Front. Oncol. Frontiers in Oncology Front. Oncol. 2234-943X Frontiers Media S.A. 10.3389/fonc.2022.1089874 Oncology Correction Corrigendum: Murine models of acute myeloid leukemia Kurtz Kristen J. 1 † Conneely Shannon E. 1 † O’Keefe Madeleine 1 Wohlan Katharina 2 Rau Rachel E. 1 * 1 Department of Pediatrics, Baylor College of Medicine, Texas Children’s Hospital, Houston, TX, United States 2 Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, United States

Edited and Reviewed by: Paraskevi Panagopoulou, Aristotle University of Thessaloniki, Greece

*Correspondence: Rachel E. Rau, Rachel.rau@bcm.edu

†These authors contributed equally to this work

This article was submitted to Pediatric Oncology, a section of the journal Frontiers in Oncology

 23 02 2023 2022 12 1089874 04 11 2022 13 12 2022 Copyright © 2023 Kurtz, Conneely, O’Keefe, Wohlan and Rau 2023 Kurtz, Conneely, O’Keefe, Wohlan and Rau

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 A corrigendum on Murine models of acute myeloid leukemia by Kurtz KJ, Conneely SE, O’Keefe M, Wohlan K and Rau RE (2022). Front. Oncol. 12:854973. doi: 10.3389/fonc.2022.854973 acute myeloid leukemia AML transgenic mouse genetically engineered mice (GEM) core binding factor acute myeloid leukemia KMT2a (MLL) rearrangements NUP98 fusion patient-derived xenograft (PDX)

In the original article, there was an error in Table 1 as published. We inadvertently omitted a CBFA2T3-GLIS2 mouse model and two NUP98 fusion models. The corrected Table 1 and its caption appear below.

Mouse models of fusion genes.

Fusion Gene Year Expression Mechanism Phenotype References
RUNX1-RUNX1T1 2006 Constitutive Retrovirus 9a isoform: AML (37)
2001 Constitutive Germline - Mrp8 promoter (myeloid specific) AML, T-ALL after ENU treatment (38)
2013 Inducible MDS (39)
2021 Inducible Tet-OneR1-CreERT2 AML, MPD (40)
CBFB-MYH11 2006 Inducible Mx1-Cre AML (41)
KMT2A-MLLT3 1996 Constitutive Germline AML (42)
2000 Inducible Lmo2-Cre AML (43)
2013 Constitutive Retrovirus AML (44)
2016 Inducible Retrovirus (Transduced LSKs > GMP)AML (45)
MLL-PTD 2012 Constitutive Germline AML (if FLT3-ITD mutated) (46)
KMT2A-MLLT1 2013 Inducible CreER ALL (47)
2014 Inducible Tet-On ALL (48)
NUP98-NSD1 2007 Constitutive Retrovirus AML (49)
2014 Constitutive Retrovirus AML (if FLT3-ITD mutated) (50)
2020 Constitutive Retrovirus AML (51)
Other NUP98 fusions 2020 Inducible Tet-On Retrovirus AML (52)
CBFA2T3-GLIS2 2019 Inducible Tet-On AML (53)
PML-RARA 1997 Constitutive Germline – Ctsg promoter (myeloid specific) AML – long latency (54)
1999 Constitutive Retrovirus Differentiation blockade, enhanced self-renewal (55)
2003 Constitutive Germline – Mrp8 promoter (myeloid specific) AML (56)

AML, acute myeloid leukemia; ENU, N-ethyl-N-nitrosurea; GMP, granulocyte-macrophage progenitor; ITD, internal tandem duplication; LSK, Lin-Sca1+Kit+; MDS, myelodysplastic syndrome; MPD, myeloproliferative disease; PTD, partial tandem duplication; T-ALL, T-acute lymphoblastic leukemia.

Text Correction

In the original article, several sections were mislabeled. The sub-section titled “Core binding factor leukemias” currently is labeled with “4”. This has been corrected to 3.1.

The sub-section titled “NUP98 Fusions” currently is labeled as section 3.4. This has been corrected to 3.3.

Missing reference

In the sub-section “NUP98 Fusions”, we failed to reference an important paper, Wang et al., 2007.

We have therefore inserted a new sentence and modified a sentence in that section.

Original text: Retroviral models of NUP98 fusions have served as the predominant mouse models to date. Mohanty et al. showed that retroviral model of NUP98-NSD1, the most common NUP98 fusion in pediatric AML, into murein HSCs followed by transplantation independently produced AML with a median survival of 250 days post-transplant with significant disease acceleration when NRAS G12D is co-expressed.

Corrected text:

Retroviral models of NUP98 fusions have served as the predominant mouse models to date. In 2007 Wang et al. showed that retroviral transduction of NUP98-NSD1, the most common NUP98 fusion in pediatric AML, into murine hematopoietic progenitors followed by transplantation independently produced AML with an average survival of 126 days post-transplant (68). Mohanty et al. created a similar retroviral model of NUP98-NSD1 and demonstrated significant disease acceleration when NRASG12D is co-expressed.

Text correction

In the sub-section, “CBFA2T3-GLIS2” we originally did not include an important mouse model reported by Lopez, et al. The corrected text appears below.

Lopez et al. (53) developed a novel transgenic model using tetracycline-inducible expression of CBFA2T3-GLIS2 in which nearly all mice developed a lethal hematologic malignancy, 20% of which displayed megakaryoblastic markers with a disease latency of 164 days, whereas the remaining mice displayed heterogeneous non-megakaryoblastic immunophenotypes with a significantly longer disease latency (79). As this fusion is predominantly found in pediatric AML, the authors sought to investigate the role of developmental stage on leukemia onset. They found that transplantation of fetal liver cells from their inducible model led to a shorter disease latency with a predominant megakaryoblastic population compared to mice transplanted with bone marrow from adult mice, demonstrating that developmental stage significantly impacts disease phenotype. The Lopez et al. transgenic model was a substantial technical advancement as prior to its description, murine models had been largely limited to patient-derived xenografts (PDXs) (80).

The authors apologize for these errors and state that they do not change the scientific conclusions of the article in any way. The original article has been updated.

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