ArticleBlood2010
Sequential treatment of CD34+ cells from patients with primary myelofibrosis with chromatin-modifying agents eliminate JAK2V617F-positive NOD/SCID marrow repopulating cells.
Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Article
- Imetelstat, a telomerase inhibitor, is capable of depleting myelofibrosis stem and progenitor cells.Blood advances · 2018Article
- A humanized bone marrow ossicle xenotransplantation model enables improved engraftment of healthy and leukemic human hematopoietic cells.Nature medicine · 2016Article
- Article
- Evolving Therapeutic Strategies for the Classic Philadelphia-Negative Myeloproliferative Neoplasms.EBioMedicine · 2016Review
- Allo-SCT for myelofibrosis: reversing the chronic phase in the JAK inhibitor era?Bone marrow transplantation · 2015Review
- C-X-C motif chemokine 12 influences the development of extramedullary hematopoiesis in the spleens of myelofibrosis patients.Experimental hematology · 2015Article
- JAK2 inhibitors do not affect stem cells present in the spleens of patients with myelofibrosis.Blood · 2014Article
- Differential effects of epigenetic modifiers on the expansion and maintenance of human cord blood stem/progenitor cells.Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation · 2014Article
- Spleens of myelofibrosis patients contain malignant hematopoietic stem cells.The Journal of clinical investigation · 2012Article
- Article
- Targeting JAK2 in the therapy of myeloproliferative neoplasms.Expert opinion on therapeutic targets · 2012Review
- A novel murine model of myeloproliferative disorders generated by overexpression of the transcription factor NF-E2.The Journal of experimental medicine · 2012Article
- Epigenetic approaches in stem cell transplantation.Clinical epigenetics · 2011Article
- Epigenetic abnormalities in myeloproliferative neoplasms: a target for novel therapeutic strategies.Clinical epigenetics · 2011Article
- Emerging drug discovery approaches for selective targeting of "precursor" metastatic breast cancer cells: highlights and perspectives.American journal of translational research · 2011Article
- New ways to use DNA methyltransferase inhibitors for the treatment of myelodysplastic syndrome.Hematology. American Society of Hematology. Education Program · 2011Review
- Recurring mutations in myeloproliferative neoplasms alter epigenetic regulation of gene expression.American journal of cancer research · 2011Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Because primary myelofibrosis (PMF) originates at the level of the pluripotent hematopoietic stem cell (HSC), we examined the effects of various therapeutic agents on the in vitro and in vivo behavior of PMF CD34(+) cells. Treatment of PMF CD34(+) cells with chromatin-modifying agents (CMAs) but not hydroxyurea, Janus kinase 2 (JAK2) inhibitors, or low doses of interferon-α led to the generation of greater numbers of CD34(+) chemokine (C-X-C motif) receptor (CXCR)4(+) cells, which were capable of migrating in response to chemokine (C-X-C motif) ligand (CXCL)12 and resulted in a reduction in the proportion of hematopoietic progenitor cells (HPCs) that were JAK2V617F(+). Furthermore, sequential treatment of PMF CD34(+) cells but not normal CD34(+) cells with decitabine (5-aza-2'-deoxycytidine [5azaD]), followed by suberoylanilide hydroxamic acid (SAHA; 5azaD/SAHA), or trichostatin A (5azaD/TSA) resulted in a higher degree of apoptosis. Two to 6 months after the transplantation of CMAs treated JAK2V617F(+) PMF CD34(+) cells into nonobese diabetic/severe combined immunodeficient (SCID)/IL-2Rγ(null) mice, the percentage of JAK2V617F/JAK2(total) in human CD45(+) marrow cells was dramatically reduced. These findings suggest that both PMF HPCs, short-term and long-term SCID repopulating cells (SRCs), are JAK2V617F(+) and that JAK2V617F(+) HPCs and SRCs can be eliminated by sequential treatment with CMAs. Sequential treatment with CMAs, therefore, represents a possible effective means of treating PMF at the level of the malignant SRC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.