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1. Gérard J, Berdin B, Portier G, Godon A, Tessier-Marteau A, Geneviève F, Zandecki M: [Bone marrow necrosis in two patients with neoplastic disorders]. Ann Biol Clin (Paris); 2007 Nov-Dec;65(6):636-42
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  • Diagnosis is done on characteristic cytological pattern of the bone marrow aspiration and/or biopsy.
  • An haematological malignancy was suspected after observation of a few peripheral blood blast cells, but necrosis was found on the bone marrow aspiration and could not lead to further haematological diagnosis.
  • Within next days, the white blood cell count and the number of blasts increased, leading to the diagnosis of acute monoblastic leukaemia.
  • The second patient, aged 28, has been hospitalized for severe bleeding a few days after the diagnosis of a metastatic gastric tumour.
  • According to literature, bone marrow necrosis is in most instances secondary to either an haematological malignancy (60%) or to a solid tumour (30%), but only at times observed with a non-malignant disorder.
  • Bone pain, fever, cytopenias and elevated serum lactic dehydrogenase and alkaline phosphatase are frequently reported, but are mostly non specific of the diagnosis in these malignant conditions.
  • Examination of the bone marrow leads to the diagnosis: cells are pycnotic, scarcely recognizable in a background of amorphous extracellular eosinophilic proteinaceous material, and histology shows disappearance of fat spaces with preservation of the bone tissue.
  • Tissue hypoxemia due to microcirculation failure may be the main mechanism leading to the necrosis, whatever the related disorder.
  • Supportive care together with specific therapy of the causal disease must be started promptly.
  • [MeSH-major] Bone Marrow / pathology. Leukemia, Monocytic, Acute / pathology. Stomach Neoplasms / pathology

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  • (PMID = 18039608.001).
  • [ISSN] 0003-3898
  • [Journal-full-title] Annales de biologie clinique
  • [ISO-abbreviation] Ann. Biol. Clin. (Paris)
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
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2. Yang J, Ikezoe T, Nishioka C, Tasaka T, Taniguchi A, Kuwayama Y, Komatsu N, Bandobashi K, Togitani K, Koeffler HP, Taguchi H, Yokoyama A: AZD1152, a novel and selective aurora B kinase inhibitor, induces growth arrest, apoptosis, and sensitization for tubulin depolymerizing agent or topoisomerase II inhibitor in human acute leukemia cells in vitro and in vivo. Blood; 2007 Sep 15;110(6):2034-40
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  • [Title] AZD1152, a novel and selective aurora B kinase inhibitor, induces growth arrest, apoptosis, and sensitization for tubulin depolymerizing agent or topoisomerase II inhibitor in human acute leukemia cells in vitro and in vivo.
  • We have recently shown that hematopoietic malignant cells including those from acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) aberrantly expressed Aurora A and B kinases, and ZM447439, a potent inhibitor of Aurora kinases, effectively induced growth arrest and apoptosis of a variety of leukemia cells.
  • The present study explored the effect of AZD1152, a highly selective inhibitor of Aurora B kinase, on various types of human leukemia cells.
  • AZD1152 inhibited the proliferation of AML lines (HL-60, NB4, MOLM13), ALL line (PALL-2), biphenotypic leukemia (MV4-11), acute eosinophilic leukemia (EOL-1), and the blast crisis of chronic myeloid leukemia K562 cells with an IC50 ranging from 3 nM to 40 nM, as measured by thymidine uptake on day 2 of culture.
  • Taken together, AZD1152 is a promising new agent for treatment of individuals with leukemia.
  • The combined administration of AZD1152 and conventional chemotherapeutic agent to patients with leukemia warrants further investigation.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Apoptosis / drug effects. Cell Proliferation / drug effects. Leukemia / drug therapy. Organophosphates / pharmacology. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Quinazolines / pharmacology. Tubulin Modulators / pharmacology

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  • Guide to Pharmacology. gene/protein/disease-specific - Aurora kinase (Aur) family - overview and references .
  • Guide to Pharmacology. gene/protein/disease-specific - aurora kinase A - data and references .
  • Guide to Pharmacology. gene/protein/disease-specific - aurora kinase B - data and references .
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  • (PMID = 17495131.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-((3-((4-((5-(2-((3-fluorophenyl)amino)-2-oxoethyl)-1H-pyrazol-3-yl)amino)quinazolin-7-yl)oxy)propyl)(ethyl)amino)ethyl dihydrogen phosphate; 0 / Antibiotics, Antineoplastic; 0 / Enzyme Inhibitors; 0 / Organophosphates; 0 / Quinazolines; 0 / Tubulin Modulators; 5J49Q6B70F / Vincristine; EC 2.7.11.1 / AURKB protein, human; EC 2.7.11.1 / Aurka protein, mouse; EC 2.7.11.1 / Aurkb protein, mouse; EC 2.7.11.1 / Aurora Kinase A; EC 2.7.11.1 / Aurora Kinase B; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; VC2W18DGKR / Thymidine; ZS7284E0ZP / Daunorubicin
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3. Schaffer JV, McNiff JM, Seropian S, Cooper DL, Bolognia JL: Lichen sclerosus and eosinophilic fasciitis as manifestations of chronic graft-versus-host disease: expanding the sclerodermoid spectrum. J Am Acad Dermatol; 2005 Oct;53(4):591-601
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  • [Title] Lichen sclerosus and eosinophilic fasciitis as manifestations of chronic graft-versus-host disease: expanding the sclerodermoid spectrum.
  • Chronic cutaneous graft-versus-host disease (GVHD) is classically divided into two major clinical categories--lichenoid and sclerodermoid.
  • Eosinophilic fasciitis (EF) (a fibrosing disorder related to deep morphea) and lichen sclerosus (LS) have also been reported as manifestations of sclerodermoid GVHD.
  • EF involved the extremities (sparing the hands and feet), and was characterized clinically by an acute onset of pain and edema followed by induration with a rippled appearance.
  • [MeSH-major] Eosinophilia / etiology. Fasciitis / etiology. Graft vs Host Disease / complications. Lichen Sclerosus et Atrophicus / etiology
  • [MeSH-minor] Adult. Chronic Disease. Female. Humans. Leukemia, Myeloid, Acute / surgery. Lymphoma, Large B-Cell, Diffuse / surgery. Magnetic Resonance Imaging. Male. Middle Aged. Remission Induction. Stem Cell Transplantation


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4. Tefferi A, Gilliland G: Classification of chronic myeloid disorders: from Dameshek towards a semi-molecular system. Best Pract Res Clin Haematol; 2006;19(3):365-85

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  • In turn, myeloid malignancies are broadly categorized into either acute myeloid leukemia (AML) or chronic myeloid disorder (CMD), depending on the presence or absence, respectively, of AML-defining cytomorphologic and cytogenetic features.
  • It has now become evident that most CMD represent clonal stem cell processes where the primary oncogenic event has been characterized in certain instances; Bcr/Abl in chronic myeloid leukemia, FIP1L1-PDGFRA or c-kit(D816V) in systemic mastocytosis, rearrangements of PDGFRB in chronic eosinophilic leukemia, and rearrangements of FGFR1 in stem cell leukemia/lymphoma syndrome.
  • In addition, Bcr/Abl-negative classic myeloproliferative disorders are characterized by recurrent JAK2(V617F) mutations, whereas other mutations affecting the RAS signaling pathway molecules have been associated with juvenile myelomonocytic leukemia.
  • [MeSH-minor] Fusion Proteins, bcr-abl / genetics. Genes, abl. Humans. Janus Kinase 2. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / classification. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Myelodysplastic Syndromes / classification. Myelodysplastic Syndromes / genetics. Protein-Tyrosine Kinases / genetics. Proto-Oncogene Proteins / genetics. Receptor, Platelet-Derived Growth Factor beta / genetics

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  • (PMID = 16781478.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  • [Number-of-references] 232
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5. Goiriz R, Guhl-Millán G, Peñas PF, Fernández-Herrera J, Daudén E, Fraga J, García-Diez A: Eosinophilic folliculitis following allogeneic peripheral blood stem cell transplantation: case report and review. J Cutan Pathol; 2007 Dec;34 Suppl 1:33-6
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  • [Title] Eosinophilic folliculitis following allogeneic peripheral blood stem cell transplantation: case report and review.
  • Eosinophilic folliculitis is considered a heterogeneous group of disorders, with several clinical subsets, sharing a common histopathological appearance.
  • We herein present a case of eosinophilic folliculitis that appeared in a 26-year-old woman 5 months after allogeneic peripheral blood stem cell transplantation as treatment for eosinophilic acute leukemia.
  • Our review of the published cases has shown that eosinophilic folliculitis in patients after BMT could be considered as a pattern of reaction related to immune dysregulation.
  • [MeSH-minor] Adult. Anti-Inflammatory Agents / therapeutic use. Female. Humans. Leukemia, Eosinophilic, Acute / therapy. Prednisone / therapeutic use. Transplantation, Homologous. Treatment Outcome

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  • (PMID = 17997736.001).
  • [ISSN] 1600-0560
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; VB0R961HZT / Prednisone
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6. Roufosse F, Goldman M, Cogan E: Hypereosinophilic syndrome: lymphoproliferative and myeloproliferative variants. Semin Respir Crit Care Med; 2006 Apr;27(2):158-70
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  • Idiopathic hypereosinophilic syndrome is a largely heterogeneous disorder defined as persistent, marked hypereosinophilia of unknown origin complicated by end-organ damage.
  • As far as prognosis of these disease variants is concerned, hypereosinophilic syndrome patients with the FIP1L1-PDGFRalpha fusion gene may develop acute myelogenous (eosinophilic) leukemia, whereas those with clonal interleukin-5-producing T-cells have an increased risk of developing T-cell lymphoma.
  • [MeSH-major] Hypereosinophilic Syndrome / classification. Hypereosinophilic Syndrome / diagnosis. Lymphoproliferative Disorders / diagnosis. Myeloproliferative Disorders / diagnosis

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  • (PMID = 16612767.001).
  • [ISSN] 1069-3424
  • [Journal-full-title] Seminars in respiratory and critical care medicine
  • [ISO-abbreviation] Semin Respir Crit Care Med
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / CD52 antigen; 0 / FIP1L1-PDGFRA fusion protein, human; 0 / Glucocorticoids; 0 / Glycoproteins; 0 / Immunologic Factors; 0 / Interleukin-5; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 0 / mRNA Cleavage and Polyadenylation Factors; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
  • [Number-of-references] 70
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