Hematology and Oncology, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Pediatric Metabolismand Inflammatory Diseases, Children's Hospital of Chongqing Medical University, 136 Zhongshanerlu, Yu Zhong district, Chongqing, 400014, China.

Chenxi Jia (C)

Chongqing Key Laboratory of Structural Birth Defect and Reconstruction, Chongqing, China.

Li Xiao (L)

Department of Hematology and Oncology, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Pediatric Metabolismand Inflammatory Diseases, Children's Hospital of Chongqing Medical University, 136 Zhongshanerlu, Yu Zhong district, Chongqing, 400014, China.

Wen Wang (W)

Shanghai University of Medicine & Health Sciences, Shanghai, China.

Yongjie Zhang (Y)

Department of Hematology and Oncology, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Pediatric Metabolismand Inflammatory Diseases, Children's Hospital of Chongqing Medical University, 136 Zhongshanerlu, Yu Zhong district, Chongqing, 400014, China.

Yan Xiang (Y)

Department of Hematology and Oncology, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Pediatric Metabolismand Inflammatory Diseases, Children's Hospital of Chongqing Medical University, 136 Zhongshanerlu, Yu Zhong district, Chongqing, 400014, China.

Lan Huang (L)

Department of Hematology and Oncology, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Pediatric Metabolismand Inflammatory Diseases, Children's Hospital of Chongqing Medical University, 136 Zhongshanerlu, Yu Zhong district, Chongqing, 400014, China.

Jie Yu (J)

Department of Hematology and Oncology, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Pediatric Metabolismand Inflammatory Diseases, Children's Hospital of Chongqing Medical University, 136 Zhongshanerlu, Yu Zhong district, Chongqing, 400014, China. yujie@hospital.cqmu.edu.cn.

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