UBTF tandem duplications in pediatric myelodysplastic syndrome and acute myeloid leukemia: implications for clinical screening and diagnosis

Recent genomic studies in adult and pediatric acute myeloid leukemia (AML) demonstrated recurrent in-frame tandem duplications (TD) in exon 13 of upstream binding transcription factor (UBTF). These alterations, which account for ~4.3% of AMLs in childhood and about 3% in adult AMLs under 60, are sub...

Celý popis

Uloženo v:
Podrobná bibliografie
Vydáno v:Haematologica (Roma) Ročník 109; číslo 8; s. 2459 - 2468
Hlavní autoři: Barajas, Juan M., Umeda, Masayuki, Contreras, Lisett, Khanlari, Mahsa, Westover, Tamara, Walsh, Michael P., Xiong, Emily, Yang, Chenchen, Otero, Brittney, Arribas-Layton, Marc, Abdelhamed, Sherif, Song, Guangchun, Ma, Xiaotu, Thomas 3rd, Melvin E., Ma, Jing, Klco, Jeffery M.
Médium: Journal Article
Jazyk:angličtina
Vydáno: Italy Fondazione Ferrata Storti 01.08.2024
Ferrata Storti Foundation
Témata:
ISSN:0390-6078, 1592-8721, 1592-8721
On-line přístup:Získat plný text
Tagy: Přidat tag
Žádné tagy, Buďte první, kdo vytvoří štítek k tomuto záznamu!
Abstract Recent genomic studies in adult and pediatric acute myeloid leukemia (AML) demonstrated recurrent in-frame tandem duplications (TD) in exon 13 of upstream binding transcription factor (UBTF). These alterations, which account for ~4.3% of AMLs in childhood and about 3% in adult AMLs under 60, are subtype-defining and associated with poor outcomes. Here, we provide a comprehensive investigation into the clinicopathological features of UBTF-TD myeloid neoplasms in childhood, including 89 unique pediatric AML and 6 myelodysplastic syndrome (MDS) cases harboring a tandem duplication in exon 13 of UBTF. We demonstrate that UBTF-TD myeloid tumors are associated with dysplastic features, low bone marrow blast infiltration, and low white blood cell count. Furthermore, using bulk and single-cell analyses, we confirm that UBTF-TD is an early and clonal event associated with a distinct transcriptional profile, whereas the acquisition of FLT3 or WT1 mutations is associated with more stem celllike programs. Lastly, we report rare duplications within exon 9 of UBTF that phenocopy exon 13 duplications, expanding the spectrum of UBTF alterations in pediatric myeloid tumors. Collectively, we comprehensively characterize pediatric AML and MDS with UBTF-TD and highlight key clinical and pathologic features that distinguish this new entity from other molecular subtypes of AML.
AbstractList Recent genomic studies in adult and pediatric acute myeloid leukemia (AML) demonstrated recurrent in-frame tandem duplications (TD) in exon 13 of upstream binding transcription factor (UBTF). These alterations, which account for ~4.3% of AMLs in childhood and about 3% in adult AMLs under 60, are subtype-defining and associated with poor outcomes. Here, we provide a comprehensive investigation into the clinicopathological features of UBTF-TD myeloid neoplasms in childhood, including 89 unique pediatric AML and 6 myelodysplastic syndrome (MDS) cases harboring a tandem duplication in exon 13 of UBTF. We demonstrate that UBTF-TD myeloid tumors are associated with dysplastic features, low bone marrow blast infiltration, and low white blood cell count. Furthermore, using bulk and single-cell analyses, we confirm that UBTF-TD is an early and clonal event associated with a distinct transcriptional profile, whereas the acquisition of FLT3 or WT1 mutations is associated with more stem celllike programs. Lastly, we report rare duplications within exon 9 of UBTF that phenocopy exon 13 duplications, expanding the spectrum of UBTF alterations in pediatric myeloid tumors. Collectively, we comprehensively characterize pediatric AML and MDS with UBTF-TD and highlight key clinical and pathologic features that distinguish this new entity from other molecular subtypes of AML.
Recent genomic studies in adult and pediatric acute myeloid leukemia (AML) demonstrated recurrent in-frame tandem duplications (TD) in exon 13 of upstream binding transcription factor (UBTF). These alterations, which account for approximately 4.3% of AML in childhood and about 3% in adult AML aged <60 years of age, are subtype-defining and associated with poor outcomes. Here, we provide a comprehensive investigation into the clinicopathological features of UBTF-TD myeloid neoplasms in childhood, including 89 unique pediatric AML and 6 myelodysplastic syndrome (MDS) cases harboring a tandem duplication in exon 13 of UBTF. We demonstrate that UBTF-TD myeloid tumors are associated with dysplastic features, low bone marrow blast infiltration, and low white blood cell count. Furthermore, using bulk and single-cell analyses, we confirm that UBTF-TD is an early and clonal event associated with a distinct transcriptional profile, whereas the acquisition of FLT3 or WT1 mutations is associated with more stem cell-like programs. Lastly, we report rare duplications within exon 9 of UBTF that phenocopy exon 13 duplications, expanding the spectrum of UBTF alterations in pediatric myeloid tumors. Collectively, we comprehensively characterize pediatric AML and MDS with UBTF-TD, and highlight key clinical and pathologic features that distinguish this new entity from other molecular subtypes of AML.Recent genomic studies in adult and pediatric acute myeloid leukemia (AML) demonstrated recurrent in-frame tandem duplications (TD) in exon 13 of upstream binding transcription factor (UBTF). These alterations, which account for approximately 4.3% of AML in childhood and about 3% in adult AML aged <60 years of age, are subtype-defining and associated with poor outcomes. Here, we provide a comprehensive investigation into the clinicopathological features of UBTF-TD myeloid neoplasms in childhood, including 89 unique pediatric AML and 6 myelodysplastic syndrome (MDS) cases harboring a tandem duplication in exon 13 of UBTF. We demonstrate that UBTF-TD myeloid tumors are associated with dysplastic features, low bone marrow blast infiltration, and low white blood cell count. Furthermore, using bulk and single-cell analyses, we confirm that UBTF-TD is an early and clonal event associated with a distinct transcriptional profile, whereas the acquisition of FLT3 or WT1 mutations is associated with more stem cell-like programs. Lastly, we report rare duplications within exon 9 of UBTF that phenocopy exon 13 duplications, expanding the spectrum of UBTF alterations in pediatric myeloid tumors. Collectively, we comprehensively characterize pediatric AML and MDS with UBTF-TD, and highlight key clinical and pathologic features that distinguish this new entity from other molecular subtypes of AML.
Recent genomic studies in adult and pediatric acute myeloid leukemia (AML) demonstrated recurrent in-frame tandem duplications (TD) in exon 13 of upstream binding transcription factor (UBTF). These alterations, which account for approximately 4.3% of AML in childhood and about 3% in adult AML aged <60 years of age, are subtype-defining and associated with poor outcomes. Here, we provide a comprehensive investigation into the clinicopathological features of UBTF-TD myeloid neoplasms in childhood, including 89 unique pediatric AML and 6 myelodysplastic syndrome (MDS) cases harboring a tandem duplication in exon 13 of UBTF. We demonstrate that UBTF-TD myeloid tumors are associated with dysplastic features, low bone marrow blast infiltration, and low white blood cell count. Furthermore, using bulk and single-cell analyses, we confirm that UBTF-TD is an early and clonal event associated with a distinct transcriptional profile, whereas the acquisition of FLT3 or WT1 mutations is associated with more stem cell-like programs. Lastly, we report rare duplications within exon 9 of UBTF that phenocopy exon 13 duplications, expanding the spectrum of UBTF alterations in pediatric myeloid tumors. Collectively, we comprehensively characterize pediatric AML and MDS with UBTF-TD, and highlight key clinical and pathologic features that distinguish this new entity from other molecular subtypes of AML.
Author Khanlari, Mahsa
Xiong, Emily
Song, Guangchun
Umeda, Masayuki
Yang, Chenchen
Westover, Tamara
Barajas, Juan M.
Ma, Xiaotu
Otero, Brittney
Arribas-Layton, Marc
Abdelhamed, Sherif
Thomas 3rd, Melvin E.
Ma, Jing
Klco, Jeffery M.
Walsh, Michael P.
Contreras, Lisett
AuthorAffiliation 3 Department of Computational Biology, St. Jude Children’s Research Hospital, Memphis, TN, USA
1 Department of Pathology, St. Jude Children’s Research Hospital, Memphis, TN
2 Mission Bio, South San Francisco, CA
AuthorAffiliation_xml – name: 2 Mission Bio, South San Francisco, CA
– name: 1 Department of Pathology, St. Jude Children’s Research Hospital, Memphis, TN
– name: 3 Department of Computational Biology, St. Jude Children’s Research Hospital, Memphis, TN, USA
Author_xml – sequence: 1
  givenname: Juan M.
  surname: Barajas
  fullname: Barajas, Juan M.
– sequence: 2
  givenname: Masayuki
  surname: Umeda
  fullname: Umeda, Masayuki
– sequence: 3
  givenname: Lisett
  surname: Contreras
  fullname: Contreras, Lisett
– sequence: 4
  givenname: Mahsa
  surname: Khanlari
  fullname: Khanlari, Mahsa
– sequence: 5
  givenname: Tamara
  surname: Westover
  fullname: Westover, Tamara
– sequence: 6
  givenname: Michael P.
  surname: Walsh
  fullname: Walsh, Michael P.
– sequence: 7
  givenname: Emily
  surname: Xiong
  fullname: Xiong, Emily
– sequence: 8
  givenname: Chenchen
  surname: Yang
  fullname: Yang, Chenchen
– sequence: 9
  givenname: Brittney
  surname: Otero
  fullname: Otero, Brittney
– sequence: 10
  givenname: Marc
  surname: Arribas-Layton
  fullname: Arribas-Layton, Marc
– sequence: 11
  givenname: Sherif
  surname: Abdelhamed
  fullname: Abdelhamed, Sherif
– sequence: 12
  givenname: Guangchun
  surname: Song
  fullname: Song, Guangchun
– sequence: 13
  givenname: Xiaotu
  surname: Ma
  fullname: Ma, Xiaotu
– sequence: 14
  givenname: Melvin E.
  surname: Thomas 3rd
  fullname: Thomas 3rd, Melvin E.
– sequence: 15
  givenname: Jing
  surname: Ma
  fullname: Ma, Jing
– sequence: 16
  givenname: Jeffery M.
  surname: Klco
  fullname: Klco, Jeffery M.
BackLink https://www.ncbi.nlm.nih.gov/pubmed/38426285$$D View this record in MEDLINE/PubMed
BookMark eNp9klFvFCEUhYmpsdvqPzCGR192ywDDQF-MNtY2aeJL-0zuALOlMrDCjMn-B3-0dLdrWh98ugHO-U7IPSfoKKboEHrfkBVjlJ_dgxthSmFFCWUrKrmQ7BVaNK2iS9nR5ggtCFNkKUgnj9FJKQ-EUKJU9wYdM8mpoLJdoN93X24v8QTRuhHbeRO8gcmnWLCPeOOshyl7g8etC8luyyZAmeq5bKPNaXS4GjGYeXJ7ibc4uPmHGz2cYz8-ww0pYxN8rBcBF5Odiz6ud_4aso6p-PIWvR4gFPfuaZ6iu8uvtxdXy5vv364vPt8sDe_aaWmpGprBEegBeischZ41YJRUorct70ULktFu4LyzBGRvjICmg970rRBGMnaKrvdcm-BBb7IfIW91Aq93FymvNeT6zeC0IbyhkilDZA3nQilhTCX2cqBDR3hlfdqzNnM_OmtcnDKEF9CXL9Hf63X6pZuGKtIyWgkfnwg5_ZxdmfToi3EhQHRpLpoqxmnX1VGlH56H_U057LMKzvcCk1Mp2Q3a-Gm3gZrtg26IfiyPPpRHP5ZH78tTzfwf84H_X9sf7C_QbQ
CitedBy_id crossref_primary_10_1016_j_intimp_2025_114433
ContentType Journal Article
Copyright Copyright© 2024 Ferrata Storti Foundation
Copyright_xml – notice: Copyright© 2024 Ferrata Storti Foundation
DBID AAYXX
CITATION
NPM
7X8
5PM
DOA
DOI 10.3324/haematol.2023.284683
DatabaseName CrossRef
PubMed
MEDLINE - Academic
PubMed Central (Full Participant titles)
DOAJ Directory of Open Access Journals
DatabaseTitle CrossRef
PubMed
MEDLINE - Academic
DatabaseTitleList
PubMed
MEDLINE - Academic
CrossRef

Database_xml – sequence: 1
  dbid: DOA
  name: DOAJ Directory of Open Access Journals
  url: https://www.doaj.org/
  sourceTypes: Open Website
– sequence: 2
  dbid: NPM
  name: PubMed
  url: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
  sourceTypes: Index Database
– sequence: 3
  dbid: 7X8
  name: MEDLINE - Academic
  url: https://search.proquest.com/medline
  sourceTypes: Aggregation Database
DeliveryMethod fulltext_linktorsrc
Discipline Medicine
Anatomy & Physiology
EISSN 1592-8721
EndPage 2468
ExternalDocumentID oai_doaj_org_article_c0412839c08c4746996ccbccb8f2f704
PMC11290532
38426285
10_3324_haematol_2023_284683
Genre Journal Article
GroupedDBID ---
29I
2WC
53G
5GY
5RE
5VS
AAFWJ
AAYXX
ADBBV
AENEX
AFPKN
ALMA_UNASSIGNED_HOLDINGS
AOIJS
BAWUL
BCNDV
BTFSW
CITATION
CS3
DIK
E3Z
EBS
EJD
F5P
FRP
GROUPED_DOAJ
H13
HYE
KQ8
OK1
OVT
P2P
RHI
RNS
RPM
SJN
TFS
TR2
W8F
WOQ
WOW
NPM
7X8
5PM
ID FETCH-LOGICAL-c475t-d29f1fe0abaabd6e2ab31ac9896bd54b65a8327f447d0a8bcc6a17abcb566c833
IEDL.DBID DOA
ISICitedReferencesCount 6
ISICitedReferencesURI http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=001381323000011&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
ISSN 0390-6078
1592-8721
IngestDate Fri Oct 03 12:53:29 EDT 2025
Tue Sep 30 17:08:21 EDT 2025
Fri Sep 05 12:04:33 EDT 2025
Mon Jul 21 06:05:42 EDT 2025
Sat Nov 29 06:33:10 EST 2025
Tue Nov 18 21:29:30 EST 2025
IsDoiOpenAccess true
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 8
Language English
License http://creativecommons.org/licenses/by-nc/4.0
This article is distributed under the terms of the Creative Commons Attribution Noncommercial License (by-nc 4.0) which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c475t-d29f1fe0abaabd6e2ab31ac9896bd54b65a8327f447d0a8bcc6a17abcb566c833
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
CY, BO and MA are employed by Mission Bio, Inc. All the other authors have no conflicts of interest to disclose.
Disclosures
OpenAccessLink https://doaj.org/article/c0412839c08c4746996ccbccb8f2f704
PMID 38426285
PQID 2934277293
PQPubID 23479
PageCount 10
ParticipantIDs doaj_primary_oai_doaj_org_article_c0412839c08c4746996ccbccb8f2f704
pubmedcentral_primary_oai_pubmedcentral_nih_gov_11290532
proquest_miscellaneous_2934277293
pubmed_primary_38426285
crossref_citationtrail_10_3324_haematol_2023_284683
crossref_primary_10_3324_haematol_2023_284683
PublicationCentury 2000
PublicationDate 2024-08-01
PublicationDateYYYYMMDD 2024-08-01
PublicationDate_xml – month: 08
  year: 2024
  text: 2024-08-01
  day: 01
PublicationDecade 2020
PublicationPlace Italy
PublicationPlace_xml – name: Italy
PublicationTitle Haematologica (Roma)
PublicationTitleAlternate Haematologica
PublicationYear 2024
Publisher Fondazione Ferrata Storti
Ferrata Storti Foundation
Publisher_xml – name: Fondazione Ferrata Storti
– name: Ferrata Storti Foundation
References 38014207 - medRxiv. 2023 Nov 13
References_xml – reference: 38014207 - medRxiv. 2023 Nov 13;:
SSID ssj0020997
Score 2.4657383
Snippet Recent genomic studies in adult and pediatric acute myeloid leukemia (AML) demonstrated recurrent in-frame tandem duplications (TD) in exon 13 of upstream...
SourceID doaj
pubmedcentral
proquest
pubmed
crossref
SourceType Open Website
Open Access Repository
Aggregation Database
Index Database
Enrichment Source
StartPage 2459
SubjectTerms Acute Myeloid Leukemia
Title UBTF tandem duplications in pediatric myelodysplastic syndrome and acute myeloid leukemia: implications for clinical screening and diagnosis
URI https://www.ncbi.nlm.nih.gov/pubmed/38426285
https://www.proquest.com/docview/2934277293
https://pubmed.ncbi.nlm.nih.gov/PMC11290532
https://doaj.org/article/c0412839c08c4746996ccbccb8f2f704
Volume 109
WOSCitedRecordID wos001381323000011&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
journalDatabaseRights – providerCode: PRVAON
  databaseName: DOAJ Directory of Open Access Journals
  customDbUrl:
  eissn: 1592-8721
  dateEnd: 99991231
  omitProxy: false
  ssIdentifier: ssj0020997
  issn: 0390-6078
  databaseCode: DOA
  dateStart: 19940101
  isFulltext: true
  titleUrlDefault: https://www.doaj.org/
  providerName: Directory of Open Access Journals
link http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV3fb9MwELZgQoiXCTZ-dIPJSIi3sDZ2HJu3DVHxABMPG-pb5LMdLaJNq7WZ1P9hf_Tu4qS0CGkvSHlKbNnyXXzf-c7fMfYhlKVWAmySglKJBJcnYIhyn5LCpIeQtTUjf33PLy70ZGJ-bpX6opywSA8cF-7UESEUWnE31E7m6MwZ5Rzgo8u0zCMTKKKe3pnqXC26D9rGDww6R2gF46U5gejh9NoSGeqcwg6p-IS7s9Jixyi13P3_Apx_501uGaLxc7bfIUh-Fmf-gj0K9QE7PKtxtNmaf-RtTmd7WH7Anv7oQueH7O7q_HLM6eAgzLhv_oSteVXzRV-wg8_WYTr36-UCUTUOwHtGA44duXXNKsQmlefT0PwOs8p-5tVWWjpHFMz7-5YcNyV0lNE8tv19zOurli_Z1fjr5ZdvSVeKIcFFz1aJT005KsPQgrXgVUgtiJF1RhsFPpOgMotbQ15Kmfuh1SgfZUe5BQcIF50W4hXbq-d1eMM40KUllRooUy8FGA2ZG9kM0BEUWQ5qwEQvi8J1POVULmNaoL9CEix6CRYkwSJKcMCSTa9F5Ol4oP05iXnTlli22xeoe0Wne8VDujdg73slKfCvpFCLrcO8WRYIomRKjgsO9DoqzWYooakKgM4GTO-o085cdr_U1XXL_E3gmEp5HP2P2R-zZ7ggMmYzvmV7q5smvGNP3O2qWt6csMf5RJ-0f9U9nGAqOA
linkProvider Directory of Open Access Journals
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=UBTF+tandem+duplications+in+pediatric+myelodysplastic+syndrome+and+acute+myeloid+leukemia%3A+implications+for+clinical+screening+and+diagnosis&rft.jtitle=Haematologica+%28Roma%29&rft.au=Barajas%2C+Juan+M.&rft.au=Umeda%2C+Masayuki&rft.au=Contreras%2C+Lisett&rft.au=Khanlari%2C+Mahsa&rft.date=2024-08-01&rft.issn=0390-6078&rft.eissn=1592-8721&rft_id=info:doi/10.3324%2Fhaematol.2023.284683&rft.externalDBID=n%2Fa&rft.externalDocID=10_3324_haematol_2023_284683
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0390-6078&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0390-6078&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0390-6078&client=summon