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Journal articles on the topic 'Reticulo cytopenia'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

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1

Deldar, A., H. Lewis, J. Bloom, and L. Weiss. "Cephalosporin-induced Changes in the Ultrastructure of Canine Bone Marrow." Veterinary Pathology 25, no. 3 (1988): 211–18. http://dx.doi.org/10.1177/030098588802500305.

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Fourteen healthy dogs were given 540 to 840 mg/kg of cefazedone (Refosporen®) intravenously for up to 4 months or until peripheral blood cell counts were depressed. Within 6 to 10 weeks treated dogs developed pancytopenia (5/14), thrombocytopenia (11/14), moderate to severe neutropenia (8/14), and/or normocytic anemia with erythroblastemia (8/14). Ultrastructural changes in bone marrow of severely cytopenic dogs included mitochondrial damage in hematopoietic and nonhematopoietic cells, thickening of endosteal bone lining layers, increased adventitial coverage of vascular sinuses, and an increa

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2

Alana Vicente, Bhavisha A. Patel, Fernanda Gutierrez-Rodrigues, et al. "Eltrombopag monotherapy can improve hematopoiesis in patients with low to intermediate risk-1 myelodysplastic syndrome." Haematologica 105, no. 12 (2020): 2785–94. http://dx.doi.org/10.3324/haematol.2020.249995.

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Myelodysplastic syndromes (MDS) are a group of clonal myeloid disorders characterized by cytopenia and a propensity to develop acute myeloid leukemia (AML). The management of lower-risk (LR) MDS with persistent cytopenias remains suboptimal. Eltrombopag (EPAG), a thrombopoietin receptor agonist, can improve platelet counts in LR-MDS and tri-lineage hematopoiesis in aplastic anemia (AA). We conducted a phase 2 dose modification study to investigate the safety and efficacy of EPAG in LR-MDS. EPAG dose was escalated from 50 mg/day, to a maximum of 150 mg/day over a period of 16 weeks. The primary

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3

Srinivas, G., D.V. Ramanjaneyulu, E. Muralinath, et al. "An Essential Parameters of Parvo Virus Include Patho Physiology, Histo Pathology, Diagnosis, Differential Diagnosis, Treatment and Prognosis." Journal of Research and Reviews in Nursing Science and Education 2, no. 2 (2025): 11–17. https://doi.org/10.5281/zenodo.15541791.

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<em>One virus that only affects people is parvovirus B19. The fifth illness, also known as erythema infectious or slapped cheek syndrome, is known to be caused by it. It primarily affects young children, though it can sometimes affect adults. In addition, it may result in Poly arthropathy, popular-purpuric gloves and socks syndrome (PPGSS) in young people, certain anemias, hydrops fetalis, particularly in pregnant women, and an aplastic crisis. Viral transmission occurs through both respiratory secretions and blood products. The virus can infect a pregnant woman and then infect her unborn chil

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4

Mathew, Josy, Surbhi Shah, and Virginia L. Kubic. "Bone Marrow Biopsy Findings in Patients with Hepatitis C Infection." Blood 120, no. 21 (2012): 4840. http://dx.doi.org/10.1182/blood.v120.21.4840.4840.

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Abstract Abstract 4840 Patients with hepatitis C often present with cytopenias - thrombocytopenia, neutropenia and less commonly anemia. Hypersplenism may contribute to cytopenias but effects on the bone marrow due to the hepatitis C infection also likely play a role in its pathogenesis. Hepatitis C infection predisposes to development of lymphomas as well. The bone marrow findings in patients with hepatitis C infection are not well described and to our knowledge there has only been one peer reviewed study published till date. In order to elucidate this further, we conducted a retrospective re

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5

Mailloux, Adam, Ling Zhang, Lynn Moscinski, et al. "Pathophysiology of cytopenias in an autoimmune lymphoproliferative disease linked to bone marrow fibrosis (P3165)." Journal of Immunology 190, no. 1_Supplement (2013): 43.44. http://dx.doi.org/10.4049/jimmunol.190.supp.43.44.

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Abstract Large Granular Lymphocyte (LGL) leukemia is associated with unexplained cytopenias, autoimmune features, and CD57+CD8+perforin+ T-cell lympoproliferation. Like many autoimmune disorders, the pathophysiology of cytopenias in LGL leukemia is unknown. Bone marrow (BM) pathology from 24 LGL leukemia patients was retrospectively studied using H&E, reticulin, and trichrome-stained sections, and revealed that BM fibrosis was present in 21 out of 24 patients (88%). Fibrosis, a previously undefined complication, was significantly associated with splenomegaly, the presence of cytopenias, an

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6

Logue, Jennifer Marilyn, Gabriel S. Krivenko, Victoria Larson, et al. "Cytopenia following axicabtagene ciloleucel (axi-cel) for refractory large B-cell lymphoma (LBCL)." Journal of Clinical Oncology 37, no. 15_suppl (2019): e14019-e14019. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e14019.

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e14019 Background: Axi-cel is an anti-CD19 CAR T-cell therapy that can lead to long term disease control for patients with refractory LBCL including DLBCL, PMBCL, HGBL, and tFL. Beyond day 30, grade 3 or higher cytopenias were reported in 17% of patients (Locke 2019). We sought to further characterize cytopenias after axi-cel. Methods: We evaluated patients with LBCL treated with axi-cel at Moffitt from May 2015 to May 2018. Counts at apheresis and days 30, 90 and 180 after axi-cel infusion were recorded. Data was censored at date of progression, death or last follow-up. AEs were per CTCAE v4.

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7

Fattizzo, Bruno, Silvia Cantoni, Rachele Zavaglia, et al. "Efficacy and Safety of Cyclosporine Treatment in Autoimmune Cytopenias: The Experience of Two Italian Reference Centers." Blood 138, Supplement 1 (2021): 3146. http://dx.doi.org/10.1182/blood-2021-149043.

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Abstract Background: Autoimmune cytopenias (immune thrombocytopenia ITP, autoimmune hemolytic anemia AIHA, and chronic idiopathic neutropenia CIN) are a heterogeneous group of disorders characterized by the presence of autoantibodies directed against platelets (PLT), erythrocytes, and neutrophils (ANC). Frontline steroids are the mainstay of treatment, although most patients relapse and require 2 nd line therapies which slightly differ according to disease subtype. Rituximab is mainly effective in AIHA, although only a fraction of cases would experience long-term relapse-free. Splenectomy may

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8

Juvvadi, R., J. M. Rossetti, R. K. Shadduck, et al. "Response to azacitidine in patients with myelodysplastic syndrome with marrow fibrosis." Journal of Clinical Oncology 25, no. 18_suppl (2007): 7089. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.7089.

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7089 Background: The Myelodysplastic syndrome (MDS) is characterized by aberrant hematopoietic progenitor cell maturation resulting in ineffective hematopoiesis, cytopenia and progression to acute myeloid leukemia. Some individuals with MDS also have fibrosis within the marrow. MDS with marrow fibrosis appears to be biologically and clinically distinct from myeloproliferative disorders with marrow fibrosis such as agnogenic myeloid metaplasia. While azacitidine (AZA), a DNA methyl transferase inhibitor has known activity in MDS, little is known about its efficacy in patients with MDS with marr

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9

Khera, Sanjeev, Priyanka Misra, Kanwaljeet Singh, and Preeti Tripathi. "Complete resolution of primary myelofibrosis in an infant with steroids and hydroxyurea." BMJ Case Reports 16, no. 11 (2023): e256210. http://dx.doi.org/10.1136/bcr-2023-256210.

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Paediatric primary myelofibrosis (PMF) is exceedingly rare and distinct compared with adult PMF. It is characterised by peripheral blood cytopenias, leucoerythroblastosis, reticulin fibrosis, extramedullary haematopoiesis and hepatosplenomegaly. In the absence of laid down diagnostic criteria, the diagnosis is largely of exclusion. Though early haematological stem cell transplant (HSCT) remains the treatment of choice, spontaneous remission or remission with steroids and/or cytoreductive agents is described in around 20% of cases of paediatric PMF. Moreover, HSCT in paediatric PMF is associate

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10

Jafarzadeh, Bita, Vahid Mehrtash, Hortense Le, et al. "A Self-Supervised Machine Learning Model Can Differentiate MDS from Clinical Mimics Based on Bone Marrow Biopsy Features." Blood 144, Supplement 1 (2024): 7496. https://doi.org/10.1182/blood-2024-211667.

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Introduction: The pathologic evaluation of bone marrow biopsies (BMBx) for diagnosing myelodysplastic syndrome (MDS) is challenging due to the limited cytologic detail provided by H&E sections. Diagnosing MDS requires a sophisticated, integrative approach because of its complex clinical and histopathological presentations. In this study, we investigate whether integrating features from both H&E and reticulin-stained BMBx slides using self-supervised learning (SSL) image analysis could address these limitations by developing an algorithm capable of reliably distinguishing MDS from its c

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11

Giri, Neelam, Irina Maric, Robert Wesley, et al. "Bone Marrow Fibrosis in Patients with Inherited Bone Marrow Failure Syndromes." Blood 114, no. 22 (2009): 3192. http://dx.doi.org/10.1182/blood.v114.22.3192.3192.

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Abstract Abstract 3192 Poster Board III-129 Introduction Bone marrow fibrosis has been reported in many benign and malignant disorders, and it may be associated with a poor prognosis in patients with chronic idiopathic myelofibrosis and adult myelodysplastic syndrome (MDS). There are no data on the incidence or significance of bone marrow fibrosis in patients with the inherited bone marrow failure syndromes (IBMFS), genetic disorders characterized by cytopenias, distinctive clinical features, varied molecular pathways and high risks of MDS and acute myeloid leukemia. We have now studied marrow

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12

Gonzalez, Maria Fernanda, and Jonathan King Freeman. "Myelofibrosis Associated with Romiplostim Treatment in a Patient with Immune Thrombocytopenia." Case Reports in Hematology 2012 (2012): 1–4. http://dx.doi.org/10.1155/2012/318597.

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Immune thrombocytopenia is characterized by antibody-mediated platelet destruction and insufficient platelet production resulting in isolated thrombocytopenia in the absence of underlying cause. Despite many treatment options, low-to-intermediate rates of remission and high rates of resistance to treatment are seen. Approximately 20% of patients do not attain a hemostatic platelet count after splenectomy or after first- and second-line medical approaches. A new option in these cases is treatment withromiplostim. Bone marrow (BM) fibrosis has been reported in clinical trials with romiplostim. W

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13

Epling-Burnette, Pearlie K., Adam W. Mailloux, Ling Zhang, et al. "Pluripotent Fibrosis Initiating Mesenchymal Stromal Cell Linked To Cytopenias In LGL Leukemia Through Genetic Reprogramming." Blood 122, no. 21 (2013): 1218. http://dx.doi.org/10.1182/blood.v122.21.1218.1218.

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Abstract Background Large Granular Lymphocyte (LGL) leukemia is associated with chronic lymphoproliferation in association with unexplained cytopenias. Discovery of somatic mutations in STAT3 provides new insights into the molecular basis of LGL leukemia, but the precise mechanism leading to cytopenias remains unresolved. To gain insight into this mechanism, bone marrow fibrosis (Fig. 1A) was found to occur in 88% of cases and is significantly associated with splenomegaly, the presence of cytopenias, and co- existence of autoimmune diseases. In this study, we are reporting the identification o

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14

Oh, Stephen T., Jamile Shammo, Vikas Gupta, et al. "Retrospective Analysis of the Relationship between Transfusion Independence and Bone Marrow Fibrosis Reduction in Patients with Myelofibrosis Treated with Pacritinib Versus Ruxolitinib." Blood 142, Supplement 1 (2023): 4566. http://dx.doi.org/10.1182/blood-2023-178753.

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Background Pacritinib is a JAK1-sparing JAK2/IRAK1/ACVR1 inhibitor for treatment of myelofibrosis (MF). In addition to improving spleen volume and symptoms, pacritinib is associated with anemia benefit in MF patients. Recent in vivo studies have shown that dual JAK2/IRAK1 inhibition is associated with improvement in both cytopenias and bone marrow reticulin fibrosis (BMF) in an inflammation-driven murine MF model ( Cuenca Zamora E, et al. EHA 2023; P987 and P990). Here, we retrospectively analyzed the relationship between achieving transfusion independence and reduction in BMF in MF patients t

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15

Mailloux, Adam W., Ling Zhang, Lili Yang, et al. "Cytopenias in Large Granular Lymphocyte Leukemia Are Mediated by Pro-Fibrotic Mesenchymal Stem Cells in the Bone Marrow Niche with Functional Restoration by FGFb." Blood 118, no. 21 (2011): 932. http://dx.doi.org/10.1182/blood.v118.21.932.932.

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Abstract Abstract 932 Large Granular Lymphocyte Leukemia (LGLL) is a chronic lymphoproliferative syndrome of clonal mature T or NK cells frequently associated with peripheral cytopenias including neutropenia and anemia. The ability of LGLL cells to lyse pro-erythrocytes, the association with secondary autoimmune disorders, and the chronically activated state of LGLL clones suggest that the disease is secondary to a systemic reactive process. Yet, the mechanism causing severe and chronic cytopenias remains unresolved. Because LGLL cells heavily reside in the bone marrow and the bone marrow micr

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16

Irene Piatek, Caroline, Maria E. Vergara-Lluri, Vinod Pullarkat, et al. "Autoimmune Myelofibrosis (AIMF) – Clinical Features, Course and Outcome." Blood 122, no. 21 (2013): 3714. http://dx.doi.org/10.1182/blood.v122.21.3714.3714.

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Abstract Background Bone marrow (BM) fibrosis is commonly recognized in the setting of primary myelofibrosis (PMF) and other myeloproliferative neoplasms. However, a variety of non-malignant conditions are associated with myelofibrosis (MF). While PMF is associated with a limited survival, other causes of MF such as AIMF appear to have a favorable clinical course (Pullarkat et al, Am J Hematol 2001;116:211). We conducted a retrospective chart review of patients diagnosed with non-malignant MF to investigate clinical presentations, therapies, and outcomes of AIMF. Methods Patients diagnosed wit

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17

Bennett, Charles L., Ari Polish, Athena T. Samaras, et al. "From Bench to Bedside: Hematopoietic Growth Factors (HGFs)- a Cause of Serious and Unanticipated Class Toxicities." Blood 114, no. 22 (2009): 4555. http://dx.doi.org/10.1182/blood.v114.22.4555.4555.

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Abstract Abstract 4555 Introduction HGFs have vastly improved the management of anemia, neutropenia, and thrombocytopenia, but are associated with unexpected toxicities. Methods Toxicities associated with granulocyte, erythroid, and thrombopoietic growth factors were reviewed. Data sources included systematic reviews, clinical trials, guidelines, and materials disseminated by the Food and Drug Administration (FDA), the European Medicines Agency (EMEA), and Canada Health and their advisory committees; product labels and safety notifications disseminated by manufacturers; and utilization data. D

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18

Schieppati, Francesca, Erin P. Demakos, Odchimar Rosalie-Reissig, Shyamala C. Navada, and Lewis R. Silverman. "Intravenous Immunoglobulin Is an Effective Treatment for LGL-Mediated Immune Cytopenias in Myelodysplastic Syndromes and Other Bone Marrow Failure Syndromes." Blood 126, no. 23 (2015): 1704. http://dx.doi.org/10.1182/blood.v126.23.1704.1704.

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Abstract Background: Myelodysplastic Syndrome (MDS) and Aplastic Anemia (AA) are often associated with clinical immune manifestations. An abnormal profile of the T-cell repertoire can be detected in these patients (pts) and is thought to play a role in bone marrow (BM) insufficiency. The presence of a co-existent large granular lymphocytic (LGL) clone may exacerbate cytopenias independent of the primary disease mechanism and offers another target for therapeutic intervention. Treatment for LGL proliferation is usually immunosuppressive therapy but there is no accepted standard of care. Methods

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Ketharnathan, Sarada, Sujata Pokharel, Sergey V. Prykhozhij, et al. "A Zebrafish Model of Parn-Deficiency Reveals Conserved Mechanisms Underlying Marrow Failure and Opportunities for Therapeutic Amelioration of Hematopoiesis." Blood 142, Supplement 1 (2023): 2737. http://dx.doi.org/10.1182/blood-2023-190331.

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Dyskeratosis congenita (DC) is a rare inherited bone marrow failure syndrome (IBMFS) and a telomere biology disorder that is characterized by physical malformations such as nail dystrophy, oral leukoplakia, reticular hyperpigmentation, multilineage cytopenia and immunodeficiency. Definitive treatment for the hematological complications is hematopoietic stem cell transplantation (HSCT), which is associated with high risk of organ toxicity and engraftment failure in this population. Further, DC patients are prone to developing myelodysplastic syndrome (MDS) and solid tumors. Germline mutations i

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Mailloux, Adam W., Fanqi Bai, Ling Zhang, et al. "Altered Collagen Production by Dysfunctional Mesenchymal Stem Cells Is Linked to T Cell Large Granular Lymphocyte Leukemia Pathophysiology." Blood 116, no. 21 (2010): 2595. http://dx.doi.org/10.1182/blood.v116.21.2595.2595.

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Abstract Abstract 2595 Large Granular Lymphocyte (LGL) leukemia is a chronic lymphoproliferative syndrome that can be broadly classified into two groups depending on whether the expanded cells are T-cells or NK-cells. The clinical characteristics of the disease include lymphocytosis, neutropenia, anemia, that can be associated with rheumatoid arthritis and pulmonary arterial hypertension (PAH). Hematologic improvement with immunosuppressive agents such as cyclosporine and low-dose methotrexate has lead to the widely accepted theory that cytopenias are mediated by autoimmune destruction of the

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Malcovati, Luca, Matteo G. Della Porta, Daniela Pietra, et al. "Granulocyte JAK2 (V617F) Mutation Status in Myeloid Neoplasms with Ringed Sideroblasts." Blood 108, no. 11 (2006): 854. http://dx.doi.org/10.1182/blood.v108.11.854.854.

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Abstract The most common type of acquired sideroblastic anemia is the myelodysplastic syndrome (MDS) defined as refractory anemia with ringed sideroblasts (RARS). We have previously demonstrated that mitochondrial iron accumulation in this condition is in the form of mitochondrial ferritin (MtF). A gain-of-function mutation of JAK2 is found in most patients with chronic myeloproliferative disorders. A high frequency of this mutation has been also reported in RARS associated with marked thrombocytosis (RARS-T), a provisional entity characterized by marked increase in platelet count, hypercellul

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22

Fajgenbaum, David C. "Novel insights and therapeutic approaches in idiopathic multicentric Castleman disease." Hematology 2018, no. 1 (2018): 318–25. http://dx.doi.org/10.1182/asheducation-2018.1.318.

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Abstract Castleman disease (CD) describes a heterogeneous group of hematologic disorders that share characteristic lymph node histopathology. Patients of all ages present with either a solitary enlarged lymph node (unicentric CD) or multicentric lymphadenopathy (MCD) with systemic inflammation, cytopenias, and life-threatening multiple organ dysfunction resulting from a cytokine storm often driven by interleukin 6 (IL-6). Uncontrolled human herpesvirus-8 (HHV-8) infection causes approximately 50% of MCD cases, whereas the etiology is unknown in the remaining HHV-8-negative/idiopathic MCD cases

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Fajgenbaum, David C. "Novel insights and therapeutic approaches in idiopathic multicentric Castleman disease." Blood 132, no. 22 (2018): 2323–30. http://dx.doi.org/10.1182/blood-2018-05-848671.

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Castleman disease (CD) describes a heterogeneous group of hematologic disorders that share characteristic lymph node histopathology. Patients of all ages present with either a solitary enlarged lymph node (unicentric CD) or multicentric lymphadenopathy (MCD) with systemic inflammation, cytopenias, and life-threatening multiple organ dysfunction resulting from a cytokine storm often driven by interleukin 6 (IL-6). Uncontrolled human herpesvirus-8 (HHV-8) infection causes approximately 50% of MCD cases, whereas the etiology is unknown in the remaining HHV-8-negative/idiopathic MCD cases (iMCD).

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24

Li, Xiaomei, Qiu Jiang, Rui Chen, and Yi Ding. "Efficacy of BTI615 on malignant cells expansion and bone marrow fibrosis in a myelofibrosis mice model." Journal of Clinical Oncology 43, no. 16_suppl (2025): 6572. https://doi.org/10.1200/jco.2025.43.16_suppl.6572.

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6572 Background: Due to the limitation of Janus kinase inhibitors and allogeneic transplant, critical unmet needs are remained in myelofibrosis (MF) patients, particularly for those with cytopenias, non-response or intolerance issues. Novel therapeutic avenues could arise from promoting bone marrow regeneration, which is dysregulated by pro-tumorigenic, fibrotic niche networked by vicious cycle of transforming growth factor β (TGF-β) signaling. Here we verified that BTI615, a synthetic active TGF-β modulating peptide, rescued malignant cells expansion and bone marrow fibrosis to restore hemato

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25

Alter, Blanche P., Neelam Giri, Peter M. Lansdorp, Gabriela M. Baerlocher, Philip S. Rosenberg, and Sharon Savage. "Longitudinal Changes In Telomere Length In Patients with Dyskeratosis Congenita." Blood 116, no. 21 (2010): 2230. http://dx.doi.org/10.1182/blood.v116.21.2230.2230.

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Abstract Abstract 2230 Dyskeratosis congenita (DC) is an inherited bone marrow failure syndrome with a complex clinical phenotype, including dysplastic nails, lacy reticular pigmentation, and oral leukoplakia (the diagnostic triad). Numerous other physical abnormalities may be present, in addition to cytopenias due to bone marrow failure, and a high risk of leukemia or solid tumors. However, many patients have no physical findings at diagnosis. Patients with DC have very short telomeres, and approximately one-half have a mutation in one of six genes important in telomere biology. Telomere leng

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26

Mangi, MH, and GJ Mufti. "Primary myelodysplastic syndromes: diagnostic and prognostic significance of immunohistochemical assessment of bone marrow biopsies." Blood 79, no. 1 (1992): 198–205. http://dx.doi.org/10.1182/blood.v79.1.198.198.

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Abstract Material from 63 cases with primary myelodysplastic syndromes (P-MDS) (French-American-British [FAB] types: refractory anemia [RA] = 21; RA with ring sideroblasts [RARS] = 8; RA with excess of blasts (RAEB) = 10; RAEB in transformation (RAEBt) = 6; chronic myelomonocytic leukemia [CMML] = 10 and unclassifiable = 8, ie, bone marrow aspiration was inadequate and stringent FAB criteria were not applicable) was analyzed for bone marrow histologic and immunohistochemical patterns. Standard Giemsa, hematoxylin and eosin (H&E) and reticulin stains were used for morphologic assessment. To

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Mangi, MH, and GJ Mufti. "Primary myelodysplastic syndromes: diagnostic and prognostic significance of immunohistochemical assessment of bone marrow biopsies." Blood 79, no. 1 (1992): 198–205. http://dx.doi.org/10.1182/blood.v79.1.198.bloodjournal791198.

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Material from 63 cases with primary myelodysplastic syndromes (P-MDS) (French-American-British [FAB] types: refractory anemia [RA] = 21; RA with ring sideroblasts [RARS] = 8; RA with excess of blasts (RAEB) = 10; RAEB in transformation (RAEBt) = 6; chronic myelomonocytic leukemia [CMML] = 10 and unclassifiable = 8, ie, bone marrow aspiration was inadequate and stringent FAB criteria were not applicable) was analyzed for bone marrow histologic and immunohistochemical patterns. Standard Giemsa, hematoxylin and eosin (H&E) and reticulin stains were used for morphologic assessment. To identify

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Chandy, Mammen, Biju George, Vikram Mathews, Auro Viswabandya, Ashish Bajel, and Alok Srivastava. "Oral Prednisolone Produces a Durable Response in Pediatric Myelodysplastic Syndromes (MDS)." Blood 106, no. 11 (2005): 4906. http://dx.doi.org/10.1182/blood.v106.11.4906.4906.

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Abstract Treatment options for children with MDS are limited except for allogeneic bone marrow transplantation. We present our experience with the use of long duration corticosteroids in children with MDS. Fifty five children (age&lt; 15 years) with pediatric MDS or myelofibrosis treated between 1991–2004 with corticosteroids were analyzed. All of these patients presented with cytopenia involving one or more lineages and a hypercellular marrow with dysplasia and increased reticulin. Prednisolone was started at 1 mg/kg daily or on alternate days for a period of 1–2 months. If there was no r

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Bourg, Wilson C., Theresa M. Launder, and Tariq I. Mughal. "Hematological Responses to Megesterol Acetate in Patients with Myelodysplastic Syndrome Involving an Abnormal Chromosome 6." Blood 106, no. 11 (2005): 4922. http://dx.doi.org/10.1182/blood.v106.11.4922.4922.

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Abstract The presence of an abnormal chromosome (chr) 6 often confers a poor prognosis on patients with myelodysplastic syndrome (MDS), particularly therapy related-MDS (t-MDS). We report two patients with MDS and an abnormal chr 6 who achieved significant improvements in their hematological parameters after being subjected to megesterol actetate at 80mg/d; one patient achieved a complete cytogenetic remission, albeit based on a limited study. The first patient, a 73 y female presented with a monocytopenia (thrombocytopenia; 43K/dl), a bone marrow consistent with MDS, blasts 6% and an abnormal

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Methuku, Nanda K., Nidhi Mishra, Gloria Fernandez, Praveena Coimbatore, and Sammy Selahi. "A Case of Hemophagocytic Lymphohistiocytosis with Acute Myelofibrosis." Blood 116, no. 21 (2010): 5070. http://dx.doi.org/10.1182/blood.v116.21.5070.5070.

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Abstract Abstract 5070 Title: A case of Hemophagocytic Lymphohistiocytosis with Acute Myelofibrosis Case report: A 60 year old previously healthy male was admitted for a four week history of non-productive cough, and intermittent fever which was getting worse since 1 week prior to presentation. He also had runny nose and nasal stuffiness 2 months prior to presentation. The patient also had significant weight loss of 30 lbs over the past month. Physical examination was remarkable for a temperature of 38°C. Patient was alert and oriented. No Lymphadenopathy or hepatosplenomegaly was found. Rest

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Ostronoff, Mauricio, Mariana Coutinho Domingues, Fabiana Ostronoff, et al. "Hemophagocytic Syndrome (HPS) after Autologous Peripheral Stem Cell Tansplantation (APSCT) for Multiple Myeloma (MM)- Successful Treatment with High Dosages of Intravenous Immunoglobulin (IVIG)." Blood 106, no. 11 (2005): 5359. http://dx.doi.org/10.1182/blood.v106.11.5359.5359.

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Abstract HPS is characterized by activation of histiocytes with prominent hemophagocytosis in bone marrow and reticulo-endothelial system, resulting in cytopenias. Reactive HPS (R-HPS) is known to be associated with infection, malignancies and autoimmune disorders. We report a case of R-HPS with massive life-threatening gastro-intestinal (GI) tract bleeding after APSCT for MM which responded to high dosages of IVIG. In May 2005, a 54-year old female diagnosed with MM stage III A, achieved CR after 4 cycles of VAD. APSCT conditioning consisted of L-PAM 140mg/m2. 2x106 CD34+ cells/kg were infuse

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32

Levy, Benjamin, Katherine Vandris, Fernando Adriano, Joshua Goldman та Richard T. Silver. "Recombinant Interferon Alpha (rIFNα) May Retard Progression of Early Primary Myelofibrosis (PM) by Reducing Splenomegaly and by Changing Marrow Morphology." Blood 112, № 11 (2008): 1758. http://dx.doi.org/10.1182/blood.v112.11.1758.1758.

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Abstract Reports of the limited effect of JAK2 inhibitors in PM, and the limited survival experienced with stem cell transplantation, led us to examine our results of treating the earlier phases of primary myelofibrosis with rIFNα. The use of rIFNα in early PM is based upon its known effects on a related myloproliferative disease, polycythemia vera, which is also characterized by myelofibrosis and its effects on megakaryopoiesis. These include decreasing megakaryocyte density and size, inhibiting thrombopoietin-induced signaling, and reducing levels of platelet derived growth factor, which pla

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Yang, Li-Jun, Ilicia L. Schlossman, Samuel E. Myrick, Haoyang Zhuang, Hai Wang та Westley H. Reeves. "Role Of Tumor Necrosis Factor α In Bone Marrow Niche Dysfunction Of Patients With Systemic Lupus Erythematosus (SLE)". Blood 122, № 21 (2013): 1036. http://dx.doi.org/10.1182/blood.v122.21.1036.1036.

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Abstract Objectives and background SLE is a chronic systemic autoimmune disorder associated with autoantibodies and cytopenias. There are few studies of the pathogenesis of anemia of chronic inflammation in lupus. This study addresses the pathogenesis of the hematological manifestations of lupus. We have shown that SLE bone marrow (BM) exhibits striking death of niche and hematopoietic cells associated with tumor necrosis factor-α (TNFα) over-production. Here, we further examined the pathogenesis of hematological BM niche dysfunction. Methods Pathology records over the past 10 years from the U

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Florez, Marcus A., Duy Le, Youngjae Jeong, et al. "Bone Marrow Stromal Antigen 2 Facilitates Activation of Hematopoietic Stem Cell through the Induction of ERK Signaling." Blood 138, Supplement 1 (2021): 1098. http://dx.doi.org/10.1182/blood-2021-151567.

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Abstract Chronic infections are prevalent worldwide and contribute to bone marrow failure syndromes. Long-term homeostatic production of all blood cells is dependent on the ability of hematopoietic stem cells (HSCs) to remain mostly quiescent and, upon activation, must carefully balance between their ability to self-renew and differentiate. However, infections trigger inflammatory cytokines, such as interferon-gamma (IFNy), that facilitate HSC proliferative exhaustion by disrupting both quiescence and self-renewal, thereby contributing to cytopenias and bone marrow failure syndromes. Our previ

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Mesa, Ruben A., Chin Yang Li, Susan Schwager, and Ayalew Tefferi. "Increased Intramedullary T Cells Corresponds with Response to Thalidomide (THAL) Therapy in Primary Myelofibrosis." Blood 112, no. 11 (2008): 5234. http://dx.doi.org/10.1182/blood.v112.11.5234.5234.

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Abstract BACKGROUND: THAL has been used as immunomodulatory therapy alone (Tefferi et. al. Blood 200;96:4007), or with steroids (Mesa et al. Blood2003;101:2534), in patients with primary myelofibrosis (PMF). Clinical benefit has been limited to improvements in cytopenias and/or splenomegaly. However, major histologic remissions of intramedullary manifestations of disease have not typically been observed. The mechanism of action of THAL in MF remains uncertain, and may involve cytokine inhibition or immunomodulation. We have previously observed increased numbers of CD8+ T lymphocytes on marrow

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Kang, Seong-Ho, Oscar Perales, Michael Michuad, and Samuel G. Katz. "Bok Promotes Erythropoiesis in a Mouse Model of Myelodysplastic Syndrome." Blood 130, Suppl_1 (2017): 922. http://dx.doi.org/10.1182/blood.v130.suppl_1.922.922.

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Abstract BCL-2 Ovarian Killer (BOK) is a pro-apoptotic member of the BCL-2 family of proteins best characterized for its putative ability to induce apoptosis in response to Endoplasmic Reticulum (ER) stress, when stabilized from ER-associated degradation (ERAD). Although ER stress appropriately activates the unfolded protein response (UPR) in BOK-disrupted cells, as measured by PERK and eIF2-alpha phosphorylation, downstream effector signaling, including ATF4 and CHOP, is defective. A functional role for BOK as a tumor suppressor is suggested by its genetic location in one of the 20 most frequ

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Kyttälä, Satu, Wolfgang Bauer, Michael Haase, Ivonne Habermann, Gerhard Ehninger, and Alexander Kiani. "Osteomyelosclerosis, Anemia and Extramedullary Hematopoiesis in Mice Deficient for the Transcription Factor NFAT (Nuclear Factor of Activated T Cells) c2." Blood 112, no. 11 (2008): 3726. http://dx.doi.org/10.1182/blood.v112.11.3726.3726.

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Abstract NFAT (Nuclear Factor of Activated T cells) is a family of five calcium-induced, calcineurin-dependent transcription factors, characterized as master regulators of inducible gene expression in T lymphocytes. In various tissues (including bone, cartilage and adipose tissue), NFAT factors have also been found to regulate processes of cellular adaptation and differentiation. NFAT family members are also expressed in human CD34+ hematopoietic progenitor cells as well as in mesenchymal stem cells; however, a biological function of NFAT in these cells, such as a role in hematopoietic differe

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Hanoun, Maher, Dachuan Zhang, Sandra Pinho та ін. "Acute Myeloid Leukemia Alters The Mesenchymal Stem Cell Potential Of The HSC Niche: Evidence For Modulation By β-Adrenergic Signals". Blood 122, № 21 (2013): 342. http://dx.doi.org/10.1182/blood.v122.21.342.342.

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Abstract Hematopoietic stem cells (HSC) reside in specific bone marrow niches comprised of perisinusoidal Nestin-GFP+ (Nes-GFP+) and leptin receptor (LepR)+ stromal cells which highly overlap with each other, as well as osteolineage and endothelial cells. These different cellular constituents regulate HSC maintenance and retention in the bone marrow (BM). Recently, our laboratory further identified rare periarteriolar Nes-GFPbright cells which have been identified to be pericytes and functionally crucial for HSC quiescence and maintenance, from the more abundant reticular Nes-GFPdim population

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Soliman, Dina Sameh, Ahmad Al-Sabbagh, Firyal Ibrahim, Halima El-Omri, Mohamed A. Yassin, and Aliaa Amer. "Local Field Radiotherapy Induced Therapy Related Myeloid Neoplasms and Bone Marrow Suppression." Blood 134, Supplement_1 (2019): 5113. http://dx.doi.org/10.1182/blood-2019-131683.

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Introduction: Different cytotoxic agents have been implicated in development of therapy related myeloid neoplasm (t-MN). These include alkylating agents, topoisomerase II inhibitors, antimetabolites, and ionizing field radiation given to large field including active bone marrow (BM) (Swerdlow, 2016). This report highlight the impact of local field radiotherapy on BM through discussing few patients diagnosed in our center who showed profound BM hypocellularity or developed t-MN following exposure to local field radiotherapy without chemotherapy. Local field Radiotherapy as a causative agent for

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Peerwani, Ziad, Ramon Tiu, Bianca Serio, Andrew Schade, Jaroslaw P. Maciejewski, and Eric D. Hsi. "Phospho-IkappaB Is Abnormally Expressed in Bone Marrow of CMML Patients." Blood 110, no. 11 (2007): 2450. http://dx.doi.org/10.1182/blood.v110.11.2450.2450.

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Abstract Introduction: Chronic myelomonocytic leukemia (CMML) is a heterogeneous group of bone marrow disorders currently grouped into the MDS/MPD overlap by WHO classification. Its clinical and laboratory features includes the presence of up to 20% blast in the bone marrow and the peripheral blood, a PB monocyte count &gt;1000/mL, splenomegaly, variable reticulin fibrosis in the bone marrow and cytopenias. The exact pathogenesis remains in question and there are no effective therapies. Recent studies in certain myeloid disorders suggest that the nuclear transcription factor NFkB regulates

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Yacoub, Abdulraheem, Coralie Pickert, and Wei Cui. "Advanced Extramedullary Hematopoiesis In a Transplanted Liver Graft As Initial Presentation Of Primary Myelofibrosis." Blood 122, no. 21 (2013): 5256. http://dx.doi.org/10.1182/blood.v122.21.5256.5256.

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Abstract Primary myelofibrosis (PMF) is one of the BCR-ABL-negative myeloproliferative neoplasms. The hallmarks of PMF include increased bone marrow (BM) fibrosis, megakaryocytic hyperplasia with hyperchromatic nuclei and abnormal lobation, leukoerythroblastosis, cytopenias, extramedullary hematopoiesis (EMH), and constitutional symptoms that can be debilitating. PMF is associated with the constitutive mobilization of CD34+ cells into the peripheral blood which characteristically occurs in the more clinically advanced phases of the disease. This dysregulation of hematopoietic stem cell (HSC) t

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Hunt, Alesia Abigael, Anjum Bashir Khan, Victoria T. Potter, et al. "Hypoplastic MDS Is a Distinct Clinico-Pathological Entity with Somatic Mutations Frequent in Patients with Prior Aplastic Anaemia with Favorable Clinical Outcome." Blood 124, no. 21 (2014): 3269. http://dx.doi.org/10.1182/blood.v124.21.3269.3269.

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Abstract Introduction: Hypocellular myelodysplastic syndrome (hMDS) is characterized by decreased marrow cellularity, and is often difficult to distinguish from aplastic anemia (AA) based on standard morphological criteria. It represents around 10-15% of patients diagnosed with MDS, but is not currently considered a separate entity by WHO. Hypocellularity is defined as bone marrow cellularity of less than 30% in patients younger than 70 years or less than 20% in those older than 70 years. Patients and Methods: We retrospectively evaluated the demographic, clinical features, bone marrow aspirat

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Li, Qiaoli, Fei Yang, Yuanyi Ling, et al. "Mitochondrial Transcriptional-Translational Conflict Contributes to Defective Erythropoiesis and Disease Progression in Splicing Factor Mutant Myelodysplastic Syndromes." Blood 144, Supplement 1 (2024): 345. https://doi.org/10.1182/blood-2024-204428.

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Myelodysplastic syndromes (MDS) are myeloid malignancies derived from hematopoietic stem progenitor cells (HSPCs), characterized by cytopenia, dysplastic and ineffective hematopoiesis and a high risk of developing acute myeloid leukemia. SF3B1 is the most frequently mutated splicing factor in MDS, especially in MDS with ring sideroblasts. Although SF3B1 mutation generally indicates good prognosis, some patients with excess blasts still harbor this mutation. Previous studies have reported SF3B1 mutation induce R-loop and DNA damage with therapeutic implications, however, the role of SF3B1 mutat

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Mertz, Jennifer A., Patricia J. Keller, Rosana D. Meyer, et al. "The BET Inhibitor, CPI-0610, Promotes Myeloid Differentiation in Myelofibrosis Patient Bone Marrow and Peripheral CD34+ Hematopoietic Stem Cells." Blood 136, Supplement 1 (2020): 37–38. http://dx.doi.org/10.1182/blood-2020-138752.

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Myelofibrosis (MF) is characterized by progressive bone marrow (BM) fibrosis resulting from aberrant megakaryopoeisis and expression of pro-inflammatory cytokines. These two processes, heavily influenced by bromodomain and extraterminal domain (BET)-mediated gene regulation, lead to myeloproliferation and cytopenias. CPI-0610 is a potent, selective and unique BET inhibitor under investigation in MF patients as monotherapy or in combination with ruxolitinib in the MANIFEST trial (NCT02158858). In ruxolitinib naïve and experienced MF patients, treatment with CPI-0610 monotherapy or in combinatio

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Masarova, Lucia, Meixian Huang, Sharon Bledsoe, et al. "A Phase Ib, Open-Label Study of Add on Therapy with CK0804 in Participants with Myelofibrosis and Suboptimal Response to Ruxolitinib." Blood 142, Supplement 1 (2023): 1813. http://dx.doi.org/10.1182/blood-2023-188051.

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Background: JAK2 inhibitor ruxolitinib leads to improvements in symptom burden and spleen volume in patients with myelofibrosis (MF), but suboptimal response represents a major unmet clinical need. Deregulated inflammatory pathways including CXCR4/CXCR12 axis might limit the therapeutic efficacy of ruxolitinib and contribute to disease progression ( Miwa et al. Pathology. 2013), where agents targeting bone marrow (BM) inflammation could be promising. Adoptive therapy with allogeneic, cord blood-derived regulatory T cells (Tregs) (CK0801- HLA 3/ 6 match, fresh infusion) showed safety and early

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Silver, Richard T., Ariella Barel, Elena Lascu та ін. "The Effect of Initial Molecular Profile on Response to Recombinant Interferon Alpha (rIFNα) Treatment in Early Myelofibrosis". Blood 128, № 22 (2016): 944. http://dx.doi.org/10.1182/blood.v128.22.944.944.

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Abstract Introduction Successful treatment of early myelofibrosis (eMF), defined as patients (pts) with low or intermediate-1 (int-1) risk and ≥15% hematopoietic foci in the marrow biopsy, with rIFNα has been reported, but effects of driver and epigenetic mutations on outcomes were not considered. We now report results of our single center phase II study of 30 pts with primary (PM) or secondary (SMF) eMF, correlating the baseline molecular profile with response to rIFNα treatment. Methods We used WHO 2008 and IWG-MRT criteria for the diagnosis of PM and post-polycythemia vera MF (pPV MF) or po

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Kumar, Mritunjay, Shruti Mishra, and Kailash Kumar. "Comparative Study of Treatment Outcomes of Patients of Aplastic Anemia with Combination Therapy Cyclosporine a + Danazol+ Eltrombopag Versus Cyclosporine a + Danazol + High Dose Romiplostim." Blood 144, Supplement 1 (2024): 5690. https://doi.org/10.1182/blood-2024-209534.

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Introduction In aplastic anemia (AA), pancytopenia and hypocellular bone marrow occur without aberrant infiltration or reticulin. Acquired AA frequently comes from an autoimmune attack on hematopoietic stem/progenitor cells, while inherited versions include Fanconi anemia, Dyskeratosis Congenita, etc. Symptoms of peripheral blood cytopenia include tiredness, bruising, and bleeding. Blood counts, bone marrow biopsy, and exclusion of Paroxysmal Nocturnal Hemoglobinuria (PNH) and hypoplastic Myelodysplastic Syndrome (hMDS) establish the diagnosis. Immunosuppressive therapy (IST) and hematopoietic

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Hakkarainen, Marja, Suvi P. M. Douglas, Tom Vulliamy, et al. "Multinational Study on the Clinical and Genetic Features of the ERCC6L2-Disease." Blood 138, Supplement 1 (2021): 864. http://dx.doi.org/10.1182/blood-2021-145039.

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Abstract Biallelic mutations in ERCC6L2 were first reported to cause bone marrow failure (BMF). Additionally, we recently described a strong predisposition to erythroid lineage-restricted acute myeloid leukemia (AML-M6). Today, 31 ERCC6L2-mutated cases have been reported. This study aims to further explore the clinical and molecular features, as well as outcomes, of the ERCC6L2 patients. By June 2021, we have gathered clinical and genetic characteristics of 46 subjects in 31 families with biallelic germ line ERCC6L2 mutations from Finland (n = 21), France (n = 8), Israel (n = 1), Sweden (n = 4

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Kanagal-Shamanna, Rashmi, Juliana E. Hidalgo Lopez, Hye Ryoun Kim, et al. "Validation of the 2016 Revision to the World Health Organization (WHO) Classification of Myelodysplastic Syndromes with Diploid Karyotype." Blood 128, no. 22 (2016): 4319. http://dx.doi.org/10.1182/blood.v128.22.4319.4319.

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Abstract Introduction: The revised 2016 WHO classification of MDS has highlighted the value of morphologic evaluation and mutation analysis of bone marrow (BM)/ peripheral blood (PB) to further refine prognostication. These highlights include: (1) increased emphasis on lineage dysplasia compared with cytopenias; (2) objective enumeration of blast % for reproducibility; (3) accurate quantification of ring sideroblasts (RS); and (4) mutation analysis for SF3B1 in cases showing RS >5% and TP53 in MDS with isolated del(5q). Most of the proposed changes are within the categories of low-grade MDS

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Jamieson, Catriona HM, Robert P. Hasserjian, Jason Gotlib, et al. "Effect Of Treatment With The JAK2-Selective Inhibitor Fedratinib (SAR302503) On Bone Marrow Histology In Patients With Myeloproliferative Neoplasms With Myelofibrosis." Blood 122, no. 21 (2013): 2823. http://dx.doi.org/10.1182/blood.v122.21.2823.2823.

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Abstract Introduction Fedratinib, a JAK2-selective inhibitor, demonstrated clinical benefit through a reduction in splenomegaly and symptoms in patients with myelofibrosis (MF), including post-polycythemia vera MF (post-PV MF), post-essential thrombocythemia MF (post-ET MF) and primary MF (PMF), in Phase I and II studies (J Clin Oncol 2011;29:789; Haematologica 2013;98:S1113). Bone marrow fibrosis (BMF) has been associated with splenomegaly and cytopenias (Ann Hematol 2006;85:226). Hence, stabilization and/or reversal of BMF remain important therapeutic goals. This report represents an explora

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