Genome editing-induced t(4;11) chromosomal translocations model B cell precursor acute lymphoblastic leukemias with KMT2A-AFF1 fusion

Feng Pan; Jolanda Sarno; Johan Jeong; Xin Yang; Astraea Jager; Tanja A Gruber; Kara L Davis; Michael L Cleary

doi:10.1172/JCI171030

Genome editing-induced t(4;11) chromosomal translocations model B cell precursor acute lymphoblastic leukemias with KMT2A-AFF1 fusion

J Clin Invest. 2024 Jan 2;134(1):e171030. doi: 10.1172/JCI171030.

Authors

Feng Pan^{1

2}, Jolanda Sarno^{3

4}, Johan Jeong¹, Xin Yang¹, Astraea Jager^{3

4}, Tanja A Gruber³, Kara L Davis^{3

4}, Michael L Cleary¹

Affiliations

¹ Department of Pathology, Stanford University School of Medicine, Stanford, California, USA.
² Department of Molecular Medicine, the University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA.
³ Division of Pediatric Hematology, Oncology, Stem Cell Transplantation and Regenerative Medicine, Stanford University School of Medicine, Stanford, California, USA.
⁴ Stanford Center for Cancer Cell Therapy, Stanford Cancer Institute, Stanford University, Stanford, California, USA.

Abstract

A t(4;11) leukemia model established from CRISPR-engineered chromosomal translocations between the KMT2A and AFF1 genes recapitulate proteomic, epigenomic, and transcriptomic features of primary patient leukemias.

Keywords: Hematology; Leukemias; Mouse models; Oncology.

MeSH terms

DNA-Binding Proteins / genetics
Gene Editing
Humans
Myeloid-Lymphoid Leukemia Protein / genetics
Precursor B-Cell Lymphoblastic Leukemia-Lymphoma* / genetics
Proteomics
Transcriptional Elongation Factors / genetics
Translocation, Genetic*

Substances

Myeloid-Lymphoid Leukemia Protein
AFF1 protein, human
DNA-Binding Proteins
Transcriptional Elongation Factors

Grants and funding

R01 CA214888/CA/NCI NIH HHS/United States