» Articles » PMID: 25486471

Genetically Engineered Mouse Models of Human B-cell Precursor Leukemias

Overview
Journal Cell Cycle
Specialty Cell Biology
Date 2014 Dec 9
PMID 25486471
Citations 4
Authors
Affiliations
Soon will be listed here.
Abstract

B-cell precursor acute lymphoblastic leukemias (pB-ALLs) are the most frequent type of malignancies of the childhood, and also affect an important proportion of adult patients. In spite of their apparent homogeneity, pB-ALL comprises a group of diseases very different both clinically and pathologically, and with very diverse outcomes as a consequence of their biology, and underlying molecular alterations. Their understanding (as a prerequisite for their cure) will require a sustained multidisciplinary effort from professionals coming from many different fields. Among all the available tools for pB-ALL research, the use of animal models stands, as of today, as the most powerful approach, not only for the understanding of the origin and evolution of the disease, but also for the development of new therapies. In this review we go over the most relevant (historically, technically or biologically) genetically engineered mouse models (GEMMs) of human pB-ALLs that have been generated over the last 20 years. Our final aim is to outline the most relevant guidelines that should be followed to generate an "ideal" animal model that could become a standard for the study of human pB-ALL leukemia, and which could be shared among research groups and drug development companies in order to unify criteria for studies like drug testing, analysis of the influence of environmental risk factors, or studying the role of both low-penetrance mutations and cancer susceptibility alterations.

Citing Articles

Challenges and Opportunities for Childhood Cancer Drug Development.

Houghton P, Kurmasheva R Pharmacol Rev. 2019; 71(4):671-697.

PMID: 31558580 PMC: 6768308. DOI: 10.1124/pr.118.016972.


Immunophenotyping of Murine Precursor B-Cell Leukemia/Lymphoma: A Comparison of Immunohistochemistry and Flow Cytometry.

Janke L, Mullighan C, Dang J, Rehg J Vet Pathol. 2019; 56(6):950-958.

PMID: 31170889 PMC: 7140381. DOI: 10.1177/0300985819852138.


Five percent of healthy newborns have an fusion as revealed by DNA-based GIPFEL screening.

Schafer D, Olsen M, Lahnemann D, Stanulla M, Slany R, Schmiegelow K Blood. 2018; 131(7):821-826.

PMID: 29311095 PMC: 5909885. DOI: 10.1182/blood-2017-09-808402.


ZNF423 and ZNF521: EBF1 Antagonists of Potential Relevance in B-Lymphoid Malignancies.

Mesuraca M, Chiarella E, Scicchitano S, Codispoti B, Giordano M, Nappo G Biomed Res Int. 2016; 2015:165238.

PMID: 26788497 PMC: 4695665. DOI: 10.1155/2015/165238.

References
1.
Wang P, Young F, Chen C, Stevens B, Neering S, Rossi R . The biologic properties of leukemias arising from BCR/ABL-mediated transformation vary as a function of developmental origin and activity of the p19ARF gene. Blood. 2008; 112(10):4184-92. PMC: 2581986. DOI: 10.1182/blood-2008-02-142190. View

2.
Jing L, Zon L . Zebrafish as a model for normal and malignant hematopoiesis. Dis Model Mech. 2011; 4(4):433-8. PMC: 3124047. DOI: 10.1242/dmm.006791. View

3.
Kantner H, Warsch W, Delogu A, Bauer E, Esterbauer H, Casanova E . ETV6/RUNX1 induces reactive oxygen species and drives the accumulation of DNA damage in B cells. Neoplasia. 2013; 15(11):1292-300. PMC: 3858895. DOI: 10.1593/neo.131310. View

4.
Bijl J, Sauvageau M, Thompson A, Sauvageau G . High incidence of proviral integrations in the Hoxa locus in a new model of E2a-PBX1-induced B-cell leukemia. Genes Dev. 2005; 19(2):224-33. PMC: 545883. DOI: 10.1101/gad.1268505. View

5.
Voncken J, Kaartinen V, Pattengale P, Germeraad W, Groffen J, Heisterkamp N . BCR/ABL P210 and P190 cause distinct leukemia in transgenic mice. Blood. 1995; 86(12):4603-11. View