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Article: Editorial: The Bone Marrow Niche in Normal and Malignant Haematopoiesis.

Colombo, Michela / Norfo, Ruggiero / Bianchi, Giada / Roccaro, Aldo M

Frontiers in cell and developmental biology

2022 Volume 10, Page(s) 870114

Language	English
Publishing date	2022-02-28
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2022.870114
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Article: Ancient genomic linkage couples metabolism with erythroid development.

Preston, Alexandra E / Frost, Joe N / Badat, Mohsin / Teh, Megan / Armitage, Andrew E / Norfo, Ruggiero / Wideman, Sarah K / Hanifi, Muhammad / White, Natasha / Roy, Noémi / Ghesquiere, Bart / Babbs, Christian / Kassouf, Mira / Davies, James / Hughes, Jim R / Beagrie, Rob / Higgs, Douglas R / Drakesmith, Hal

bioRxiv : the preprint server for biology

2023

Abstract: Generation of mature cells from progenitors requires tight coupling of differentiation and metabolism. During erythropoiesis, erythroblasts are required to massively upregulate globin synthesis then clear extraneous material and enucleate to produce ... ...

Abstract	Generation of mature cells from progenitors requires tight coupling of differentiation and metabolism. During erythropoiesis, erythroblasts are required to massively upregulate globin synthesis then clear extraneous material and enucleate to produce erythrocytes
Language	English
Publishing date	2023-09-25
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.09.25.558944
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Article ; Online: Loss of endothelial membrane KIT ligand affects systemic KIT ligand levels but not bone marrow hematopoietic stem cells.

Matsuoka, Sahoko / Facchini, Raffaella / Luis, Tiago C / Carrelha, Joana / Woll, Petter S / Mizukami, Takuo / Wu, Bishan / Boukarabila, Hanane / Buono, Mario / Norfo, Ruggiero / Arai, Fumio / Suda, Toshio / Mead, Adam J / Nerlov, Claus / Jacobsen, Sten Eirik W

Blood

2023 Volume 142, Issue 19, Page(s) 1622–1632

Abstract: A critical regulatory role of hematopoietic stem cell (HSC) vascular niches in the bone marrow has been implicated to occur through endothelial niche cell expression of KIT ligand. However, endothelial-derived KIT ligand is expressed in both a soluble ... ...

Abstract	A critical regulatory role of hematopoietic stem cell (HSC) vascular niches in the bone marrow has been implicated to occur through endothelial niche cell expression of KIT ligand. However, endothelial-derived KIT ligand is expressed in both a soluble and membrane-bound form and not unique to bone marrow niches, and it is also systemically distributed through the circulatory system. Here, we confirm that upon deletion of both the soluble and membrane-bound forms of endothelial-derived KIT ligand, HSCs are reduced in mouse bone marrow. However, the deletion of endothelial-derived KIT ligand was also accompanied by reduced soluble KIT ligand levels in the blood, precluding any conclusion as to whether the reduction in HSC numbers reflects reduced endothelial expression of KIT ligand within HSC niches, elsewhere in the bone marrow, and/or systemic soluble KIT ligand produced by endothelial cells outside of the bone marrow. Notably, endothelial deletion, specifically of the membrane-bound form of KIT ligand, also reduced systemic levels of soluble KIT ligand, although with no effect on stem cell numbers, implicating an HSC regulatory role primarily of soluble rather than membrane KIT ligand expression in endothelial cells. In support of a role of systemic rather than local niche expression of soluble KIT ligand, HSCs were unaffected in KIT ligand deleted bones implanted into mice with normal systemic levels of soluble KIT ligand. Our findings highlight the need for more specific tools to unravel niche-specific roles of regulatory cues expressed in hematopoietic niche cells in the bone marrow.
MeSH term(s)	Mice ; Animals ; Stem Cell Factor/metabolism ; Endothelial Cells ; Hematopoietic Stem Cells/metabolism ; Bone Marrow/metabolism ; Bone and Bones ; Stem Cell Niche ; Bone Marrow Cells/metabolism
Chemical Substances	Stem Cell Factor
Language	English
Publishing date	2023-08-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood.2022019018
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Article ; Online: Genomic landscape of megakaryopoiesis and platelet function defects.

Bianchi, Elisa / Norfo, Ruggiero / Pennucci, Valentina / Zini, Roberta / Manfredini, Rossella

Blood

2016 Volume 127, Issue 10, Page(s) 1249–1259

Abstract: Megakaryopoiesis is a complex, stepwise process that takes place largely in the bone marrow. At the apex of the hierarchy, hematopoietic stem cells undergo a number of lineage commitment decisions that ultimately lead to the production of polyploid ... ...

Abstract	Megakaryopoiesis is a complex, stepwise process that takes place largely in the bone marrow. At the apex of the hierarchy, hematopoietic stem cells undergo a number of lineage commitment decisions that ultimately lead to the production of polyploid megakaryocytes. On average, megakaryocytes release 10(11) platelets per day into the blood that repair vascular injuries and prevent excessive bleeding. This differentiation process is tightly controlled by exogenous and endogenous factors, which have been the topics of intense research in the hematopoietic field. Indeed, a skewing of megakaryocyte commitment and differentiation may entail the onset of myeloproliferative neoplasms and other preleukemic disorders together with acute megakaryoblastic leukemia, whereas quantitative or qualitative defects in platelet production can lead to inherited platelet disorders. The recent advent of next-generation sequencing has prompted mapping of the genomic landscape of these conditions to provide an accurate view of the underlying lesions. The aims of this review are to introduce the physiological pathways of megakaryopoiesis and to present landmark studies on acquired and inherited disorders that target them. These studies have not only introduced a new era in the fields of molecular medicine and targeted therapies but may also provide us with a better understanding of the mechanisms underlying normal megakaryopoiesis and thrombopoiesis that can inform efforts to create alternative sources of megakaryocytes and platelets.
MeSH term(s)	Animals ; Blood Platelet Disorders/genetics ; Blood Platelet Disorders/metabolism ; Blood Platelet Disorders/pathology ; Blood Platelets/metabolism ; Blood Platelets/pathology ; Genetic Diseases, Inborn/genetics ; Genetic Diseases, Inborn/metabolism ; Genetic Diseases, Inborn/pathology ; Genome, Human ; High-Throughput Nucleotide Sequencing ; Humans ; Megakaryocytes/metabolism ; Megakaryocytes/pathology ; Thrombopoiesis/genetics
Language	English
Publishing date	2016-01-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2015-07-607952
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Article ; Online: Perivascular niche cells sense thrombocytopenia and activate hematopoietic stem cells in an IL-1 dependent manner.

Nature communications

2023 Volume 14, Issue 1, Page(s) 6062

Abstract: Hematopoietic stem cells (HSCs) residing in specialized niches in the bone marrow are responsible for the balanced output of multiple short-lived blood cell lineages in steady-state and in response to different challenges. However, feedback mechanisms by ...

Abstract	Hematopoietic stem cells (HSCs) residing in specialized niches in the bone marrow are responsible for the balanced output of multiple short-lived blood cell lineages in steady-state and in response to different challenges. However, feedback mechanisms by which HSCs, through their niches, sense acute losses of specific blood cell lineages remain to be established. While all HSCs replenish platelets, previous studies have shown that a large fraction of HSCs are molecularly primed for the megakaryocyte-platelet lineage and are rapidly recruited into proliferation upon platelet depletion. Platelets normally turnover in an activation-dependent manner, herein mimicked by antibodies inducing platelet activation and depletion. Antibody-mediated platelet activation upregulates expression of Interleukin-1 (IL-1) in platelets, and in bone marrow extracellular fluid in vivo. Genetic experiments demonstrate that rather than IL-1 directly activating HSCs, activation of bone marrow Lepr
MeSH term(s)	Humans ; Interleukin-1/metabolism ; Hematopoietic Stem Cells/metabolism ; Bone Marrow/metabolism ; Megakaryocytes ; Thrombocytopenia/metabolism
Chemical Substances	Interleukin-1
Language	English
Publishing date	2023-09-28
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-41691-y
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Article ; Online: Rapid Emergence of Chronic Lymphocytic Leukemia During JAK2 Inhibitor Therapy in a Patient With Myelofibrosis.

Sousos, Nikolaos / Buck, Gemma / Rodriguez-Meira, Alba / Norfo, Ruggiero / Hamblin, Angela / Pezzella, Francesco / Davies, Jennifer / Hublitz, Philip / Psaila, Bethan / Mead, Adam J

HemaSphere

2020 Volume 4, Issue 3, Page(s) e356

Language	English
Publishing date	2020-05-27
Publishing country	United States
Document type	Letter
ISSN	2572-9241
ISSN (online)	2572-9241
DOI	10.1097/HS9.0000000000000356
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Article ; Online: Single-cell multi-omics identifies chronic inflammation as a driver of TP53-mutant leukemic evolution.

Rodriguez-Meira, Alba / Norfo, Ruggiero / Wen, Sean / Chédeville, Agathe L / Rahman, Haseeb / O'Sullivan, Jennifer / Wang, Guanlin / Louka, Eleni / Kretzschmar, Warren W / Paterson, Aimee / Brierley, Charlotte / Martin, Jean-Edouard / Demeule, Caroline / Bashton, Matthew / Sousos, Nikolaos / Moralli, Daniela / Subha Meem, Lamia / Carrelha, Joana / Wu, Bishan /

Hamblin, Angela / Guermouche, Helene / Pasquier, Florence / Marzac, Christophe / Girodon, François / Vainchenker, William / Drummond, Mark / Harrison, Claire / Chapman, J Ross / Plo, Isabelle / Jacobsen, Sten Eirik W / Psaila, Bethan / Thongjuea, Supat / Antony-Debré, Iléana / Mead, Adam J

Nature genetics

2023 Volume 55, Issue 9, Page(s) 1531–1541

Abstract: Understanding the genetic and nongenetic determinants of tumor protein 53 (TP53)-mutation-driven clonal evolution and subsequent transformation is a crucial step toward the design of rational therapeutic strategies. Here we carry out allelic resolution ... ...

Abstract	Understanding the genetic and nongenetic determinants of tumor protein 53 (TP53)-mutation-driven clonal evolution and subsequent transformation is a crucial step toward the design of rational therapeutic strategies. Here we carry out allelic resolution single-cell multi-omic analysis of hematopoietic stem/progenitor cells (HSPCs) from patients with a myeloproliferative neoplasm who transform to TP53-mutant secondary acute myeloid leukemia (sAML). All patients showed dominant TP53 'multihit' HSPC clones at transformation, with a leukemia stem cell transcriptional signature strongly predictive of adverse outcomes in independent cohorts, across both TP53-mutant and wild-type (WT) AML. Through analysis of serial samples, antecedent TP53-heterozygous clones and in vivo perturbations, we demonstrate a hitherto unrecognized effect of chronic inflammation, which suppressed TP53 WT HSPCs while enhancing the fitness advantage of TP53-mutant cells and promoted genetic evolution. Our findings will facilitate the development of risk-stratification, early detection and treatment strategies for TP53-mutant leukemia, and are of broad relevance to other cancer types.
MeSH term(s)	Humans ; Multiomics ; Neoplasm Proteins ; Inflammation/genetics ; Alleles ; Leukemia/genetics ; Tumor Suppressor Protein p53/genetics
Chemical Substances	Neoplasm Proteins ; TP53 protein, human ; Tumor Suppressor Protein p53
Language	English
Publishing date	2023-09-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1108734-1
ISSN	1546-1718 ; 1061-4036
ISSN (online)	1546-1718
ISSN	1061-4036
DOI	10.1038/s41588-023-01480-1
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Article ; Online: miR-382-5p Controls Hematopoietic Stem Cell Differentiation Through the Downregulation of MXD1.

Zini, Roberta / Rossi, Chiara / Norfo, Ruggiero / Pennucci, Valentina / Barbieri, Greta / Ruberti, Samantha / Rontauroli, Sebastiano / Salati, Simona / Bianchi, Elisa / Manfredini, Rossella

Stem cells and development

2016 Volume 25, Issue 19, Page(s) 1433–1443

Abstract: microRNAs are key regulators of gene expression that control stem cell fate by posttranscriptional downregulation of hundreds of target genes through seed pairing in their 3' untranslated region. In fact, miRNAs tightly regulate fundamental stem cell ... ...

Abstract	microRNAs are key regulators of gene expression that control stem cell fate by posttranscriptional downregulation of hundreds of target genes through seed pairing in their 3' untranslated region. In fact, miRNAs tightly regulate fundamental stem cell processes, like self-renewal, proliferation, and differentiation; therefore, miRNA deregulation may contribute to the development of solid tumors and hematological malignancies. miR-382-5p has been found to be upregulated in patients with myeloid neoplasms, but its role in normal hematopoiesis is still unknown. In this study, we demonstrated that miR-382-5p overexpression in CD34(+) hematopoietic stem/progenitor cells (HSPCs) leads to a significant decrease of megakaryocyte precursors coupled to increase of granulocyte ones. Furthermore, by means of a computational analysis using different prediction algorithms, we identified several putative mRNA targets of miR-382-5p that are downregulated upon miRNA overexpression (ie, FLI1, GATA2, MAF, MXD1, RUNX1, and SGK1). Among these, we validated MXD1 as real target of miR-382-5p by luciferase reporter assay. Finally, we showed that MXD1 knockdown mimics the effects of miR-382-5p overexpression on granulocyte and megakaryocyte differentiation of CD34(+) cells. Overall, our results demonstrated that miR-382-5p expression favors the expansion of granulocyte lineage and impairs megakaryocyte commitment through MXD1 downregulation. Therefore, our data showed for the first time that the miR-382-5p/MXD1 axis plays a critical role in myelopoiesis by affecting the lineage choice of CD34(+) HSPCs.
MeSH term(s)	Antigens, CD34/metabolism ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/genetics ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/metabolism ; Cell Differentiation/drug effects ; Cell Differentiation/genetics ; Cell Lineage/drug effects ; Cell Lineage/genetics ; Cells, Cultured ; Clone Cells ; Collagen/pharmacology ; Down-Regulation/drug effects ; Down-Regulation/genetics ; Gene Silencing/drug effects ; Genes, Reporter ; Hematopoietic Stem Cells/cytology ; Hematopoietic Stem Cells/drug effects ; Hematopoietic Stem Cells/metabolism ; Humans ; Luciferases/metabolism ; Methylcellulose/pharmacology ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Repressor Proteins/genetics ; Repressor Proteins/metabolism ; Reproducibility of Results
Chemical Substances	Antigens, CD34 ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; MIRN382 microRNA, human ; MXD1 protein, human ; MicroRNAs ; Repressor Proteins ; Methylcellulose (9004-67-5) ; Collagen (9007-34-5) ; Luciferases (EC 1.13.12.-)
Language	English
Publishing date	2016-10-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	2142214-X
ISSN	1557-8534 ; 1547-3287
ISSN (online)	1557-8534
ISSN	1547-3287
DOI	10.1089/scd.2016.0150
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Article ; Online: Heterogeneous disease-propagating stem cells in juvenile myelomonocytic leukemia.

The Journal of experimental medicine

2021 Volume 218, Issue 2

Abstract: Juvenile myelomonocytic leukemia (JMML) is a poor-prognosis childhood leukemia usually caused by RAS-pathway mutations. The cellular hierarchy in JMML is poorly characterized, including the identity of leukemia stem cells (LSCs). FACS and single-cell RNA ...

Abstract	Juvenile myelomonocytic leukemia (JMML) is a poor-prognosis childhood leukemia usually caused by RAS-pathway mutations. The cellular hierarchy in JMML is poorly characterized, including the identity of leukemia stem cells (LSCs). FACS and single-cell RNA sequencing reveal marked heterogeneity of JMML hematopoietic stem/progenitor cells (HSPCs), including an aberrant Lin-CD34+CD38-CD90+CD45RA+ population. Single-cell HSPC index-sorting and clonogenic assays show that (1) all somatic mutations can be backtracked to the phenotypic HSC compartment, with RAS-pathway mutations as a "first hit," (2) mutations are acquired with both linear and branching patterns of clonal evolution, and (3) mutant HSPCs are present after allogeneic HSC transplant before molecular/clinical evidence of relapse. Stem cell assays reveal interpatient heterogeneity of JMML LSCs, which are present in, but not confined to, the phenotypic HSC compartment. RNA sequencing of JMML LSC reveals up-regulation of stem cell and fetal genes (HLF, MEIS1, CNN3, VNN2, and HMGA2) and candidate therapeutic targets/biomarkers (MTOR, SLC2A1, and CD96), paving the way for LSC-directed disease monitoring and therapy in this disease.
MeSH term(s)	Animals ; Biomarkers, Tumor/genetics ; Cell Line ; Female ; Hematopoietic Stem Cells/pathology ; Humans ; Leukemia, Myelomonocytic, Juvenile/genetics ; Leukemia, Myelomonocytic, Juvenile/pathology ; Male ; Mice ; Mutation/genetics ; Neoplastic Stem Cells/pathology ; Signal Transduction/genetics ; Up-Regulation/genetics
Chemical Substances	Biomarkers, Tumor
Language	English
Publishing date	2021-01-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20180853
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Article ; Online: Cell-intrinsic depletion of Aml1-ETO-expressing pre-leukemic hematopoietic stem cells by K-Ras activating mutation.

Di Genua, Cristina / Norfo, Ruggiero / Rodriguez-Meira, Alba / Wen, Wei Xiong / Drissen, Roy / Booth, Christopher A G / Povinelli, Benjamin / Repapi, Emmanouela / Gray, Nicki / Carrelha, Joana / Kettyle, Laura M / Jamieson, Lauren / Neo, Wen Hao / Thongjuea, Supat / Nerlov, Claus / Mead, Adam J

Haematologica

2019 Volume 104, Issue 11, Page(s) 2215–2224

Abstract: Somatic mutations in acute myeloid leukemia are acquired sequentially and hierarchically. First, pre-leukemic mutations, such as t(8;21) that encodes AML1-ETO, are acquired within the hematopoietic stem cell (HSC) compartment, while signaling pathway ... ...

Abstract	Somatic mutations in acute myeloid leukemia are acquired sequentially and hierarchically. First, pre-leukemic mutations, such as t(8;21) that encodes AML1-ETO, are acquired within the hematopoietic stem cell (HSC) compartment, while signaling pathway mutations, including KRAS activating mutations, are late events acquired during transformation of leukemic progenitor cells and are rarely detectable in HSC. This raises the possibility that signaling pathway mutations are detrimental to clonal expansion of pre-leukemic HSC. To address this hypothesis, we used conditional genetics to introduce Aml1-ETO and K-RasG12D into murine HSC, either individually or in combination. In the absence of activated Ras, Aml1-ETO-expressing HSC conferred a competitive advantage. However, activated K-Ras had a marked detrimental effect on Aml1-ETO-expressing HSC, leading to loss of both phenotypic and functional HSC. Cell cycle analysis revealed a loss of quiescence in HSC co-expressing Aml1-ETO and K-RasG12D, accompanied by an enrichment in E2F and Myc target gene expression and depletion of HSC self-renewal-associated gene expression. These findings provide a mechanistic basis for the observed absence of KRAS signaling mutations in the pre-malignant HSC compartment.
MeSH term(s)	Animals ; Cell Proliferation/genetics ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; Core Binding Factor Alpha 2 Subunit/genetics ; Core Binding Factor Alpha 2 Subunit/metabolism ; Gene Expression ; Gene Expression Profiling ; Hematopoietic Stem Cells/metabolism ; Hematopoietic Stem Cells/pathology ; Humans ; Mice ; Mice, Transgenic ; Models, Animal ; Models, Biological ; Mutation ; Oncogene Proteins, Fusion/genetics ; Oncogene Proteins, Fusion/metabolism ; Precancerous Conditions/genetics ; Precancerous Conditions/metabolism ; Proto-Oncogene Proteins p21(ras)/genetics ; RUNX1 Translocation Partner 1 Protein/genetics ; RUNX1 Translocation Partner 1 Protein/metabolism
Chemical Substances	AML1-ETO fusion protein, human ; Core Binding Factor Alpha 2 Subunit ; KRAS protein, human ; Oncogene Proteins, Fusion ; RUNX1 Translocation Partner 1 Protein ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
Language	English
Publishing date	2019-04-11
Publishing country	Italy
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2333-4
ISSN	1592-8721 ; 0017-6567 ; 0390-6078
ISSN (online)	1592-8721
ISSN	0017-6567 ; 0390-6078
DOI	10.3324/haematol.2018.205351
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