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Journal articles on the topic 'Haematopoeitic'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 2022

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1

MacMillan, Margaret L., and John E. Wagner. "Haematopoeitic cell transplantation for Fanconi anaemia - when and how?" British Journal of Haematology 149, no. 1 (April 2010): 14–21. http://dx.doi.org/10.1111/j.1365-2141.2010.08078.x.

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2

Yapa, H. Manisha N., Donal P. McLornan, Kavita Raj, Matthew Streetly, Majid Kazmi, Kirsty Cuthill, John Laurie, Padma A. Menon, and Eithne MacMahon. "Pneumonitis post-haematopoeitic stem cell transplant – Cytopathology clinches diagnosis." Journal of Clinical Virology 55, no. 3 (November 2012): 278–81. http://dx.doi.org/10.1016/j.jcv.2012.08.007.

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3

Weilbacher, K. "PL9.2. Haematopoeitic cell and growth factor – tumour cell interactions." Cancer Treatment Reviews 34 (2008): 49. http://dx.doi.org/10.1016/j.ctrv.2008.03.138.

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4

Chakraborty, Sohini, Shobha Badiger, Sharat Damodar, and Sunil Bhat. "Haploidentical haematopoeitic stem cell transplants (Hsct) in paediatric acute leukemia." Pediatric Hematology Oncology Journal 2, no. 2 (2017): S5. http://dx.doi.org/10.1016/j.phoj.2017.11.141.

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5

Oldreive, Ceri, Tatjana Stankovic, Philip J. Byrd, Grant S. Stewart, Anna Smith, Alexander J. Taylor, Peggy Fooks, et al. "PALB2 Mutational Status in Haematopoeitic Malignancies - a Potential Therapeutic Target?" Blood 128, no. 22 (December 2, 2016): 2726. http://dx.doi.org/10.1182/blood.v128.22.2726.2726.

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Abstract PALB2 protein is one of the principal components of Homologous Recombination Repair (HRR) that facilitates recruitment of other HRR proteins such as BRCA1, BRCA2 and Rad51. Biallelic PALB2 inactivation is associated with a severe form of Fanconi Anemia (FA-N), however, biallelic PALB2 mutations also occur in patients with a FA-N syndrome variant characterised by a predisposition to B-cell lymphoma development. The association of PALB2 with FA-N and FA-N variant suggests that PALB2 may play a pathogenic role in a wider range of sporadic haematopoietic malignancies. To address this possibility, the mutational status of the PALB2 gene was assessed in 30 myelodysplastic syndrome (MDS) samples, 23 acute lymphoblastic leukaemias (ALL), 171 chronic lymphocytic leukaemias (CLL) and 24 paediatric non-Hodgkin lymphomas (NHL) of T- or B-cell origin. Overall, pathogenic (truncating or splicing errors)orlikely pathogenic sequence changes (missense alterations not previously reported but predicted to alter protein function) were detected in 17 (6.7%) of these patients. PALB2 was most frequently altered in NHL (25%), followed by MDS (6%), CLL (5%) and ALL (4%). The overall incidence of changes observed for B-cell NHL was higher than the frequency detected in T-cell NHL. PALB2 sequence changes were distributed across the whole gene including the DNA binding, BRCA1-interacting and BRCA2-interacting domains. Of note, a single truncating mutation; in the BRCA1-interacting domain, c.886delA; was detected in three cases, two with progressive CLL and one with MDS and interestingly only became detectable in one of these CLL patients following ibrutinib treatment. Furthermore, a polymorphic variant (c.2993G>A), previously associated with an increased breast cancer risk, was present at higher frequency than in the general population in cohorts of both CLL and ALL patients. HRR defective tumour cells can be targeted by pharmacological inhibition of co-operating DNA repair pathways using the principal of synthetic lethality. To explore whether this concept can be utilised in the context of PALB2 deficiency, we evaluated the effectiveness of inhibition of two pathways; PARP and ATR; that co-operate with PALB2. The cytotoxicity induced by either an ATR inhibitor or a PARP inhibitor was assessed in lymphoblastoid cell lines derived from a paediatric B-cell NHL patient carrying the c.1676_1677delAAinsG and c.2586+1G>A mutations. As predicted, exposure of lymphoid cells with PALB2 mutations to either ATR or PARP inhibitor alone exerted a cytotoxic effect which was enhanced when both inhibitors were applied in combination. In conclusion, our results suggest that PALB2 is altered in a subset of patients with different haematopoietic malignancies. This potentially provides another avenue for targeted therapies utilising the concept of synthetic lethality via application of PARP and ATR inhibitors that are currently being tested in clinical trials. Disclosures Janic: Novo Nordisk: Other: Paid Instructor, Research Funding; Baxter: Other: Paid Instructor, Research Funding; Bayer: Other: Paid Instructor, Research Funding; Pfizer: Other: Paid Instructor, Research Funding; Octopharma: Research Funding.

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6

Foster, H., J. Davidson, E. Baildam, M. Abinun, and L. R. Wedderburn. "Autologous haematopoeitic stem cell rescue (AHSCR) for severe rheumatic disease in children." Rheumatology 45, no. 12 (October 31, 2006): 1570–71. http://dx.doi.org/10.1093/rheumatology/kel319a.

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7

Din, Nazzlin Dizana. "Thalassaemia Care in Terengganu – A Local Report." Malaysian Journal of Paediatrics and Child Health 26, no. 2 (July 28, 2020): 1–5. http://dx.doi.org/10.51407/mjpch.v26i2.79.

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Inherited thalassaemia disease is commonly found in many countries of the world. Care of the disease requires comprehensive management strategies comprising of clinical management of both transfusion dependant thalassaemia (TDT) and non-transfusion dependant thalassaemia (NTDT). It also includes preventive measures such as screening programmes and genetic counseling in order to contain the genetic transmission. At the moment, the only cure is through haematopoeitic stem cell transplant (HSCT). This report illustrates thalassaemia disease prevalence in the Terengganu state and the evolution of care since National Thalassaemia Programme was launched in 2009.

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8

Zhu, Grace G., Benjamin L. Witt, Thomas C. Winter III, and Douglas M. Rogers. "Multiple enlarging hepatic and retroperitoneal myelolipomas in the setting of Cushing disease." BMJ Case Reports 14, no. 2 (February 2021): e239107. http://dx.doi.org/10.1136/bcr-2020-239107.

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Myelolipomas are benign tumours typically occurring in the adrenal glands, made up of fat and trilineage haematopoeitic cells resembling bone marrow. Their aetiology is not well understood; however, they have a clear association with elevated serum adrenocorticotropic hormone (ACTH). Extra-adrenal myelolipomas are rare, and to our knowledge there are no previously reported cases of multiple enlarging hepatic and retroperitoneal myelolipomas in the setting of Cushing disease. We present the case of a patient with an ACTH-producing pituitary adenoma who developed multiple enlarging fat containing lesions in the liver and retroperitoneum, which were histologically proven multifocal myelolipomas.

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9

Robenshtok, E., A. Gafter-Gvili, M. Paul, E. Goldberg, L. Vidal, and L. Leibovici. "P964 Antifungal prophylaxis for patients undergoing chemotherapy or haematopoeitic stem cell transplantation-meta-analysis." International Journal of Antimicrobial Agents 29 (March 2007): S254. http://dx.doi.org/10.1016/s0924-8579(07)70805-1.

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10

H, Ariffin, Daud SS, and Ibrahim K. "QUANTITATIVE EVALUATION OF CHIMERISM STATUS FOLLOWING HAEMATOPOEITIC STEM CELL TRANSPLANTATION USING A MICROCHIP ELECTROPHORESIS SYSTEM." Journal of Health and Translational Medicine 10, no. 1 (June 25, 2007): 11–16. http://dx.doi.org/10.22452/jummec.vol10no1.3.

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11

Aung, A. K., J. A. Trubiano, and D. W. Spelman. "Travel risk assessment, advice and vaccinations in immunocompromised travellers (HIV, solid organ transplant and haematopoeitic stem cell transplant recipients): A review." Travel Medicine and Infectious Disease 13, no. 1 (January 2015): 31–47. http://dx.doi.org/10.1016/j.tmaid.2014.12.007.

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12

Teoh, Ching Soon, and Ai Sim Goh. "Relapsed Chronic Lymphocytic Leukaemia with Concomitant Extensive Chronic Graft versus Host Disease after Allogeneic Haematopoietic Stem Cell Transplantation Successfully Treated with Oral Venetoclax." Case Reports in Transplantation 2021 (January 22, 2021): 1–6. http://dx.doi.org/10.1155/2021/8831125.

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A middle-aged gentleman who was diagnosed with high-risk chronic lymphocytic leukaemia (CLL), Rai stage IV, Binet C with del(17p) and del(13q) underwent allogeneic haematopoeitic stem cell transplantation (allo-HSCT) from a human leukocyte antigen (HLA) identical sister. The patient developed extensive skin, oral, and liver chronic graft versus host disease (GVHD) required tacrolimus, mycophenolate mofetil (MMF), and prednisolone. At seventh month after allo-HSCT, the patient presented with systemic symptoms, right cervical lymphadenopathy, splenomegaly, marked pancytopaenia, and elevated lactate dehydrogenase (LDH). Bone marrow study, immunophenotyping (IP), chromosome analysis, and PET-CT scan confirmed relapsed CLL with no evidence of Richter’s transformation or posttransplant lymphoproliferative disease (PTLD). Withdrawal of immunosuppressant (IS) worsened cutaneous and liver GVHD. Chemotherapy was not a suitable treatment option in view of immunodeficiency. The patient underwent extracorporeal photopheresis (ECP) therapy eventually for extensive chronic GVHD, and the IS were gradually tapered to the minimal effective dose. The relapsed CLL was treated successfully with oral venetoclax accessible via a compassionate drug program. This case highlights challenges in managing relapsed CLL and loss of graft-versus-leukaemia (GVL) effect despite extensive chronic GVHD. Venetoclax is an effective and well-tolerated oral novel agent for relapsed CLL after allo-HSCT.

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13

Wainwright, S. D., M. J. A. Tanner, G. E. M. Martin, J. E. Yendle, and C. Holmes. "Monoclonal antibodies to the membrane domain of the human erythrocyte anion transport protein. Localization of the C-terminus of the protein to the cytoplasmic side of the red cell membrane and distribution of the protein in some human tissues." Biochemical Journal 258, no. 1 (February 15, 1989): 211–20. http://dx.doi.org/10.1042/bj2580211.

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(1) We have prepared murine monoclonal antibodies to the membrane domain of the human erythrocyte anion transport protein (band 3). (2) All of these antibodies react with regions of the protein located at the cytoplasmic surface of the red cell. (3) One of the antibodies reacts with an epitope present on a cytoplasmic loop of the protein located between the C-terminus and a point 168 amino acids from the C-terminus. The other antibodies recognize different epitopes on the C-terminal tail of the protein and the sequences likely to be involved in these epitopes are defined. (4) Our results show that the C-terminus of the red-cell anion transport protein is located on the cytoplasmic side of the red-cell membrane. (5) None of the antibodies inhibited sulphate exchange transport when introduced into resealed red-cell membranes; however, the bivalent form of one of the antibodies reduced the inhibitory potency of 4-acetamido-4'-isothiocyanatostilbene disulphonate on sulphate exchange transport in resealed erythrocyte membranes. (6) Immunostaining of human kidney sections with the antibodies showed strong staining of the basolateral membrane of some but not all of the epithelial cells of distal tubules and the initial connecting segment of collecting tubules. With human liver, only the haematopoeitic cells of fetal liver reacted with all the antibodies.

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14

Lim, Zi Yi, Laurence Pearce, Aloysius Y. Ho, Linda Barber, Wendy Ingram, Monica Usai, Khalid Tobal, Stephen Devereux, Antonio Pagliuca, and Ghulam J. Mufti. "Delayed attainment of full donor chimaerism following alemtuzumab-based reduced-intensity conditioning haematopoeitic stem cell transplantation for acute myeloid leukaemia and myelodysplastic syndromes is associated with improved outcomes." British Journal of Haematology 138, no. 4 (August 2007): 517–26. http://dx.doi.org/10.1111/j.1365-2141.2007.06676.x.

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15

Ismail, F., L. Huang, Z. Lockhat, S. Ellemdin, and L. Van der Linde. "Extramedullary haematopoeisis causing spinal cord compression." South African Journal of Radiology 14, no. 3 (August 30, 2010): 62. http://dx.doi.org/10.4102/sajr.v14i3.472.

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Extramedullary haematopoeisis (EMH) is a rare cause of spinal cord compression. However, in a patient with a haematological disorder and in particular thalassaemia, EMH with paraspinal masses should be considered and imaging planned appropriately.

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16

Kottaridis, Panagiotis, Diana Brazma, Julie Howard-Reeves, Helen Mazzullo, and Elisabeth P. Nacheva. "A Cell Line SYRMO Derived From AML with EVI 1 Rearrangements Following Imatinib Mesylate Therapy for Chronic Myeloid Leukaemia." Blood 116, no. 21 (November 19, 2010): 4470. http://dx.doi.org/10.1182/blood.v116.21.4470.4470.

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Abstract Abstract 4470 Chronic Myeloid Leukaemia (CML) is a malignant disorder of the haematopoeitic stem cell, usually characterised by the t(9;22) giving rise to the Philadelphia chromosome (Ph), and by the BCR-ABL gene rearrangement at the molecular level. Imatinib mesylate (IM), which targets the tyrosine kinase (TK) activity of BCR-ABL, has become the first line therapy for CML patients. Dasatinib or Nilotinib is now indicated as a second line therapy for patients who develop resistance or intolerance to IM. Here we report the case of a 51 year old woman who was diagnosed in Cyprus (2007) with BCR/ABL1 positive CML. After failing to respond to IM therapy, she was treated with Dasatinib achieving complete cytogenetic remission (CCR), and subsequent complete molecular remission. In July 2009 the patient presented with 88% blasts in the bone marrow. Immunophenotyping showed the presence of CD34+, CD117+ myeloblasts, and a diagnosis of AML was confirmed. Analysis of G banded metaphases from cultured peripheral blood revealed a complex karyotype: 46,XX, t(2;3)(p21;q26),t(4;8)(q12;q22), del(6)(q13;q23)[1]/45,idem,der(6)ins(6;6)(q23;),-7[9]. FISH revealed EVI 1 rearrangement resulting from the t(2;3) in the absence of BCR/ABL1 fusion and confirmed the secondary monosomy 7. The patients failed to respond to treatment and passed away shortly afterwards. Whole genome screening by aCGH using a 244K platform (Agilent) confirmed the loss of chromosome 7 and the 6q22/23 region. Clonal cytogenetic abnormalities (CCA) in Ph-negative metaphases are known to develop in some patients during IM therapy. The most frequent of these abnormalities are trisomy 8, -7, del(7q), and del(20q), which are also associated with MDS and AML. These abnormalities are usually transient and disappear after a short time, or have no clinical consequence (Deininger et al., Cancer 2007). However, reports of development of high risk MDS or AML in association with CCA in Ph-negative cells are rare, but patients with chromosome 7 abnormalities appear to be at greater risk. The t(2;3) is a non random abnormality in MDS and AML, including therapy-related leukaemias, frequently associated with -7 and a complex karyotype with a poor prognosis (Stevens-Kroef et al Leukemia 2004). This is the first report of a CML patient on TKI treatment with t(2;3) and EVI1 gene rearrangements in Ph(-) cells. This cryptic translocation could easily be overlooked in the presence of a monosomy 7 with a dramatic effect on patient management. Disclosures: No relevant conflicts of interest to declare.

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17

Beirne, Michelle, Eileen Butler, and Michael Fitzpatrick. "P040 Monitoring defibrotide usage in paediatric patients undergoing HSCT with known risk factors for developing VOD/SOS." Archives of Disease in Childhood 104, no. 7 (June 19, 2019): e2.46-e2. http://dx.doi.org/10.1136/archdischild-2019-nppc.50.

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AimDefibrotide is licensed for the treatment of hepatic venous occlusive disease (VOD) following haematopoeitic stem cell transplant (HSCT). Up to April 2015 defibrotide was used as prophylaxis against VOD in our HSCT patients who were considered at high-risk for developing VOD. This practice was discontinued due to the lack of evidence of efficacy and increasing costs of the drug. The aims of this audit were to identify patients undergoing HSCT who had one or more risk factors for the development of VOD, to measure the incidence of VOD in this patient cohort after the discontinuation of prophylactic defibrotide and calculate the cost savings associated with the discontinuation of prophylaxis.MethodsAll patients who underwent HSCT between Oct 2015 and Dec 2016 were included. Patient’s medical records were reviewed and risk factors for VOD were identified. Risk factors for developing VOD post HSCT in our patient cohort were defined following a literature review of peer-reviewed papers identifying paediatric specific risk factors.1 2 These were namely: patients aged ≤2 years, patients receiving a second transplant, conditioning with IV busulfan ± cyclophosphamide, and previous treatment with gemtuzumab ozogamicin. The theoretical dose of defibrotide for patients with known risk factors was calculated based on their weight at start of conditioning and the duration of treatment was based on the number of days conditioning the patient received plus 30 days following the date of transplant. The cost of a theoretical course of defibrotide for these patients was calculated to determine cost savings.ResultsOf the 27 patients included in the study, 16 (59%) had one or more risk factors. The most common risk factor identified was conditioning with busulfan in patients ≤2 years of age (26% of patients). At present no patient post HSCT has developed VOD requiring treatment. One patient developed sub-clinical VOD which required no treatment and resolved spontaneously. Another patient received defibrotide as prophylaxis for VOD due to severe liver dysfunction prior to HSCT. There were substantial cost savings following the discontinuation of prophylactic defibrotide with a total of 2876 vials (180 vials/patient) saved during this time period.ConclusionThis audit validates our decision to discontinue use of prophylactic defibrotide and reserve its use for treatment of early VOD.ReferencesCheuk D, Wang P, Lee T, Chiang A, Ha S, Lau Y, Chan G. Risk factors and mortality predictors of hepatic veno-occlusive disease after pediatric hematopoietic stem cell transplantation. Bone Marrow Transplantation. 2007;40:935–944.Mohty M, Malard F, Abecassis M, Aerts E, Alaskar A, Alijurf M, NiChonghaile M. Sinusoidal obstruction syndrome/veno- occlusive disease: current situation and perspectives- a position statement from the European Society for Blood and Marrow Transplantation (EBMT). 2015; Bone Marrow Transplantation. 2015;50:781–789.

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18

Ablett, Mark J., and Pauline Vosylius. "Perirenal extramedullary haematopoeisis in myelofibrosis demonstrated on computed tomography." British Journal of Haematology 124, no. 4 (January 14, 2004): 406. http://dx.doi.org/10.1046/j.1365-2141.2003.04687.x.

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19

Lange, Beverly. "The Management of Neoplastic Disorders of Haematopoeisis in Children with Down's Syndrome." British Journal of Haematology 110, no. 3 (September 2000): 512–24. http://dx.doi.org/10.1046/j.1365-2141.2000.02027.x.

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20

Deambrosis, David, Ryan Hum, Prashant Hiwarkar, Kay Poulton, Denise Bonney, Helen Jane Campbell, and Robert Wynn. "Immune Mediated Cytopenia's Following Cord Blood Transplantation for Hurler's Syndrome: A Failure of Pre-Transplant Immune Suppression." Blood 132, Supplement 1 (November 29, 2018): 3374. http://dx.doi.org/10.1182/blood-2018-99-112995.

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Abstract Background: Hurler's syndrome is the most severe phenotype of Mucopolysaccharidosis 1 (MPS1H) with severe deficiency of the lysosomal enzyme alpha-L-iduronidase causing heparan and dermatan sulfate accumulation, CNS and somatic manifestations and premature death. Haematopoeitic Stem Cell Transplant (HSCT) alters the disease phenotype and prevents early death, and is standard of care in this condition. The use of an established 'donor hierarchy' recommending Unrelated Cord Blood Transplantation (UCBT) in the absence of a HLA-matched, non-carrier sibling, has resulted in improved engrafted and surviving rates and better post-enzyme levels with improved somatic and CNS clinical outcomes. However, UCBT for malignant and non-malignant conditions has led to high rates of post-transplant autoimmune disease, most frequently Autoimmune Cytopenia (AIC). We report a large cohort of MPS1H patients receiving busulfan-based UCBT and show that AIC is a frequently encountered complication of treatment with significant associated morbidity and we identify important risk factors for its occurrence. Methods: This was a retrospective observational study of patients undergoing first UCBT for Hurler's Syndrome at the Royal Manchester Children's Hospital between 30th September 2004 and 15th March 2018. An episode of AIC was defined as an episode of single or multi-lineage cytopenia occurring post-engraftment, confirmed by the presence of antibodies or diagnosed on the basis of clinical, biochemical and pathologic features. All patients received pK targeted busulfan to achieve myeloablative levels between 80-90 mg/L x hr. Conditioning between 2004 and May 2010 was with Busulfan and Cyclophosphamide (BuCy), and Fludarabine and Busulfan (FluBu) thereafter based on the reported equivocal efficacy and favourable toxicity profile of FluBu conditioning. All patients received serotherapy with Anti-Thymocyte Globulin (ATG) 10mg/kg for In Vivo T-Cell depletion. Timing of ATG was either distal (day -4 to -1) or proximal (day - 9 to -6) in accordance with international consensus at the time. Variables assessed in statistical analysis were conditioning drugs, ATG timing, Absolute Lymphocyte Count pre-conditioning, age-at-transplant, Graft-versus-Host Disease (GVHD) and Total Nucleated Cell dose. Results and Discussion: Thirty-six patients underwent first UCBT for Hurler's Syndrome. There were 8 episodes of AIC (22%), with median onset post-UCBT of 66 days (range 22-236 days). The median number of therapies required was 4 (range 0-8), with duration of illness ranging from 10 to 215 days. There were no deaths, though there were 2 episodes of life-threatening bleeding. Absolute Lymphocyte Count pre-conditioning (p=0.004), FluBu conditioning (p=0.03) and use of proximal-ATG (p=0.016) were significant risk factors for AIC in univariate analysis(see figure 1). Absolute Lymphocyte Count pre-conditioning was the most significant predictor in multivariable analysis (AOR 5.796, CI 0.921-36.474). This confirms that AIC is a frequent, serious but survivable complication of UCBT for Hurler's Syndrome. This data indicates that the balance between recipient immunity and graft immunity impacts AIC risk and severity, mandating a larger international review of registry data to define the frequency of AIC in this population, and an analysis of the risk factors that predispose to it. By better defining these risk factors, we can identify patients in whom conditioning might be altered to reduce risk. Figure 1. Univariate analysis of variables predicting an episode of Autoimmune Cytopenia. ALC (p=0.004), ATG timing (0.016) and Conditioning drugs (p=0.032) were significant risk factors. GVHD= Graft-versus-Host Disease ATG= Anti-Thymocyte Globulin Disclosures Wynn: Orchard SAB: Membership on an entity's Board of Directors or advisory committees; Orchard Therapeutics: Equity Ownership; Chimerix: Research Funding; Genzyme: Honoraria; Bluebird Bio: Consultancy; Orchard Therapeutics: Consultancy; Chimerix: Consultancy.

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21

Mahdi, Ali Jassem, Phillip Connor, and Indu Thakur. "McCune-Albright syndrome-associated bone marrow failure and extramedullary haematopoeisis secondary to fibrous dysplasia." British Journal of Haematology 178, no. 2 (June 14, 2017): 179. http://dx.doi.org/10.1111/bjh.14690.

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22

Soman, Shardul, G. D. Tharadara, Naitik Chhatrala, and Shubham Jain. "A case report of extramedullary haematopoeisis in lumbosacral region presenting as cauda equina syndrome." International Journal of Spine Surgery 10 (2016): 25. http://dx.doi.org/10.14444/3025.

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23

Chan, Lap Shu Alan, Rena Buckstein, Marciano D. Reis, Alden Chesney, Adam Lam, Matthew C. Cheung, Eugenia Piliotis, Lilly Chunhong Gu, and Richard A. Wells. "Iron Overload and Haematopoiesis in MDS: Does Blood Transfusion Promote Progression to AML?" Blood 112, no. 11 (November 16, 2008): 2685. http://dx.doi.org/10.1182/blood.v112.11.2685.2685.

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Abstract Introduction: The biology of myelodysplastic syndrome (MDS) is poorly understood, and treatment options are limited. Thus, most MDS patients require chronic red blood cell transfusion, and many develop secondary iron overload. Although the pathophysiological consequences of iron overload to the heart, liver, and endocrine organs have been well characterized, its effects on haematopoiesis have not been studied. However, it has been observed that chelation therapy in iron-overloaded MDS patients may result in reduction of transfusion requirements, and recent studies have suggested a correlation between the use of iron chelation therapy and improvement in leukaemia-free survival in MDS. At the cellular level, iron toxicity is mediated in large part via the generation of reactive oxygen species (ROS). It has been shown in animal models that accumulation of ROS leads to senescence of haematopoietic stem cells, and that ROS cause DNA damage and promote the development of malignancy. These effects of ROS may be particularly important in MDS, in which haematopoiesis is already severely compromised and genetic instability is a striking feature. Hypothesis: We hypothesize that iron overload secondary to transfusion leads to increased levels of intracellular ROS in early haematopoeitic cells in MDS. The increase in intracellular ROS in MDS would be predicted to lead further impairment of haematopoiesis via stem cell exhaustion and while promoting accumulation of DNA damage by myelodysplastic stem cells and early progenitors, thus accelerating progression of MDS to acute leukaemia. Results: To test this hypothesis, we examined the relationship between transfusion-related iron overload and ROS content of CD34+ bone marrow cells in MDS. ROS content was measured in CD34+ cells by flow cytometry in bone marrow aspirates from 34 consecutive MDS patients (CMML=4, MDS/MPD=2, RA=4, RARS=3, RCMD=2, RAEB 1=6, RAEB 2=12, RAEB-t/AML=1). The patients represented a wide range of prior transfusion burden (0->300 units PRBC) and serum ferritin levels (11->10000 μg/L). ROS was strongly correlated with serum ferritin concentration for patients with iron overload (serum ferritin >1000 μg/L; n=14, R=0.733, p<0.005). The correlation between ROS and ferritin level was even stronger in the subset of patients with RAEB 1 or RAEB 2 and iron overload (n=11, R=0.838, p<0.005). In contrast, no correlation between ROS and ferritin level was demonstrated for patients with serum ferritin <1000 μg/L (n=20). Importantly, iron chelation therapy was associated with a reduction in CD34+ cell ROS content in one patient. To assess the effect of iron overload on normal stem cell and progenitor function, we established a mouse model of subacute bone marrow iron overload. B6D2F1 mice were loaded with iron dextran by intraperitoneal injection (150mg total iron load over 21 days), and sacrificed three days after the end of iron loading. Iron staining of tissue sections confirmed iron deposition in the bone marrow, liver, and myocardium. The development of splenomegaly was noted in iron-loaded animals. Flow cytometric analysis revealed increased apoptosis of bone marrow cells in iron loaded mice based on annexin V+/7 AAD-staining (6.26±0.96% versus 3.54±0.99% for control mice, paired student’s t-Test p<0.005). However, ROS content in CD117+ progenitors of iron loaded mice was similar to control mice. Thus, subacute iron loading in mice increases apoptosis but does not alter the ROS content of HSCs; we postulate that chronic iron overload is required to achieve this effect. Conclusions: These results establish a relationship between CD34+ cell ROS content and serum ferritin concentration in MDS patients with iron overload, and indicate that iron chelation therapy in this patient population reverses this ROS accumulation. The physiological consequences of this relationship are currently being investigated in this patient set by haematopoietic colony assays and assessment of DNA damage in CD34+ cells. Nonethelesss, these data may have key implications for the deployment of iron chelation therapy in MDS patients, and may explain the association between the use of iron chelation and improved leukaemia-free survival in MDS.

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24

Hockings, Catherine, Victoria Deaner, Yvette Hoade, Phoebe Dace, Alex Lubin, and Elspeth Payne. "A Zebrafish Model of Cooperating C and N Terminal CEBPA Mutations Reveals Defects in Early Myelopoeisis and HSPCs Leading to Leukaemogenesis." Blood 132, Supplement 1 (November 29, 2018): 1343. http://dx.doi.org/10.1182/blood-2018-99-119336.

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Abstract Acute Myeloid Leukaemia (AML) is thought to occur due to stepwise accumulation of mutations in haematopoietic stem and progenitor cells (HSPCs) or early myeloid progenitor cells (EMPs) to either block differentiation or increase proliferation. In around 10% of sporadic AML cases and several known germline predisposition kindreds the myeloid transcription factor CEBPA is mutated. 50% of cases possess biallelic mutations in both C and N terminae (dm) and 50% monoallelic mutation (sm). Using TALENs we have created both C and N terminal mutants in zebrafish to study their cooperating effects in the development of AML. Our first observation was of striking defects in mature myelocytes and monocytes in all double mutants (cebpamut/mut) as assessed by Sudan black staining at 5 days post fertilisation (dpf) and apoeb whole mount in situ hybridisation (WISH) at 3dpf. In situ hybridisation revealed defects in myelopoeisis in all cebpamut/mut fry as early as 28hpf, with markedly decreased expression of coronin and l-plastin. We then interrogated the model further to assess when and where the differentiation block was occurring. We utilised the transcription factor pu.1 both as an in vivo transgenic marker Tg(pu.1:GFP) and WISH probe at earlier time points. In primitive haematopoiesis (until 22hpf) pu.1 expression showed no defects in dm mutants. However, pu.1 expressing cells were markedly reduced in dm mutants in establishment of myelopoeisis in the caudal haematopoietic tissue (CHT), fetal liver equivalent. Following formation of the CHT at around 30hpf, differing patterns of pu.1 expression were seen in sm mutants, with cebpaWT/Cterm having significantly increased staining, which was reduced in cebpaWT/Nterm (see figure 1). HSPC numbers in cebpamut/mut were seen to be normal by WISH for gata2b and runx1 and flow cytometry in Tg(CD41:GFP) fry during early haematopoeisis (2-5dpf). However, myb expression was markedly increased at 36hpf and 3 days but only in cebpaCterm/Nterm and cebpaNterm/Nterm dm mutants (see figure 2). This suggests an accumulation of early progenitors with myeloid potential but not commitment, as implied by absence of pu.1 expression but normal CD41lo numbers and other stem cell marker expression. Absence of MCherry expression in the transgenic LysC:MCherry, which highlights mature myeloid cells in vivo, was sufficiently reliable to genotype all cebpamut/mut fry and observe them for impaired survival compared to wild-type and heterozygous siblings and for the development of leukaemia. Similarly to the increase in myb staining, leukaemic transformation was only observed in dm mutants with at least one N terminal mutation, as assessed by development of anaemia and florid Tg(CD41:GFP) expression. Flow cytometry in juvenile fish (4-6weeks) also identifies a developing pre-leukaemic phenotype with moderate yet significant expansion of HSPCs and continuing absence LysC expression in cebpaNterm/Cterm and cebpaNTerm/NTerm. However, survival is poor in all dm fish, likely due to the metabolic role of cebpa and vulnerability to infection secondary to the severe myelomonocytic defect. Our results show that absence of WT cebpa has dramatic effects myelopoiesis from early stages of differentiation in definitive haematopoiesis. In addition, accumulation of myb expressing progenitors occurs as they arise from the aorta in dm mutants, identifying this as a sub-population of HSPC vulnerable to further leukaemogenic hits. Ongoing work will define the mechanism of these effects in sm and dm mutants and include comparative expression profiling in myb and pu.1 positive cells. Disclosures No relevant conflicts of interest to declare.

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Bahoush, Gholamreza, and Maryam Vafapour. "A case report of severe veno-occlusive disease following autologous stem cell transplantation successfully treated with Defibrotide." European Journal of Translational Myology, September 15, 2020. http://dx.doi.org/10.4081/ejtm.0.9161.

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Veno-occlusive disease (VOD) is one of the complications of hematopoietic stem cell transplantation that can also be caused by high-dose chemotherapy. This complication can lead to high mortality following bone marrow transplantation. It is more common after allogeneic stem cell transplantation, and is rare after autologous stem cell transplantation. While mild cases of VOD may reduce over a period of a few weeks, very severe cases can cause multi-organ damage, which has a high mortality. is therefore required with early diagnosis and treatment of this complication. In this paper, we present a sever VOD case after autologous stem cell transplantation, that was treated successfully with Defibrotide. The patient was a 14-month-old girl who has neuroblastoma with bone metastasis. VOD should be considered in the differential diagnosis of haematopoietic stem cell transplantation recipients who present with unexplained liver injuries, ascites and/or multi organ failure. Recipients of haematopoeitic stem cell transplantation who present with unexplained liver injuries, ascites and/or multi organ failure should have VOD considered in their differential diagnosis. If there is severe VOD diagnosed, then Defibrotide could be an option for treatment.

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Bahoush, Gholamreza, and Maryam Vafapour. "A case report of severe veno-occlusive disease following autologous stem cell transplantation successfully treated with Defibrotide." European Journal of Translational Myology 30, no. 3 (September 15, 2020). http://dx.doi.org/10.4081/ejtm.2020.9161.

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Veno-occlusive disease (VOD) is one of the complications of hematopoietic stem cell transplantation that can also be caused by high-dose chemotherapy. This complication can lead to high mortality following bone marrow transplantation. It is more common after allogeneic stem cell transplantation, and is rare after autologous stem cell transplantation. While mild cases of VOD may reduce over a period of a few weeks, very severe cases can cause multi-organ damage, which has a high mortality. is therefore required with early diagnosis and treatment of this complication. In this paper, we present a sever VOD case after autologous stem cell transplantation, that was treated successfully with Defibrotide. The patient was a 14-month-old girl who has neuroblastoma with bone metastasis. VOD should be considered in the differential diagnosis of haematopoietic stem cell transplantation recipients who present with unexplained liver injuries, ascites and/or multi organ failure. Recipients of haematopoeitic stem cell transplantation who present with unexplained liver injuries, ascites and/or multi organ failure should have VOD considered in their differential diagnosis. If there is severe VOD diagnosed, then Defibrotide could be an option for treatment.

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Crossland, Rachel E., Jean Norden, Sakhila Ghimire, Mateja Kralj Juric, Kim F. Pearce, Clare Lendrem, Matthew Collin, et al. "Profiling Tissue and Biofluid miR-155-5p, miR-155*, and miR-146a-5p Expression in Graft vs. Host Disease." Frontiers in Immunology 12 (March 15, 2021). http://dx.doi.org/10.3389/fimmu.2021.639171.

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Introduction: Acute graft vs. host disease (aGvHD) is a frequent complication following allogeneic haematopoeitic transplantation (HSCT). Despite recent advances, there are no universally accepted biomarkers to determine development of aGvHD. MicroRNAs miR-146a and miR-155 have been previously associated with aGvHD and show promise as clinically translatable biomarkers. In this study, we performed comprehensive expression profiling of miR-146a, miR-155, and miR-155* expression in aGvHD target tissue and biofluids and relate expression to post-HSCT outcomes.Materials and Methods: MicroRNA expression was assessed by qRT-PCR in gastrointestinal (n = 31) and skin (n = 31) biopsies as well as serum (exploratory cohort n = 34, verification cohort n = 81, diagnostic cohort n = 65) and urine (exploratory cohort n = 30, verification cohort n = 56, diagnostic cohort n = 20) biofluids, including extracellular vesicle (EV) cohorts (serum EV n = 15, urine EV n = 30). Expression was related to aGvHD incidence, severity and overall survival.Results: In GI samples, expression of miR-155 (p = 0.03) and miR-146a (p = 0.03) was higher at aGvHD onset compared to patients with no GvHD. In skin biopsies, expression of miR-155 (p = 0.004) was upregulated in aGvHD patients compared to normal control skin. Expression of miR-146a was higher in aGvHD compared to no aGvHD biopsies (p = 0.002). In serum, miR-155 (p = 0.03) and miR-146a (p = 0.02) expression was higher at day 14 (D14), while in urine expression was elevated at D7 post-HSCT in patients who developed aGvHD compared to those disease-free. This was verified in an independent serum (miR-155 p = 0.005, miR-146a p = 0.003) and urine (miR-155 p = 0.02, miR-146a p = 0.04) cohort, where both microRNAs were also associated with aGvHD by ROC analysis. In serum and urine samples taken at the time of aGvHD symptoms, expression of miR-155 and miR-146a was also elevated (serum miR-155 p = 0.03, miR-146a p < 0.001; urine miR-155 p = 0.02, miR-146a p = 0.02). In contrast, miR-146a and miR-155 were downregulated at D14 in serum EVs and at D7 in urine EVs in patients who developed aGvHD compared to those that remained disease-free, in both an exploratory (serum miR-155 p = 0.02, miR-146a p = 0.06; urine miR-155 p = 0.02, miR-146a p = 0.07) and an independent cohort (serum miR-155 p = 0.01, miR-146a p = 0.02).Conclusions: These results further support a role for miR-155 and miR-146a as non-invasive, clinically relevant biomarkers for aGvHD. However, the link between their involvement in generalized inflammation and in specific pathophysiology requires further investigation at a systemic level.

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Martinez-Losada, Carmen, Maria R. Alhambra-Exposito, Rafael Sanchez-Sanchez, Javier Casaño, Carmen Tenorio-Jimenez, and Joaquin Sanchez-Garcia. "Dysplastic extramedullary haematopoeisis with ringed sideroblasts mimicking adrenal adenoma." Histopathology, August 2013, n/a. http://dx.doi.org/10.1111/his.12181.

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Panda, Ananya, Sheragaru Hanumanthappa Chandrashekhara, Aruna Nambirajan, and Pravas Mishra. "Idiopathic myelofibrosis with disseminated hepatosplenic, mesenteric, renal and pulmonary extramedullary haematopoeisis, portal hypertension and tuberculosis: initial presentation and 2 years follow-up." BMJ Case Reports, December 23, 2016, bcr2016217854. http://dx.doi.org/10.1136/bcr-2016-217854.

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