Clarification of the clinical significance of an intron variant in a case of Peutz–Jeghers syndrome with abnormal RNA splicing of STK11

Abstract Peutz–Jeghers syndrome is an autosomal dominant disease characterized by intestinal polyposis, mucocutaneous pigmentation, and an increased risk of various types of cancer. Germline mutations in STK11 (LKB1), which encodes serine/threonine kinase 11, have been identified as the major cause...

Full description

Saved in:
Bibliographic Details
Main Authors: Aki Ishikawa, Masahiro Gotoh, Mineko Ushiama, Hiromi Sakamoto, Noriko Tanabe, Tomoko Watanabe, Hourin Cho, Masayoshi Yamada, Kokichi Sugano, Kouya Shiraishi, Makoto Hirata, Teruhiko Yoshida, Akihiro Sakurai
Format: Article
Language:English
Published: BMC 2025-08-01
Series:Molecular Cytogenetics
Subjects:
Online Access:https://doi.org/10.1186/s13039-025-00710-x
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849225933502808064
author Aki Ishikawa
Masahiro Gotoh
Mineko Ushiama
Hiromi Sakamoto
Noriko Tanabe
Tomoko Watanabe
Hourin Cho
Masayoshi Yamada
Kokichi Sugano
Kouya Shiraishi
Makoto Hirata
Teruhiko Yoshida
Akihiro Sakurai
author_facet Aki Ishikawa
Masahiro Gotoh
Mineko Ushiama
Hiromi Sakamoto
Noriko Tanabe
Tomoko Watanabe
Hourin Cho
Masayoshi Yamada
Kokichi Sugano
Kouya Shiraishi
Makoto Hirata
Teruhiko Yoshida
Akihiro Sakurai
author_sort Aki Ishikawa
collection DOAJ
description Abstract Peutz–Jeghers syndrome is an autosomal dominant disease characterized by intestinal polyposis, mucocutaneous pigmentation, and an increased risk of various types of cancer. Germline mutations in STK11 (LKB1), which encodes serine/threonine kinase 11, have been identified as the major cause of Peutz–Jeghers syndrome. Here, we detected a rare variant of undetermined significance in intron 2 of STK11 using multi-gene panel analysis in a girl with clinically suspected Peutz–Jeghers syndrome. We confirmed this variant caused abnormal splicing in exons 2 and 3 using reverse transcription-PCR and Sanger sequencing. To validate the predicted impact of this variant on splicing, we performed functional analysis using a minigene assay. Functional analysis experiments demonstrated that this variant suppresses normal splicing, and the clinical significance of the STK11 variant, which was initially considered a variant of “uncertain significance,” was reclassified as “likely pathogenic” based on functional analysis. The interpretation of U12-type intronic variants remains particularly challenging due to limited data and the absence of specific recommendations in existing guidelines [1, 2], and when segregation analysis is difficult, functional analysis from splicing assays is essential to provide accurate genetic diagnosis and information for clinical management. However, further familial segregation analysis and further validation of potential exon-skipping events are necessary to fully characterize the splicing impact of this variant.
format Article
id doaj-art-ad50c55b23af4a23b6dd0bb370c7df6a
institution Kabale University
issn 1755-8166
language English
publishDate 2025-08-01
publisher BMC
record_format Article
series Molecular Cytogenetics
spelling doaj-art-ad50c55b23af4a23b6dd0bb370c7df6a2025-08-24T11:52:14ZengBMCMolecular Cytogenetics1755-81662025-08-011811810.1186/s13039-025-00710-xClarification of the clinical significance of an intron variant in a case of Peutz–Jeghers syndrome with abnormal RNA splicing of STK11Aki Ishikawa0Masahiro Gotoh1Mineko Ushiama2Hiromi Sakamoto3Noriko Tanabe4Tomoko Watanabe5Hourin Cho6Masayoshi Yamada7Kokichi Sugano8Kouya Shiraishi9Makoto Hirata10Teruhiko Yoshida11Akihiro Sakurai12Department of Medical Genetics and Genomics, School of Medicine, Sapporo Medical UniversityDepartment of Clinical Genomics, National Cancer Center Research InstituteDepartment of Clinical Genomics, National Cancer Center Research InstituteDepartment of Clinical Genomics, National Cancer Center Research InstituteDepartment of Genetic Medicine and Services, National Cancer Center HospitalDepartment of Genetic Medicine and Services, National Cancer Center HospitalDepartment of Genetic Medicine and Services, National Cancer Center HospitalDepartment of Genetic Medicine and Services, National Cancer Center HospitalDepartment of Genetic Medicine and Services, National Cancer Center HospitalDepartment of Clinical Genomics, National Cancer Center Research InstituteDepartment of Genetic Medicine and Services, National Cancer Center HospitalDepartment of Clinical Genomics, National Cancer Center Research InstituteDepartment of Medical Genetics and Genomics, School of Medicine, Sapporo Medical UniversityAbstract Peutz–Jeghers syndrome is an autosomal dominant disease characterized by intestinal polyposis, mucocutaneous pigmentation, and an increased risk of various types of cancer. Germline mutations in STK11 (LKB1), which encodes serine/threonine kinase 11, have been identified as the major cause of Peutz–Jeghers syndrome. Here, we detected a rare variant of undetermined significance in intron 2 of STK11 using multi-gene panel analysis in a girl with clinically suspected Peutz–Jeghers syndrome. We confirmed this variant caused abnormal splicing in exons 2 and 3 using reverse transcription-PCR and Sanger sequencing. To validate the predicted impact of this variant on splicing, we performed functional analysis using a minigene assay. Functional analysis experiments demonstrated that this variant suppresses normal splicing, and the clinical significance of the STK11 variant, which was initially considered a variant of “uncertain significance,” was reclassified as “likely pathogenic” based on functional analysis. The interpretation of U12-type intronic variants remains particularly challenging due to limited data and the absence of specific recommendations in existing guidelines [1, 2], and when segregation analysis is difficult, functional analysis from splicing assays is essential to provide accurate genetic diagnosis and information for clinical management. However, further familial segregation analysis and further validation of potential exon-skipping events are necessary to fully characterize the splicing impact of this variant.https://doi.org/10.1186/s13039-025-00710-xPeutz–jeghers syndromeSTK11Abnormal splicingGenetic analysisClinical relevanceU12-type intron
spellingShingle Aki Ishikawa
Masahiro Gotoh
Mineko Ushiama
Hiromi Sakamoto
Noriko Tanabe
Tomoko Watanabe
Hourin Cho
Masayoshi Yamada
Kokichi Sugano
Kouya Shiraishi
Makoto Hirata
Teruhiko Yoshida
Akihiro Sakurai
Clarification of the clinical significance of an intron variant in a case of Peutz–Jeghers syndrome with abnormal RNA splicing of STK11
Molecular Cytogenetics
Peutz–jeghers syndrome
STK11
Abnormal splicing
Genetic analysis
Clinical relevance
U12-type intron
title Clarification of the clinical significance of an intron variant in a case of Peutz–Jeghers syndrome with abnormal RNA splicing of STK11
title_full Clarification of the clinical significance of an intron variant in a case of Peutz–Jeghers syndrome with abnormal RNA splicing of STK11
title_fullStr Clarification of the clinical significance of an intron variant in a case of Peutz–Jeghers syndrome with abnormal RNA splicing of STK11
title_full_unstemmed Clarification of the clinical significance of an intron variant in a case of Peutz–Jeghers syndrome with abnormal RNA splicing of STK11
title_short Clarification of the clinical significance of an intron variant in a case of Peutz–Jeghers syndrome with abnormal RNA splicing of STK11
title_sort clarification of the clinical significance of an intron variant in a case of peutz jeghers syndrome with abnormal rna splicing of stk11
topic Peutz–jeghers syndrome
STK11
Abnormal splicing
Genetic analysis
Clinical relevance
U12-type intron
url https://doi.org/10.1186/s13039-025-00710-x
work_keys_str_mv AT akiishikawa clarificationoftheclinicalsignificanceofanintronvariantinacaseofpeutzjegherssyndromewithabnormalrnasplicingofstk11
AT masahirogotoh clarificationoftheclinicalsignificanceofanintronvariantinacaseofpeutzjegherssyndromewithabnormalrnasplicingofstk11
AT minekoushiama clarificationoftheclinicalsignificanceofanintronvariantinacaseofpeutzjegherssyndromewithabnormalrnasplicingofstk11
AT hiromisakamoto clarificationoftheclinicalsignificanceofanintronvariantinacaseofpeutzjegherssyndromewithabnormalrnasplicingofstk11
AT norikotanabe clarificationoftheclinicalsignificanceofanintronvariantinacaseofpeutzjegherssyndromewithabnormalrnasplicingofstk11
AT tomokowatanabe clarificationoftheclinicalsignificanceofanintronvariantinacaseofpeutzjegherssyndromewithabnormalrnasplicingofstk11
AT hourincho clarificationoftheclinicalsignificanceofanintronvariantinacaseofpeutzjegherssyndromewithabnormalrnasplicingofstk11
AT masayoshiyamada clarificationoftheclinicalsignificanceofanintronvariantinacaseofpeutzjegherssyndromewithabnormalrnasplicingofstk11
AT kokichisugano clarificationoftheclinicalsignificanceofanintronvariantinacaseofpeutzjegherssyndromewithabnormalrnasplicingofstk11
AT kouyashiraishi clarificationoftheclinicalsignificanceofanintronvariantinacaseofpeutzjegherssyndromewithabnormalrnasplicingofstk11
AT makotohirata clarificationoftheclinicalsignificanceofanintronvariantinacaseofpeutzjegherssyndromewithabnormalrnasplicingofstk11
AT teruhikoyoshida clarificationoftheclinicalsignificanceofanintronvariantinacaseofpeutzjegherssyndromewithabnormalrnasplicingofstk11
AT akihirosakurai clarificationoftheclinicalsignificanceofanintronvariantinacaseofpeutzjegherssyndromewithabnormalrnasplicingofstk11