Persistence of <i>UBTF</i> tandem duplications in remission in acute myeloid leukaemia-Reference-Cited by-同舟云学术

Persistence of UBTF tandem duplications in remission in acute myeloid leukaemia

Published:2023-10-19 Issue:4 Volume:4 Page:1105-1109
ISSN:2688-6146
Container-title:eJHaem
language:en
Short-container-title:eJHaem

Author:

Harrop Sean¹^ORCID,Nguyen Phillip C.¹,Byrne David¹,Wilson Clarissa¹,Ryland Georgina L.¹²^ORCID,Nguyen Tamia¹,Anderson Mary Ann¹,Khaw Seong Lin³⁴,Martin Michelle⁵,Tiong Ing Soo¹,Sanij Elaine¹⁶⁷²⁸,Blombery Piers¹²^ORCID

Affiliation:

1. Peter MacCallum Cancer Centre Melbourne Victoria Australia

2. Sir Peter MacCallum Department of Oncology University of Melbourne Parkville Victoria Australia

3. Royal Children's Hospital Melbourne Victoria Australia

4. Murdoch Children's Research Institute Melbourne Victoria Australia

5. Monash Children's Hospital Melbourne Victoria Australia

6. St Vincent's Institute of Medical Research Fitzroy Victoria Australia

7. Department of Medicine St Vincent's Hospital University of Melbourne Melbourne Victoria Australia

8. Department of Biochemistry and Molecular Biology Monash University Clayton Victoria Australia

Abstract

AbstractUBTF tandem duplications are recurrent in adult and paediatric acute myeloid leukaemia and have been reported to be associated with a poor prognosis. Co‐mutations in WT1 and FLT3 are common while morphological dysplasia is frequent. The role of UBTF‐TDs in leukemogenesis is yet to be elucidated; however they have been proposed as early initiating events, making them attractive for assessment of MRD and a potential therapeutic target. We present two cases where the UBTF‐TD was observed in remission and discuss the implications of these findings in the clinicobiological understanding of this emerging entity.

Publisher

Wiley

Subject

General Earth and Planetary Sciences

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1002/jha2.808

Reference18 articles.

1. Integrated Genomic Analysis Identifies UBTF Tandem Duplications as a Recurrent Lesion in Pediatric Acute Myeloid Leukemia

2. UBTF tandem duplications define a distinct subtype of adult de novo acute myeloid leukemia

3. A novel role for the Pol I transcription factor UBTF in maintaining genome stability through the regulation of highly transcribed Pol II genes

4. DNA looping in the RNA polymerase I enhancesome is the result of non-cooperative in-phase bending by two UBF molecules

5. Growth Factor Signaling Regulates Elongation of RNA Polymerase I Transcription in Mammals via UBF Phosphorylation and r-Chromatin Remodeling