Subjects -> MEDICAL SCIENCES (Total: 8185 journals)
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HEMATOLOGY (160 journals)                     

Showing 1 - 151 of 151 Journals sorted alphabetically
Acta Angiologica     Open Access   (Followers: 2)
Acta Haematologica     Full-text available via subscription   (Followers: 23)
Acta Haematologica Polonica     Open Access  
Adipocyte     Open Access  
Advances in Hematology     Open Access   (Followers: 13)
Africa Sanguine     Full-text available via subscription  
American Journal of Hematology     Hybrid Journal   (Followers: 52)
Anemia     Open Access   (Followers: 6)
Annals of Hematology     Hybrid Journal   (Followers: 15)
Archives of Hematology Case Reports and Reviews     Open Access  
Arteriosclerosis, Thrombosis and Vascular Biology     Full-text available via subscription   (Followers: 29)
Artery Research     Hybrid Journal   (Followers: 4)
Artificial Cells, Nanomedicine and Biotechnology     Hybrid Journal   (Followers: 4)
ASAIO Journal     Hybrid Journal   (Followers: 2)
Best Practice & Research Clinical Haematology     Hybrid Journal   (Followers: 5)
Blood     Hybrid Journal   (Followers: 296)
Blood Advances     Open Access   (Followers: 7)
Blood and Lymphatic Cancer : Targets and Therapy     Open Access   (Followers: 7)
Blood Cancer Journal     Open Access   (Followers: 18)
Blood Cells, Molecules, and Diseases     Hybrid Journal   (Followers: 8)
Blood Coagulation & Fibrinolysis     Hybrid Journal   (Followers: 60)
Blood Pressure     Open Access  
Blood Pressure Monitoring     Hybrid Journal   (Followers: 1)
Blood Purification     Full-text available via subscription   (Followers: 6)
Blood Reviews     Hybrid Journal   (Followers: 26)
BMC Hematology     Open Access   (Followers: 7)
BMJ Open Diabetes Research & Care     Open Access   (Followers: 29)
Bone Marrow Transplantation     Hybrid Journal   (Followers: 17)
British Journal of Diabetes & Vascular Disease     Open Access   (Followers: 21)
British Journal of Haematology     Hybrid Journal   (Followers: 60)
British Journal of Primary Care Nursing - Cardiovascular Disease, Diabetes and Kidney Care     Full-text available via subscription   (Followers: 10)
Canadian Journal of Diabetes     Hybrid Journal   (Followers: 28)
Case Reports in Hematology     Open Access   (Followers: 10)
Clinical and Applied Thrombosis/Hemostasis     Open Access   (Followers: 32)
Clinical Diabetes     Full-text available via subscription   (Followers: 39)
Clinical Diabetes and Endocrinology     Open Access   (Followers: 20)
Clinical Lymphoma & Myeloma     Full-text available via subscription   (Followers: 2)
Clinical Lymphoma Myeloma and Leukemia     Hybrid Journal   (Followers: 5)
Clinical Medicine Insights : Blood Disorders     Open Access   (Followers: 1)
Conquest : The Official Journal of Diabetes Australia     Full-text available via subscription   (Followers: 3)
Current Angiogenesis     Hybrid Journal   (Followers: 1)
Current Diabetes Reports     Hybrid Journal   (Followers: 24)
Current Diabetes Reviews     Hybrid Journal   (Followers: 27)
Current Hematologic Malignancy Reports     Hybrid Journal   (Followers: 2)
Current Opinion in Hematology     Hybrid Journal   (Followers: 20)
Cytotherapy     Full-text available via subscription   (Followers: 2)
Der Diabetologe     Hybrid Journal   (Followers: 2)
Diabetes     Full-text available via subscription   (Followers: 411)
Diabetes aktuell     Hybrid Journal   (Followers: 3)
Diabetes and Vascular Disease Research     Hybrid Journal   (Followers: 20)
Diabetes Care     Full-text available via subscription   (Followers: 469)
Diabetes Case Reports     Open Access  
Diabetes Educator     Hybrid Journal   (Followers: 27)
Diabetes Management     Full-text available via subscription   (Followers: 15)
Diabetes Research and Clinical Practice     Hybrid Journal   (Followers: 70)
Diabetes Spectrum     Full-text available via subscription   (Followers: 16)
Diabetes Technology & Therapeutics     Hybrid Journal   (Followers: 50)
Diabetes Therapy     Open Access   (Followers: 23)
Diabetic Foot & Ankle     Open Access   (Followers: 10)
Diabetic Medicine     Hybrid Journal   (Followers: 147)
Diabetologia     Hybrid Journal   (Followers: 207)
Diabetologia Kliniczna     Hybrid Journal  
Diabetologie und Stoffwechsel     Hybrid Journal   (Followers: 2)
Egyptian Journal of Haematology     Open Access  
eJHaem     Open Access  
European Journal of Haematology     Hybrid Journal   (Followers: 16)
Experimental Hematology     Hybrid Journal   (Followers: 6)
Experimental Hematology & Oncology     Open Access   (Followers: 6)
Expert Review of Hematology     Hybrid Journal   (Followers: 5)
Fluids and Barriers of the CNS     Open Access   (Followers: 1)
Global Journal of Transfusion Medicine     Open Access   (Followers: 1)
Haematologica - the Hematology journal     Open Access   (Followers: 33)
Haemophilia     Hybrid Journal   (Followers: 66)
Hematologia     Full-text available via subscription   (Followers: 3)
Hematología     Open Access  
Hematology     Open Access   (Followers: 15)
Hematology Reports     Open Access   (Followers: 4)
Hematology, Transfusion and Cell Therapy     Open Access   (Followers: 2)
Hematology/Oncology and Stem Cell Therapy     Open Access   (Followers: 6)
Hemodialysis International     Hybrid Journal   (Followers: 3)
Hepatitis Monthly     Open Access   (Followers: 3)
Immunohematology : Journal of Blood Group Serology and Molecular Genetics     Hybrid Journal   (Followers: 1)
Indian Journal of Hematology and Blood Transfusion     Hybrid Journal   (Followers: 2)
Info Diabetologie     Full-text available via subscription   (Followers: 1)
InFo Hämatologie + Onkologie : Interdisziplinäre Fortbildung von Ärzten für Ärzte     Full-text available via subscription  
Integrated Blood Pressure Control     Open Access  
International Blood Research & Reviews     Open Access  
International Journal of Clinical Transfusion Medicine     Open Access   (Followers: 3)
International Journal of Diabetes in Developing Countries     Hybrid Journal   (Followers: 6)
International Journal of Diabetes Research     Open Access   (Followers: 8)
International Journal of Hematologic Oncology     Open Access   (Followers: 2)
International Journal of Hematology     Hybrid Journal   (Followers: 4)
International Journal of Hematology Research     Open Access   (Followers: 2)
International Journal of Hematology-Oncology and Stem Cell Research     Open Access   (Followers: 2)
International Journal of Laboratory Hematology     Hybrid Journal   (Followers: 25)
Iraqi Journal of Hematology     Open Access  
JMIR Diabetes     Open Access  
Journal of Blood Disorders & Transfusion     Open Access   (Followers: 3)
Journal of Applied Hematology     Open Access   (Followers: 2)
Journal of Blood Medicine     Open Access   (Followers: 1)
Journal of Cerebral Blood Flow & Metabolism     Hybrid Journal   (Followers: 3)
Journal of Diabetes     Open Access   (Followers: 20)
Journal of Diabetes and its Complications     Hybrid Journal   (Followers: 25)
Journal of Diabetes and Metabolic Disorders     Open Access   (Followers: 8)
Journal of Diabetes Investigation     Open Access   (Followers: 12)
Journal of Diabetes Mellitus     Open Access   (Followers: 5)
Journal of Diabetes Research     Open Access   (Followers: 13)
Journal of Diabetes Research     Open Access   (Followers: 9)
Journal of Hematological Malignancies     Open Access  
Journal of Hematology     Open Access   (Followers: 2)
Journal of Hematology and Transfusion Medicine     Open Access   (Followers: 1)
Journal of Hematopathology     Hybrid Journal   (Followers: 3)
Journal of Hypo & Hyperglycemia     Partially Free  
Journal of Pediatric Hematology/Oncology     Hybrid Journal   (Followers: 8)
Journal of Social Health and Diabetes     Open Access   (Followers: 1)
Journal of Thrombosis and Haemostasis     Hybrid Journal   (Followers: 81)
Journal of Thrombosis and Thrombolysis     Hybrid Journal   (Followers: 35)
Journal of Transfusion Medicine     Full-text available via subscription  
Kidney and Blood Pressure Research     Open Access   (Followers: 4)
Leukemia     Hybrid Journal   (Followers: 22)
Leukemia and Lymphoma     Hybrid Journal   (Followers: 12)
Leukemia Research     Hybrid Journal   (Followers: 8)
Leukemia Research Reports     Open Access   (Followers: 1)
Leukemia Supplements     Full-text available via subscription  
Mediterranean Journal of Hematology and Infectious Diseases     Open Access  
Nederlands Tijdschrift voor Diabetologie     Hybrid Journal  
Nutrition & Diabetes     Open Access   (Followers: 20)
Oncohematology     Open Access   (Followers: 1)
Open Diabetes Journal     Open Access  
Open Hematology Journal     Open Access   (Followers: 1)
Open Hypertension Journal     Open Access  
Open Journal of Blood Diseases     Open Access  
Pediatric Blood & Cancer     Hybrid Journal   (Followers: 8)
Pediatric Hematology Oncology Journal     Open Access   (Followers: 3)
Peritoneal Dialysis International     Hybrid Journal  
Platelets     Hybrid Journal   (Followers: 3)
Practical Diabetes     Hybrid Journal   (Followers: 7)
Primary Care Diabetes     Hybrid Journal   (Followers: 26)
Research & Reviews : Journal of Oncology and Hematology     Full-text available via subscription   (Followers: 1)
Research and Practice in Thrombosis and Haemostasis     Open Access   (Followers: 1)
Revista Cubana de Hematología, Inmunología y Hemoterapia     Open Access  
Seminars in Hematology     Hybrid Journal   (Followers: 12)
Seminars in Thrombosis and Hemostasis     Hybrid Journal   (Followers: 45)
Thalassemia Reports     Open Access   (Followers: 1)
The Lancet Haematology     Full-text available via subscription   (Followers: 38)
Therapeutic Advances in Hematology     Hybrid Journal  
Thrombosis & Haemostasis     Hybrid Journal   (Followers: 145)
Thrombosis Research     Hybrid Journal   (Followers: 47)
Transfusionsmedizin - Immunhämatologie, Hämotherapie, Immungenetik, Zelltherapie     Hybrid Journal  
Transplantation and Cellular Therapy     Hybrid Journal   (Followers: 13)
Veins and Lymphatics     Open Access   (Followers: 1)


Similar Journals
Journal Cover
Haematologica - the Hematology journal
Journal Prestige (SJR): 3.063
Citation Impact (citeScore): 4
Number of Followers: 33  

  This is an Open Access Journal Open Access journal
ISSN (Print) 0390-6078 - ISSN (Online) 1592-8721
Published by Ferrata Storti Foundation Homepage  [1 journal]
  • Images from the Haematologica Atlas of Hematologic Cytology:
           myelodysplastic syndrome with isolated del(5q)

    • Authors: Rosangela Invernizzi
      PubDate: Sat, 01 Oct 2022 00:00:00 +000
  • How we changed our approach to venous thromboembolism

    • Authors: Walter Ageno
      PubDate: Sat, 01 Oct 2022 00:00:00 +000
  • Association of FLT3-internal tandem duplication length with overall

    • Authors: Tobias B. Polak; Joost van Rosmalen, Stijn Dirven, Julia K. Herzig, Jacqueline Cloos, Soheil Meshinchi, Konstanze Döhner, Jeroen J.W.M. Janssen, David G.J. Cucchi
      PubDate: Thu, 07 Jul 2022 00:00:00 +000
  • Platelet functional abnormalities and clinical presentation in pediatric
           patients with germline RUNX1, ANKRD26, and ETV6 mutations

    • Authors: Galina S. Ovsyannikova; Daria V. Fedorova, Ivan P. Tesakov, Alexey A. Martyanov, Anastasia A. Ignatova, Evgeniya A. Ponomarenko, Pavel A. Zharkov, Anna V. Pavlova, Elena V. Raykina, Michael A. Maschan, Mikhail A. Panteleev, Galina A. Novichkova, Anastasia N. Sveshnikova, Nataliya S. Smetanina
      PubDate: Thu, 07 Jul 2022 00:00:00 +000
  • A myeloablative fractionated busulfan conditioning regimen with
           post-transplant cyclophosphamide in HLA-matched and haploidentical
           transplantation: results of a phase II study

    • Authors: Uday R. Popat; Borje S Andersson, Roland Bassett, Jitesh Kawedia, Ben C. Valdez, Amin M. Alousi, Gheath Al-Atrash, Qaiser Bashir, Chitra M. Hosing, Jin S. Im, Partow Kebriaei, David Marin, Yago Nieto, Betul Oran, Amanda Olson, Muzaffar H. Qazilbash, Samer A. Srour, Elizabeth J. Shpall, Richard E. Champlin, Rohtesh S. Mehta
      PubDate: Thu, 30 Jun 2022 00:00:00 +000
  • Molecular predictors of response to venetoclax plus hypomethylating agent
           in treatment-naïve acute myeloid leukemia

    • Authors: Naseema Gangat; Isla Johnson, Kristen McCullough, Faiqa Farrukh, Aref Al-Kali, Hassan Alkhateeb, Kebede Begna, Abhishek Mangaonkar, Mark Litzow, William Hogan, Mithun Shah, Mrinal Patnaik, Animesh Pardanani, Ayalew Tefferi
      PubDate: Thu, 30 Jun 2022 00:00:00 +000
  • Daunorubicin-60 versus daunorubicin-90 versus idarubicin-12 for induction
           chemotherapy in acute myeloid leukemia: a retrospective analysis of the
           Mayo Clinic experience

    • Authors: Ayalew Tefferi; Naseema Gangat, Mithun Shah, Hassan Alkhateeb, Mrinal S. Patnaik, Aref Al-Kali, Michelle A. Elliott, William J. Hogan, Mark R. Litzow, Christopher C. Hook, Abhishek Mangaonkar, David Viswanatha, Dong Chen, Animesh Pardanani, Rhett P. Ketterling, Kebede H. Begna
      PubDate: Thu, 23 Jun 2022 00:00:00 +000
  • SARS-CoV-2-specific cellular response following third COVID-19 vaccination
           in patients with chronic lymphocytic leukemia

    • Authors: Sibylle C. Mellinghoff; Leonie Mayer, Sandra Robrecht, Leonie M. Weskamm, Christine Dahlke, Henning Gruell, Maike Schlotz, Kanika Vanshylla, Hans A. Schloser, Martin Thelen, Anna-Maria Fink, Kirsten Fischer, Florian Klein, Marylyn M. Addo, Barbara Eichhorst, Michael Hallek, Petra Langerbeins
      PubDate: Thu, 23 Jun 2022 00:00:00 +000
  • Primary outcomes by 1q21+ status for isatuximab-treated patients with
           relapsed/refractory multiple myeloma: subgroup analyses from ICARIA-MM and

    • Authors: Tom Martin; Paul G Richardson, Thierry Facon, Philippe Moreau, Aurore Perrot, Ivan Spicka, Kamlesh Bisht, Marlene Inchauspé, France Casca, Sandrine Macé, Helgi van de Velde, Kenshi Suzuki
      PubDate: Thu, 23 Jun 2022 00:00:00 +000
  • COVID-19 vaccine-induced adverse events predict immunogenicity among
           recipients of allogeneic hematopoietic stem cell transplantation

    • Authors: Hanna Grauers Wiktorin; Sigrun Einarsdottir, Andreas Törnell, Mohammad Arabpour, Nuttida Issdisai, Jesper Waldenström, Johan Ringlander, Magnus Lindh, Martin Lagging, Kristoffer Hellstrand, Anna Martner
      PubDate: Thu, 23 Jun 2022 00:00:00 +000
  • Daratumumab for treatment-refractory acquired idiopathic pure red cell

    • Authors: Naseema Gangat; Jonathan Bleeker, Douglas Lynch, Horatiu Olteanu, Louis Letendre, Ayalew Tefferi
      PubDate: Thu, 09 Jun 2022 00:00:00 +000
  • The successful use of eculizumab for treatment of thrombotic
           microangiopathy in pediatric acute SARSCoV2 infection and multisystem
           inflammatory syndrome in children

    • Authors: Tarun Aurora; Noel Joseph, Senthil Velan Bhoopalan, Miguela A. Caniza, Tim Flerlage, Saad Ghafoor, Jane Hankins, Diego R. Hijano, Rohith Jesudas, Justin Kirkham, Hugo Martinez, Gabriela Maron Alfaro, Akshay Sharma, Melissa Hines
      PubDate: Thu, 26 May 2022 00:00:00 +000
  • Genomic determinants impacting the clinical outcome of mogamulizumab
           treatment for adult T-cell leukemia/lymphoma

    • Authors: Norio Tanaka; Seiichi Mori, Kazuma Kiyotani, Yuki Ota, Osamu Gotoh, Shigeru Kusumoto, Nobuaki Nakano, Youko Suehiro, Asahi Ito, Ilseung Choi, Eiichi Ohtsuka, Michihiro Hidaka, Kisato Nosaka, Makoto Yoshimitsu, Yoshitaka Imaizumi, Shinsuke Iida, Atae Utsunomiya, Tetsuo Noda, Hiroyoshi Nishikawa, Ryuzo Ueda, Takashi Ishida
      Abstract: In order to identify genomic biomarkers for the outcome of mogamulizumab-containing treatment, an integrated molecular analysis of adult T-cell leukemia/lymphoma (ATL) was conducted on 64 mogamulizumab-naïve patients. Among driver genes, CCR4 and CCR7 alterations were observed in 22% and 11% of the patients, respectively, both consisting of single nucleotide variants (SNV)/insertion-deletions (indels) in the C-terminus. Patients with CCR4 alterations or without CCR7 alterations exhibited a more favorable clinical response (complete response [CR] rate 93%, 13/14; P=0.024, and CR rate 71%, 40/56; P=0.036, respectively). Additionally, TP53, CD28, and CD274 alterations were identified in 35%, 16%, and 10% of the patients, respectively. TP53 alterations included SNV/indels or copy number variations (CNV) such as homozygous deletion; CD28 alterations included SNV, CNV such as amplification, or fusion; CD274 alterations included CNV such as amplification, or structural variants. Univariate analysis revealed that TP53, CD28 or CD274 alterations were associated with worse overall survival (OS) (hazard ratio [HR]: 2.330, 95% confidence interval [CI]: 1.183-4.589; HR: 3.191, 95% CI: 1.287- 7.911; HR: 3.301, 95% CI: 1.130-9.641, respectively) but that CCR4 alterations were associated with better OS (HR: 0.286, 95% CI: 0.087-0.933). Multivariate analysis indicated that in addition to performance status, TP53, CCR4 or CD274 alterations (HR: 2.467, 95% CI: 1.197-5.085; HR: 0.155, 95% CI: 0.031-0.778; HR: 14.393, 95% CI: 2.437-85.005, respectively) were independently and significantly associated with OS. The present study contributes to the establishment of precision medicine using mogamulizumab in ATL patients.
      PubDate: Thu, 14 Apr 2022 00:00:00 +000
  • Factors associated with left ventricular hypertrophy in children with
           sickle cell disease: results from the DISPLACE study

    • Authors: Najibah A. Galadanci; Walter Johnson, April Carson, Gerhard Hellemann, Virginia Howard, Julie Kanter
      Abstract: Cardiopulmonary complications remain a leading cause of morbidity and mortality in sickle cell disease (SCD). The overall goals of this study were to evaluate the relationship between left ventricular hypertrophy (LVH) and laboratory markers of hemolysis and determine the association between LVH and SCD-specific therapies (hydroxyurea and chronic red cell transfusion). Data from the DISPLACE (Dissemination and Implementation of Stroke Prevention Looking at the Care Environment) study cohort was used. LVH was defined based on the left ventricular mass indexed to the body surface area as left ventricular mass index >103.0 g/m2 for males and >84.2 g/m2 for females. There were 1,409 children included in the analysis and 20.3% had LVH. Results of multivariable analysis of LVH showed baseline hemoglobin levels were associated with the lower odds of having LVH (odds ratio [OR]: 0.71, 95% confidence interval [CI]: 0.60– 0.84). The odds of LVH increases for every 1-year increase in age (OR: 1.07, 95% CI: 1.02-1.13). Similarly, the odds of LVH were lower among males than females (OR: 0.59, 95% CI: 0.38-0.93). The odds of LVH were higher among those on hydroxyurea compared to no therapy (OR: 1.83, 95% CI: 1.41–2.37). Overall results of the study showed that LVH occurs early in children with SCD and the risk increases with increasing age and with lower hemoglobin. Further, we found higher use of hydroxyurea among those with LVH, suggesting that the need for hydroxyurea conveys a risk of cardiovascular remodeling.
      PubDate: Thu, 14 Apr 2022 00:00:00 +000
  • Treatment-free remission in chronic myeloid leukemia patients treated
           front-line with nilotinib: 10-year followup of the GIMEMA CML 0307 study

    • Authors: Gabriele Gugliotta; Fausto Castagnetti, Massimo Breccia, Luciano Levato, Tamara Intermesoli, Mariella D'Adda, Marzia Salvucci, Fabio Stagno, Giovanna Rege-Cambrin, Mario Tiribelli, Bruno Martino, Monica Bocchia, Michele Cedrone, Elena Trabacchi, Francesco Cavazzini, Ferdinando Porretto, Federica Sorà, Maria Pina Simula, Francesco Albano, Simona Soverini, Robin Foà, Fabrizio Pane, Michele Cavo, Giuseppe Saglio, Michele Baccarani, Gianantonio Rosti
      Abstract: We report the final analysis, with a 10-year follow-up, of the phase II study GIMEMA CML 0307 (NCT 00481052), which enrolled 73 adult patients (median age 51 years; range, 18-83) with newly diagnosed chronic-phase chronic myeloid leukemia to investigate the efficacy and the toxicity of front-line treatment with nilotinib. The initial dose was 400 mg twice daily; the dose was reduced to 300 mg twice daily as soon as this dose was approved and registered. The 10-year overall survival and progression- free survival were 94.5%. At the last contact, 36 (49.3%) patients were continuing nilotinib (22 patients at 300 mg twice daily, 14 at lower doses), 18 (24.7%) patients were in treatment-free remission, 14 (19.2%) were receiving other tyrosinekinase inhibitors and four (5.5%) patients have died. The rates of major and deep molecular responses by 10 years were 96% and 83%, respectively. The median times to major and deep molecular response were 6 and 18 months, respectively. After a median duration of nilotinib treatment of 88 months, 24 (32.9%) patients discontinued nilotinib while in stable deep molecular response. In these patients, the 2-year estimated treatment-free survival was 72.6%. The overall treatment-free remission rate, calculated on all enrolled patients, was 24.7% (18/73 patients). Seventeen patients (23.3%), at a median age of 69 years, had at least one arterial obstructive event. In conclusion, the use of nilotinib front-line in chronic phase chronic myeloid leukemia can induce a stable treatment-free remission in a relevant number of patients, although cardiovascular toxicity remains of concern.
      PubDate: Thu, 07 Apr 2022 00:00:00 +000
  • The deglycosylated form of 1E12 inhibits platelet activation and
           prothrombotic effects induced by VITT antibodies

    • Authors: Caroline Vayne; Raghavendra Palankar, Sandra Billy, Stefan Handtke, Thomas Thiele, Charlotte Cordonnier, Claire Pouplard, Andreas Greinacher, Yves Gruel, Jérôme Rollin
      Abstract: In order to improve the safety of COVID-19 vaccines, there is an urgent need to unravel the pathogenesis of vaccineinduced immune thrombotic thrombocytopenia (VITT), a severe complication of recombinant adenoviral vector vaccines used to prevent COVID-19, and likely due to anti-platelet factor 4 (PF4) IgG antibodies. In this study, we demonstrated that 1E12, a chimeric anti-PF4 antibody with a human Fc fragment, fully mimics the effects of human VITT antibodies, as it activates platelets to a similar level in the presence of platelet factor 4 (PF4). Incubated with neutrophils, platelets and PF4, 1E12 also strongly induces NETosis, and in a microfluidic model of whole blood thrombosis, it triggers the formation of large platelet/leukocyte thrombi containing fibrin(ogen). In addition, a deglycosylated form of 1E12 (DG-1E12), which still binds PF4 but no longer interacts with Fcγ receptors, inhibits platelet, granulocyte and clotting activation induced by human anti-PF4 VITT antibodies. This strongly supports that 1E12 and VITT antibodies recognize overlapping epitopes on PF4. In conclusion, 1E12 is a potentially important tool to study the pathophysiology of VITT, and for establishing mouse models. On the other hand, DG-1E12 may help the development of a new drug that specifically neutralizes the pathogenic effect of autoimmune anti-PF4 antibodies, such as those associated with VITT.
      PubDate: Thu, 07 Apr 2022 00:00:00 +000
  • Iron- and erythropoietin-resistant anemia in a spontaneous breast cancer
           mouse model

    • Authors: Nuria Fabregas Bregolat; Maja Ruetten, Milene Costa da Silva, Mostafa A. Aboouf, Hyrije Ademi, Nadine von Büren, Julia Armbruster, Martina Stirn, Sandro Altamura, Oriana Marques, Josep M. Monné Rodriguez, Victor J. Samillan, Rashim Pal Singh, Ben Wielockx, Martina U. Muckenthaler, Max Gassmann, Markus Thiersch
      Abstract: Anemia of cancer (AoC) with its multifactorial etiology and complex pathology is a poor prognostic indicator for cancer patients. One of the main causes of AoC is cancer-associated inflammation that activates mechanisms, commonly observed in anemia of inflammation, whereby functional iron deficiency and iron-restricted erythropoiesis are induced by increased hepcidin levels in response to raised levels of interleukin-6. So far only a few AoC mouse models have been described, and most of them did not fully recapitulate the interplay of anemia, increased hepcidin levels and functional iron deficiency in human patients. To test if the selection and the complexity of AoC mouse models dictates the pathology or if AoC in mice per se develops independently of iron deficiency, we characterized AoC in Trp53floxWapCre mice that spontaneously develop breast cancer. These mice developed AoC associated with high levels of interleukin-6 and iron deficiency. However, hepcidin levels were not increased and hypoferremia coincided with anemia rather than causing it. Instead, an early shift in the commitment of common myeloid progenitors from the erythroid to the myeloid lineage resulted in increased myelopoiesis and in the excessive production of neutrophils that accumulate in necrotic tumor regions. This process could not be prevented by either iron or erythropoietin treatment. Trp53floxWapCre mice are the first mouse model in which erythropoietin-resistant anemia is described and may serve as a disease model to test therapeutic approaches for a subpopulation of human cancer patients with normal or corrected iron levels who do not respond to erythropoietin.
      PubDate: Thu, 07 Apr 2022 00:00:00 +000
  • TAL1 cooperates with PI3K/AKT pathway activation in T-cell acute
           lymphoblastic leukemia

    • Authors: Naomi Thielemans; Sofie Demeyer, Nicole Mentens, Olga Gielen, Sarah Provost, Jan Cools
      Abstract: TAL1 is ectopically expressed in about 30% of T-cell acute lymphoblastic leukemia (T-ALL) due to chromosomal rearrangements leading to the STIL-TAL1 fusion genes or due to non-coding mutations leading to a de novo enhancer driving TAL1 expression. Analysis of sequence data from T-ALL cases demonstrates a significant association between TAL1 expression and activating mutations of the PI3K-AKT pathway. We investigated the oncogenic function of TAL1 and the possible cooperation with PI3K-AKT pathway activation using isogenic pro-T-cell cultures ex vivo and in vivo leukemia models. We found that TAL1 on its own suppressed T-cell growth, in part by affecting apoptosis genes, while the combination with AKT pathway activation reduced apoptosis and was strongly driving cell proliferation ex vivo and leukemia development in vivo. As a consequence, we found that TAL1+AKTE17K transformed cells are more sensitive to PI3K-AKT pathway inhibition compared to AKTE17K transformed cells, related to the negative effect of TAL1 in the absence of activated PI3K-AKT signaling. We also found that both TAL1 and PI3K-AKT signaling increased the DNA-repair signature in T cells resulting in synergy between PARP and PI3K-AKT pathway inhibition. In conclusion, we have developed a novel mouse model for TAL1+AKTE17K driven T-ALL development and have identified a vulnerability of these leukemia cells to PI3K-AKT and PARP inhibitors.
      PubDate: Thu, 31 Mar 2022 00:00:00 +000
  • Acute central nervous system toxicity during treatment of pediatric acute
           lymphoblastic leukemia: phenotypes, risk factors and genotypes

    • Authors: Stavroula Anastasopoulou; Rikke Linnemann Nielsen, Bodil Als-Nielsen, Joanna Banerjee, Mats A. Eriksson, Marianne Helenius, Mats M. Heyman, Inga Maria Johannsdottir, Olafur Gisli Jonsson, Stuart MacGregor, Marion K. Mateos, Chelsea Mayoh, Sirje Mikkel, Ida Hed Myrberg, Riitta Niinimäki, Kjeld Schmiegelow, Mervi Taskinen, Goda Vaitkeviciene, Anna Warnqvist, Benjamin Wolthers, Arja Harila-Saari, Susanna Ranta
      Abstract: Central nervous system (CNS) toxicity is common at diagnosis and during treatment of pediatric acute lymphoblastic leukemia (ALL). We studied CNS toxicity in 1,464 children aged 1.0–17.9 years, diagnosed with ALL and treated according to the Nordic Society of Pediatric Hematology and Oncology ALL2008 protocol. Genome-wide association studies, and a candidate single-nucleotide polymorphism (SNP; n=19) study were performed in 1,166 patients. Findings were validated in an independent Australian cohort of children with ALL (n=797) in whom two phenotypes were evaluated: diverse CNS toxicities (n=103) and methotrexate-related CNS toxicity (n=48). In total, 135/1,464 (9.2%) patients experienced CNS toxicity for a cumulative incidence of 8.7% (95% confidence interval: 7.31–10.20) at 12 months from diagnosis. Patients aged ≥10 years had a higher risk of CNS toxicity than had younger patients (16.3% vs. 7.4%; P<0.001). The most common CNS toxicities were posterior reversible encephalopathy syndrome (n=52, 43 with seizures), sinus venous thrombosis (n=28, 9 with seizures), and isolated seizures (n=16). The most significant SNP identified by the genome-wide association studies did not reach genomic significance (lowest P-value: 1.11x10-6), but several were annotated in genes regulating neuronal functions. In candidate SNP analysis, ATXN1 rs68082256, related to epilepsy, was associated with seizures in patients <10 years (P=0.01). ATXN1 rs68082256 was validated in the Australian cohort with diverse CNS toxicities (P=0.04). The role of ATXN1 as well as the novel SNP in neurotoxicity in pediatric ALL should be further explored.
      PubDate: Thu, 31 Mar 2022 00:00:00 +000
  • The glycolytic enzyme PFKFB3 determines bone marrow endothelial progenitor
           cell damage after chemotherapy and irradiation

    • Authors: Zhong-Shi Lyu; Shu-Qian Tang, Tong Xing, Yang Zhou, Meng Lv, Hai-Xia Fu, Yu Wang, Lan-Ping Xu, Xiao-Hui Zhang, Hsiang-Ying Lee, Yuan Kong, Xiao-Jun Huang
      Abstract: Bone marrow (BM) endothelial progenitor cell (EPC) damage of unknown mechanism delays the repair of endothelial cells (EC) and recovery of hematopoiesis after chemo-radiotherapy. We found increased levels of the glycolytic enzyme PFKFB3 in the damaged BM EPC of patients with poor graft function, a clinical model of EPC damage-associated poor hematopoiesis after allogeneic hematopoietic stem cell transplantation. Moreover, in vitro the glycolysis inhibitor 3-(3-pyridinyl)- 1-(4-pyridinyl)-2-propen-1-one (3PO) alleviated the damaged BM EPC from patients with poor graft function. Consistently, PFKFB3 overexpression triggered BM EPC damage after 5-fluorouracil treatment and impaired hematopoiesis-supporting ability in vitro. Mechanistically, PFKFB3 facilitated pro-apoptotic transcription factor FOXO3A and expression of its downstream genes, including p21, p27, and FAS, after 5-fluorouracil treatment in vitro. Moreover, PFKFB3 induced activation of NF-κB and expression of its downstream adhesion molecule E-selectin, while it reduced hematopoietic factor SDF-1 expression, which could be rescued by FOXO3A silencing. High expression of PFKFB3 was found in damaged BM EC of murine models of chemo-radiotherapy-induced myelosuppression. Furthermore, a murine model of BM EC-specific PFKFB3 overexpression demonstrated that PFKFB3 aggravated BM EC damage, and impaired the recovery of hematopoiesis after chemotherapy in vivo, effects which could be mitigated by 3PO, indicating a critical role of PFKFB3 in regulating BM EC damage. Clinically, PFKFB3-induced FOXO3A expression and NF-κB activation were confirmed to contribute to the damaged BM EPC of patients with acute leukemia after chemotherapy. 3PO repaired the damaged BM EPC by reducing FOXO3A expression and phospho-NF-κB p65 in patients after chemotherapy. In summary, our results reveal a critical role of PFKFB3 in triggering BM EPC damage and indicate that endothelial-PFKFB3 may be a potential therapeutic target for myelosuppressive injury.
      PubDate: Thu, 31 Mar 2022 00:00:00 +000
  • Preclinical evaluation and structural optimization of anti-BCMA CAR to
           target multiple myeloma

    • Authors: Ortal Harush; Nathalie Asherie, Shlomit Kfir-Erenfeld, Galit Adler, Tilda Barliya, Miri Assayag, Moshe E. Gatt, Polina Stepensky, Cyrille J. Cohen
      Abstract: Chimeric antigen receptor (CAR) T-cell based immunotherapy has become a promising treatment mainly for hematological malignancies. Following the major success of CD19-targeted CAR, new potential targets for other malignancies are required. As such, B-cell maturation antigen (BCMA) is an attractive tumor-associated antigen to be targeted in multiple myeloma (MM). Herein, we aimed at assessing the function and optimal configuration of different BCMA-specific CAR, based on the same targeting moiety but with a different hinge and co-stimulatory domain. We compared their function to that of a previously characterized BCMA-CAR used in clinical trials. All constructs were expressed at high levels by primary human T cells and could trigger cytokine production and cytotoxicity upon co-culture with multiple myeloma targets. Nonetheless, critical differences were observed in off-target activation, exhaustion, and activation marker expression and in vivo antitumoral activity mediated by these different constructs. Interestingly, we noted that CD8-based hinge, combined with a 4-1BB intracellular domain, proved superior compared to IgG4-connecting regions, and/or a CD28-signaling moiety respectively. Overall, this study emphasizes the influence of CAR primary structure on its function and led to the identification of a highly efficient BCMA-specific CAR, namely H8BB, which displayed superior anti-tumoral activity both in vitro and long-term in vivo efficacy.
      PubDate: Thu, 31 Mar 2022 00:00:00 +000
  • Final analysis of the phase III non-inferiority COLUMBA study of
           subcutaneous versus intravenous daratumumab in patients with relapsed or
           refractory multiple myeloma

    • Authors: Saad Z. Usmani; Hareth Nahi, Wojciech Legiec, Sebastian Grosicki, Vladimir Vorobyev, Ivan Spicka, Vania Hungria, Sibirina Korenkova, Nizar J. Bahlis, Max Flogegard, Joan Bladé, Philippe Moreau, Martin Kaiser, Shinsuke Iida, Jacob Laubach, Hila Magen, Michele Cavo, Cyrille Hulin, Darrell White, Valerio De Stefano, Kristen Lantz, Lisa O’Rourke, Christoph Heuck, Maria Delioukina, Xiang Qin, Ivo Nnane, Ming Qi, Maria-Victoria Mateos
      Abstract: In the primary analysis of the phase III COLUMBA study, daratumumab by subcutaneous administration (DARA SC) demonstrated non-inferiority to intravenous administration (DARA IV) for relapsed or refractory multiple myeloma (RRMM). Here, we report the final analysis of efficacy and safety from COLUMBA after a median of 29.3 months follow-up (additional 21.8 months after the primary analysis). In total, 522 patients were randomized (DARA SC, n=263; DARA IV, n=259). With longer follow-up, DARA SC and DARA IV continued to show consistent efficacy and maximum trough daratumumab concentration as compared with the primary analysis. The overall response rate was 43.7% for DARA SC and 39.8% for DARA IV. The maximum mean (standard deviation [SD]) trough concentration (cycle 3, day 1 pre-dose) of serum DARA was 581 (SD, 315) μg/mL for DARA SC and 496 (SD, 231) μg/mL for DARA IV. Median progression-free survival was 5.6 months for DARA SC and 6.1 months for DARA IV; median overall survival was 28.2 months and 25.6 months, respectively. Grade 3/4 treatment-emergent adverse events occurred in 50.8% of patients in the DARA SC group and 52.7% in the DARA IV group; the most common (≥10%) were thrombocytopenia (DARA SC, 14.2%; DARA IV, 13.6%), anemia (13.8%; 15.1%), and neutropenia (13.1%; 7.8%). The safety profile remained consistent with the primary analysis after longer follow-up. In summary, DARA SC and DARA IV continue to demonstrate similar efficacy and safety, with a low rate of infusion-related reactions (12.7% vs. 34.5%, respectively) and shorter administration time (3-5 minutes vs. 3-7 hours) supporting DARA SC as a preferable therapeutic choice. (Clinicaltrials gov. Identifier: NCT03277105.
      PubDate: Thu, 31 Mar 2022 00:00:00 +000
  • Fc galactosylation of anti-platelet human IgG1 alloantibodies enhances
           complement activation on platelets

    • Authors: Thijs L.J. van Osch; Janita J. Oosterhoff, Arthur E. H. Bentlage, Jan Nouta, Carolien A. M. Koeleman, Dionne M. Geerdes, Juk Yee Mok, Sebastiaan Heidt, Arend Mulder, Wim J. E. van Esch, Rick Kapur, Leendert Porcelijn, C. Ellen van der Schoot, Masja de Haas, Manfred Wuhrer, Jan Voorberg, Gestur Vidarsson
      Abstract: Approximately 20% of patients receiving multiple platelet transfusions develop platelet alloantibodies, which can be directed against human leukocyte antigens (HLA) and, to a lesser extent, against human platelet antigens (HPA). These antibodies can lead to the rapid clearance of donor platelets, presumably through IgG-Fc receptor (FcγR)-mediated phagocytosis or via complement activation, resulting in platelet refractoriness. Strikingly, not all patients with anti-HLA or -HPA antibodies develop platelet refractoriness upon unmatched platelet transfusions. Previously, we found that IgG Fc glycosylation of anti-HLA antibodies was highly variable between patients with platelet refractoriness, especially with respect to galactosylation and sialylation of the Fc-bound sugar moiety. Here, we produced recombinant glycoengineered anti-HLA and anti- HPA-1a monoclonal antibodies with varying Fc galactosylation and sialylation levels and studied their ability to activate the classical complement pathway. We observed that anti-HLA monoclonal antibodies with different specificities, binding simultaneously to the same HLA-molecules, or anti-HLA in combination with anti-HPA-1a monoclonal antibodies interacted synergistically with C1q, the first component of the classical pathway. Elevated Fc galactosylation and, to a lesser extent, sialylation significantly increased the complement-activating properties of anti-HLA and anti-HPA-1a monoclonal antibodies. We propose that both the breadth of the polyclonal immune response, with recognition of different HLA epitopes and in some cases HPA antigens, and the type of Fc glycosylation can provide an optimal stoichiometry for C1q binding and subsequent complement activation. These factors can shift the effect of a platelet alloimmune response to a clinically relevant response, leading to complement-mediated clearance of donor platelets, as observed in platelet refractoriness.
      PubDate: Thu, 31 Mar 2022 00:00:00 +000
  • A self-assembled leucine polymer sensitizes leukemic stem cells to
           chemotherapy by inhibiting autophagy in acute myeloid leukemia

    • Authors: Xi Xu; Jian Wang, Tong Tong, Wenwen Zhang, Jin Wang, Weiwei Ma, Shunqing Wang, Dunhua Zhou, Jun Wu, Linjia Jiang, Meng Zhao
      Abstract: Chemotherapy is the primary treatment option for acute myeloid leukemia (AML), but leukemic stem cells (LSC) can survive chemotherapy for disease recurrence and refractory. Here, we found that AML cells obtained from relapsed patients had increased autophagy levels than de novo AML cells. Furthermore, doxorubicin (DOX) treatment stimulated autophagy in LSC by repressing the mTOR pathway, and pharmaceutical inhibition of autophagy rendered chemoresistant LSC sensitive to DOX treatment in MLL-AF9 induced murine AML. Moreover, we developed a self-assembled leucine polymer, which activated mTOR to inhibit autophagy in AML cells by releasing leucine. The leucine polymer loaded DOX (Leu-DOX) induced much less autophagy but more robust apoptosis in AML cells than the DOX treatment. Notably, the leucine polymer and Leu-DOX were specifically taken up by AML cells and LSC but not by normal hematopoietic cells and hematopoietic stem/progenitor cells in the bone marrow. Consequently, Leu-DOX efficiently reduced LSC and prolonged the survival of AML mice, with more limited myeloablation and tissue damage side effects than DOX treatment. Overall, we proposed that the newly developed Leu-DOX is an effective autophagy inhibitor and an ideal drug to efficiently eliminate LSC, thus serving as a revolutionary strategy to enhance the chemotherapy efficacy in AML.
      PubDate: Thu, 17 Mar 2022 00:00:00 +000
  • YTHDF3 as a new player in hematopoietic stem cell regulation

    • Authors: Xinjian Mao; Linheng Li
      PubDate: Thu, 03 Feb 2022 00:00:00 +000
  • How do mTOR inhibitors fit in the landscape of treatment for relapsed
           acute lymphoblastic leukemia'

    • Authors: Ashley Pinchinat; Elizabeth Raetz
      PubDate: Thu, 03 Feb 2022 00:00:00 +000
  • Temsirolimus combined with cyclophosphamide and etoposide for pediatric
           patients with relapsed/refractory acute lymphoblastic leukemia: a
           Therapeutic Advances in Childhood Leukemia Consortium trial (TACL

    • Authors: Sarah K. Tasian; Lewis B. Silverman, James A. Whitlock, Richard Sposto, Joseph P. Loftus, Eric S. Schafer, Kirk R. Schultz, Raymond J. Hutchinson, Paul S. Gaynon, Etan Orgel, Caroline M. Bateman, Todd M. Cooper, Theodore W. Laetsch, Maria Luisa Sulis, Yueh-Yun Chi, Jemily Malvar, Alan S. Wayne, Susan R. Rheingold
      Abstract: Phosphatidylinositol 3-kinase (PI3K)/mammalian target of rapamycin (mTOR) signaling is commonly dysregulated in acute lymphoblastic leukemia (ALL). The TACL2014-001 phase I trial of the mTOR inhibitor temsirolimus in combination with cyclophosphamide and etoposide was performed in children and adolescents with relapsed/refractory ALL. Temsirolimus was administered intravenously (IV) on days 1 and 8 with cyclophosphamide 440 mg/m2 and etoposide 100 mg/m2 IV daily on days 1-5. The starting dose of temsirolimus was 7.5 mg/m2 (DL1) with escalation to 10 mg/m2 (DL2), 15 mg/m2 (DL3), and 25 mg/m2 (DL4). PI3K/mTOR pathway inhibition was measured by phosphoflow cytometry analysis of peripheral blood specimens from treated patients. Sixteen heavily-pretreated patients were enrolled with 15 evaluable for toxicity. One dose-limiting toxicity of grade 4 pleural and pericardial effusions occurred in a patient treated at DL3. Additional dose-limiting toxicities were not seen in the DL3 expansion or DL4 cohort. Grade 3/4 non-hematologic toxicities occurring in three or more patients included febrile neutropenia, elevated alanine aminotransferase, hypokalemia, mucositis, and tumor lysis syndrome and occurred across all doses. Response and complete were observed at all dose levels with a 47% overall response rate and 27% complete response rate. Pharmacodynamic correlative studies demonstrated dose-dependent inhibition of PI3K/mTOR pathway phosphoproteins in all studied patients. Temsirolimus at doses up to 25 mg/m2 with cyclophosphamide and etoposide had an acceptable safety profile in children with relapsed/refractory ALL. Pharmacodynamic mTOR target inhibition was achieved and appeared to correlate with temsirolimus dose. Future testing of next-generation PI3K/mTOR pathway inhibitors with chemotherapy may be warranted to increase response rates in children with relapsed/refractory ALL.
      PubDate: Thu, 03 Feb 2022 00:00:00 +000
  • YTHDF3 modulates hematopoietic stem cells by recognizing RNA m6A
           modification on Ccnd1

    • Authors: Xiaofei Zhang; Tingting Cong, Lei Wei, Bixi Zhong, Xiaowo Wang, Jin Sun, Shuxia Wang, Meng Michelle Xu, Ping Zhu, Hong Jiang, Jianwei Wang
      Abstract: Hematopoietic stem cells (HSC) give rise to the cells of the blood system over the whole lifespan. N6-methyladenosine (m6A), the most prevalent RNA modification, modulates gene expression via the processes of “writing” and “reading”. Recent studies showed that m6A “writer” genes (Mettl3 and Mettl14) play an essential role in HSC. However, which reader deciphers the m6A modification to modulate HSC remains unknown. In this study, we observed that dysfunction of Ythdf3 and Ccnd1 severely impaired the reconstitution capacity of HSC, which phenocopies Mettl3-deficient HSC. Dysfunction of Ythdf3 and Mettl3 results in a translational defect of Ccnd1. Ythdf3 and Mettl3 regulate HSC by transmitting m6A RNA methylation on the 5’ untranslated region of Ccnd1. Enforced Ccnd1 expression completely rescued the defect of Ythdf3-/- HSC and partially rescued Mettl3-compromised HSC. Taken together, this study identified, for the first time, that Ccnd1 is the target of METTL3 and YTHDF3 to transmit the m6A RNA methylation signal and thereby regulate the reconstitution capacity of HSC.
      PubDate: Thu, 03 Feb 2022 00:00:00 +000
  • Proteomics: a new era in pediatric acute myeloid leukemia research

    • Authors: Jatinder K. Lamba; Stanley Pounds
      PubDate: Thu, 13 Jan 2022 00:00:00 +000
  • Clinical relevance of proteomic profiling in de novo pediatric acute
           myeloid leukemia: a Children’s Oncology Group study

    • Authors: Fieke W. Hoff; Anneke D. van Dijk, Yihua Qiu, Chenyue W. Hu, Rhonda E. Ries, Andrew Ligeralde, Gaye N. Jenkins, Robert B. Gerbing, Alan S. Gamis, Richard Aplenc, E. Anders Kolb, Todd A. Alonzo, Soheil Meshinchi, Amina A. Qutub, Eveline S.J.M. de Bont, Terzah M. Horton, Steven M. Kornblau
      Abstract: Pediatric acute myeloid leukemia (AML) remains a fatal disease for at least 30% of patients, stressing the need for improved therapies and better risk stratification. As proteins are the unifying feature of (epi)genetic and environmental alterations, and are often targeted by novel chemotherapeutic agents, we studied the proteomic landscape of pediatric AML. Protein expression and activation levels were measured in 500 bulk leukemic patients’ samples and 30 control CD34+ cell samples, using reverse phase protein arrays with 296 strictly validated antibodies. The multistep MetaGalaxy analysis methodology was applied and identified nine protein expression signatures (PrSIG), based on strong recurrent protein expression patterns. PrSIG were associated with cytogenetics and mutational state, and with favorable or unfavorable prognosis. Analysis based on treatment (i.e., ADE vs. ADE plus bortezomib) identified three PrSIG that did better with ADE plus bortezomib than with ADE alone. When PrSIG were studied in the context of cytogenetic risk groups, PrSIG were independently prognostic after multivariate analysis, suggesting a potential value for proteomics in combination with current classification systems. Proteins with universally increased (n=7) or decreased (n=17) expression were observed across PrSIG. Certain proteins significantly differentially expressed from normal could be identified, forming a hypothetical platform for personalized medicine.
      PubDate: Thu, 13 Jan 2022 00:00:00 +000
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