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Sustained fetal hematopoiesis causes juvenile death from leukemia: evidence from a dual-age–specific mouse model

Vara, Nitza, Liu, Yuqing, Yan, Yan, Lensing, Shelly Y., Colorado, Natalia, Robinson, Delli, Zhang, Jingliao, Zhang, Xin, Peterson, Erich A., Baltz, Nicholas J., Zhou, Daohong, Bertaina, Alice, Johann, Donald J., Emanuel, Peter D., Liu, Y. Lucy·2020·Blood Advances
DOI 10.1182/bloodadvances.2020002326
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Abstract

It is not clear whether disrupted age-specific hematopoiesis contributes to the complex manifestations in leukemia patients who carry identical mutations, particularly in pediatric and adult patients with similar clinical characteristics. By studying a dual-age–specific mouse model, we demonstrate that (1) loss of Pten during the fetal-to-adult hematopoiesis switch (hematopoiesis switch) causes sustained fetal hematopoiesis, resulting in death in juvenile leukemia; (2) myeloid-biased hematopoiesis in juvenile mice is associated with the sustained fetal properties of hematopoietic stem cells (HSCs); (3) the age specificity of juvenile myelomonocytic leukemia depends on the copy number of Pten and Nf1; (4) single-allelic Pten deletion during the hematopoiesis switch causes constitutive activation of MAPK in juvenile mice with Nf1 loss of heterozygosity (LOH); and (5) Nf1 LOH causes monocytosis in juvenile mice with Pten haploinsufficiency but does not cause lethality until adulthood. Our data suggest that 1 copy of Pten is sufficient to maintain an intact negative-feedback loop of the Akt pathway and HSC function in reconstitution, despite MAPK being constitutively activated in juvenile Pten+/ΔNf1LOH mice. However, 2 copies of Pten are required to maintain the integrity of the MAPK pathway in juvenile mice with Nf1 haploinsufficiency. Our data indicate that previous investigations of Pten function in wild-type mice may not reflect the impact of Pten loss in mice with Nf1 mutations or other genetic defects. We provide a proof of concept that disassociated age-specific hematopoiesis contributes to leukemogenesis and pediatric demise.

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Research works printed but not linked: 42

  1. Niemeyer, 1997, Chronic myelomonocytic leukemia in childhood: a retrospective analysis of 110 cases, Blood, 89, 3534
  2. Alfonso, 2017, Natural history of chronic myelomonocytic leukemia treated with hypomethylating agents, Am J Hematol, 92, 599, 10.1002/ajh.24735 · DOI
  3. Geissler, 2016, Chronic myelomonocytic leukemia patients with RAS pathway mutations show high in vitro myeloid colony formation in the absence of exogenous growth factors, Leukemia, 30, 2280, 10.1038/leu.2016.235 · DOI
  4. Sakaguchi, 2013, Exome sequencing identifies secondary mutations of SETBP1 and JAK3 in juvenile myelomonocytic leukemia, Nat Genet, 45, 937, 10.1038/ng.2698 · DOI
  5. Hofmans, 2018, The long non-coding RNA landscape in juvenile myelomonocytic leukemia, Haematologica, 103, e501, 10.3324/haematol.2018.189977 · DOI
  6. Stieglitz, 2015, The genomic landscape of juvenile myelomonocytic leukemia [published correction appears in Nat Genet. 2016;48(1):101], Nat Genet, 47, 1326, 10.1038/ng.3400 · DOI
  7. Lipka, 2017, RAS-pathway mutation patterns define epigenetic subclasses in juvenile myelomonocytic leukemia, Nat Commun, 8, 2126, 10.1038/s41467-017-02177-w · DOI
  8. Leoncini, 2018, Whole genome MBD-seq reveals different CpG methylation patterns in azacytidine-treated juvenile myelomonocytic leukaemia (JMML) patients, Br J Haematol, 182, 909, 10.1111/bjh.14876 · DOI
  9. Leoncini, 2016, MicroRNA fingerprints in juvenile myelomonocytic leukemia (JMML) identified miR-150-5p as a tumor suppressor and potential target for treatment, Oncotarget, 7, 55395, 10.18632/oncotarget.10577 · DOI
  10. Liu, 2016, Timing of the loss of Pten protein determines disease severity in a mouse model of myeloid malignancy, Blood, 127, 1912, 10.1182/blood-2015-05-646216 · DOI
  11. Chang, 2016, Clearance of senescent cells by ABT263 rejuvenates aged hematopoietic stem cells in mice, Nat Med, 22, 78, 10.1038/nm.4010 · DOI · Paper page
  12. Liu, 2009, PTEN deficiency is a common defect in juvenile myelomonocytic leukemia, Leuk Res, 33, 671, 10.1016/j.leukres.2008.09.036 · DOI
  13. Steinemann, 2010, Mitotic recombination and compound-heterozygous mutations are predominant NF1-inactivating mechanisms in children with juvenile myelomonocytic leukemia and neurofibromatosis type 1, Haematologica, 95, 320, 10.3324/haematol.2009.010355 · DOI
  14. Niemeyer, 2018, JMML genomics and decisions, Hematology (Am Soc Hematol Educ Program), 2018, 307, 10.1182/asheducation-2018.1.307 · DOI
  15. Bollag, 1996, Loss of NF1 results in activation of the Ras signaling pathway and leads to aberrant growth in haematopoietic cells [published correction appears in Nat Genet. 1996;12:458], Nat Genet, 12, 144, 10.1038/ng0296-144 · DOI
  16. Kikuchi, 2006, Developmental switch of mouse hematopoietic stem cells from fetal to adult type occurs in bone marrow after birth, Proc Natl Acad Sci USA, 103, 17852, 10.1073/pnas.0603368103 · DOI
  17. Copley, 2013, Developmental changes in hematopoietic stem cell properties, Exp Mol Med, 45, e55, 10.1038/emm.2013.98 · DOI
  18. Itzykson, 2013, An evolutionary perspective on chronic myelomonocytic leukemia, Leukemia, 27, 1441, 10.1038/leu.2013.100 · DOI
  19. Tyner, 2009, High-throughput sequencing screen reveals novel, transforming RAS mutations in myeloid leukemia patients, Blood, 113, 1749, 10.1182/blood-2008-04-152157 · DOI
  20. Zhang, 2018, PTEN is indispensable for cells to respond to MAPK inhibitors in myeloid leukemia, Cell Signal, 50, 72, 10.1016/j.cellsig.2018.06.004 · DOI
  21. Le, 2004, Somatic inactivation of Nf1 in hematopoietic cells results in a progressive myeloproliferative disorder, Blood, 103, 4243, 10.1182/blood-2003-08-2650 · DOI
  22. Chang, 2013, Sustained MEK inhibition abrogates myeloproliferative disease in Nf1 mutant mice, J Clin Invest, 123, 335, 10.1172/JCI63193 · DOI
  23. Christensen, 2009, The CBC: reference ranges for neonates, Semin Perinatol, 33, 3, 10.1053/j.semperi.2008.10.010 · DOI
  24. Melioli, 2011, Reference values of blood cell counts in the first days of life, Front Biosci (Elite Ed), 3, 871, 10.2741/e295 · DOI
  25. Helsmoortel, 2016, LIN28B overexpression defines a novel fetal-like subgroup of juvenile myelomonocytic leukemia, Blood, 127, 1163, 10.1182/blood-2015-09-667808 · DOI
  26. Carey, 2008, Repertoire-based selection into the marginal zone compartment during B cell development, J Exp Med, 205, 2043, 10.1084/jem.20080559 · DOI
  27. Yoshimoto, 2011, Embryonic day 9 yolk sac and intra-embryonic hemogenic endothelium independently generate a B-1 and marginal zone progenitor lacking B-2 potential, Proc Natl Acad Sci USA, 108, 1468, 10.1073/pnas.1015841108 · DOI
  28. Ghosn, 2012, Distinct B-cell lineage commitment distinguishes adult bone marrow hematopoietic stem cells, Proc Natl Acad Sci USA, 109, 5394, 10.1073/pnas.1121632109 · DOI
  29. Magee, 2012, Temporal changes in PTEN and mTORC2 regulation of hematopoietic stem cell self-renewal and leukemia suppression, Cell Stem Cell, 11, 415, 10.1016/j.stem.2012.05.026 · DOI
  30. West, 1987, Fetal alcohol-induced brain damage and the problem of determining temporal vulnerability: a review, Alcohol Drug Res, 7, 423
  31. Lai, 2014, Cell fate decisions in malignant hematopoiesis: leukemia phenotype is determined by distinct functional domains of the MN1 oncogene, PLoS One, 9, e112671, 10.1371/journal.pone.0112671 · DOI
  32. Wohrer, 2014, Distinct stromal cell factor combinations can separately control hematopoietic stem cell survival, proliferation, and self-renewal, Cell Rep, 7, 1956, 10.1016/j.celrep.2014.05.014 · DOI
  33. Tukey, 1977, Exploratory Data Analysis
  34. Manesia, 2017, Distinct molecular signature of murine fetal liver and adult hematopoietic stem cells identify novel regulators of hematopoietic stem cell function, Stem Cells Dev, 26, 573, 10.1089/scd.2016.0294 · DOI
  35. Bowie, 2007, Identification of a new intrinsically timed developmental checkpoint that reprograms key hematopoietic stem cell properties, Proc Natl Acad Sci USA, 104, 5878, 10.1073/pnas.0700460104 · DOI
  36. Babovic, 2014, Hierarchical organization of fetal and adult hematopoietic stem cells, Exp Cell Res, 329, 185, 10.1016/j.yexcr.2014.08.005 · DOI
  37. Dykstra, 2007, Long-term propagation of distinct hematopoietic differentiation programs in vivo, Cell Stem Cell, 1, 218, 10.1016/j.stem.2007.05.015 · DOI · Paper page
  38. Beaudin, 2016, A transient developmental hematopoietic stem cell gives rise to innate-like B and T cells, Cell Stem Cell, 19, 768, 10.1016/j.stem.2016.08.013 · DOI · Paper page
  39. Peng, 2018, Luteinizing hormone signaling restricts hematopoietic stem cell expansion during puberty, EMBO J, 37, e98984, 10.15252/embj.201898984 · DOI
  40. Copley, 2013, The Lin28b-let-7-Hmga2 axis determines the higher self-renewal potential of fetal haematopoietic stem cells, Nat Cell Biol, 15, 916, 10.1038/ncb2783 · DOI
  41. Baumgartner, 2018, An ERK-dependent feedback mechanism prevents hematopoietic stem cell exhaustion, Cell Stem Cell, 22, 879, 10.1016/j.stem.2018.05.003 · DOI
  42. Helsmoortel, 2016, LIN28BM overexpression defines a novel fetal-like subgroup of juvenile myelomonocytic leukemia, Blood, 127, 1163, 10.1182/blood-2015-09-667808 · DOI

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Metadata

Authors
Vara, N., Liu, Y., Yan, Y., Lensing, S. Y., Colorado, N., Robinson, D., Zhang, J., Zhang, X., Peterson, E. A., Baltz, N. J., Zhou, D., Bertaina, A., Johann, D. J., Emanuel, P. D., & Liu, Y. L.
Venue
Blood Advances
Publisher
American Society of Hematology
Published
2020-08-10
Volume
4
Issue
15
Pages
3728-3740
ISSN
  • 2473-9529
  • 2473-9537
DOI
10.1182/bloodadvances.2020002326
Cited by
5
References
2
Language
en

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