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acute leukemia pathophysiology

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https://www.readbyqxmd.com/read/28239141/chronic-myeloid-leukemia-associated-hypercalcemia-a-case-report-and-literature-review
#1
David Toro-Tobón, Sarimar Agosto, Sara Ahmadi, Maureen Koops, Jan M Bruder
BACKGROUND Hypercalcemia associated with chronic myeloid leukemia (CML) is an ominous sign. Although rare, several cases have been reported and multiple pathophysiologic mechanisms have been independently proposed. We present a patient case and a literature review of the clinical presentation and mechanisms of CML-associated hypercalcemia. CASE REPORT A 58-year-old male with a past medical history of CML diagnosed six years earlier, presented to the emergency department with one week of acute confusion, disorientation, polyuria, and polydipsia...
February 27, 2017: American Journal of Case Reports
https://www.readbyqxmd.com/read/28154779/molecular-landscape-in-acute-myeloid-leukemia-where-do-we-stand-in-2016
#2
Karam Al-Issa, Aziz Nazha
Acute myeloid leukemia (AML) is a clonal disorder characterized by the accumulation of complex genomic alterations that define the disease pathophysiology and overall outcome. Recent advances in sequencing technologies have described the molecular landscape of AML and identified several somatic alterations that impact overall survival. Despite all these advancement, several challenges remain in translating this information into effective therapy. Herein we will review the molecular landscape of AML and discuss the impact of the most common somatic mutations on disease biology and outcome...
December 2016: Cancer Biology & Medicine
https://www.readbyqxmd.com/read/28122581/acute-myeloid-leukemia-strategies-and-challenges-for-targeting-oncogenic-hedgehog-gli-signaling
#3
REVIEW
Fritz Aberger, Evelyn Hutterer, Christina Sternberg, Pedro J Del Burgo, Tanja N Hartmann
Treatment of acute myeloid leukemia (AML), an aggressive and heterogeneous hematological malignancy, remains a challenge. Despite advances in our understanding of the complex genetics and biology of AML pathophysiology, these findings have been translated to the clinic with only limited success, and poor outcomes persist for the majority of patients. Thus, novel treatment strategies are clearly needed for achieving deeper and prolonged remissions and for avoiding the development of resistance. Due to its profound role in (cancer) stem cell biology and differentiation, the Hedgehog (HH)/Glioma-associated Oncogene Homolog (GLI) signaling pathway may be an attractive novel therapeutic target in AML...
January 25, 2017: Cell Communication and Signaling: CCS
https://www.readbyqxmd.com/read/28090484/mesenchymal-stromal-cells-in-myeloid-malignancies
#4
REVIEW
Thomas Schroeder, Stefanie Geyh, Ulrich Germing, Rainer Haas
Myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) are clonal myeloid disorders characterized by hematopoietic insufficiency. As MDS and AML are considered to originate from genetic and molecular defects of hematopoietic stem and progenitor cells (HSPC), the main focus of research in this field has focused on the characterization of these cells. Recently, the contribution of BM microenvironment to the pathogenesis of myeloid malignancies, in particular MDS and AML has gained more interest. This is based on a better understanding of its physiological role in the regulation of hematopoiesis...
December 2016: Blood Research
https://www.readbyqxmd.com/read/28060109/posterior-reversible-encephalopathy-syndrome-and-cerebral-sinus-thrombosis-in-a-case-of-pediatric-b-cell-all
#5
Ellen Fraint, Robin Miller, Andrew Walter
Posterior reversible encephalopathy syndrome (PRES) and cerebral sinus thrombosis are 2 known complications of acute lymphoblastic leukemia and its treatment. We describe a patient with acute lymphoblastic leukemia whose course was complicated by both of these conditions. This case is novel both for the fact that PRES developed before the initiation of therapy and that PRES was followed shortly by the development of cerebral sinus thrombosis. Our patient's story raises questions about our current understanding of the pathophysiology of PRES, and it suggests that PRES may actually be a predisposing risk factor for cerebral sinus thrombosis...
March 2017: Journal of Pediatric Hematology/oncology
https://www.readbyqxmd.com/read/28013226/disseminated-intravascular-coagulation
#6
REVIEW
Benjamin M Boral, Dennis J Williams, Leonard I Boral
OBJECTIVES: To provide a review of the definition, pathophysiology, differential diagnosis, and treatment of disseminated intravascular coagulation (DIC). METHODS: A case scenario and a review of the literature related to the pertinent facts concerning DIC are provided. RESULTS: DIC is a systemic pathophysiologic process and not a single disease entity, resulting from an overwhelming activation of coagulation that consumes platelets and coagulation factors and causes microvascular fibrin thrombi, which can result in multiorgan dysfunction syndrome from tissue ischemia...
December 2016: American Journal of Clinical Pathology
https://www.readbyqxmd.com/read/28008177/mass-cytometry-analysis-reveals-hyperactive-nf-kappa-b-signaling-in-myelofibrosis-and-secondary-acute-myeloid-leukemia
#7
D A C Fisher, O Malkova, E K Engle, C A Miner, M C Fulbright, G K Behbehani, T B Collins, S Bandyopadhyay, A Zhou, G P Nolan, S T Oh
Myeloproliferative neoplasms (MPNs) feature a malignant clone containing the JAK2 V617F mutation, or another mutation causing dysregulated JAK2 kinase activity. The multiple disease phenotypes of MPNs, and their tendency to transform phenotypically, suggest pathophysiologic heterogeneities beyond a common phenomenon of JAK2 hyperactivation. JAK2 has the potential to activate multiple other signaling molecules, either directly through downstream effectors, or indirectly through induction of target gene expression...
February 3, 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/27913501/mutations-in-aml-prognostic-and-therapeutic-implications
#8
Courtney D DiNardo, Jorge E Cortes
Acute myeloid leukemia (AML) is a heterogeneous hematologic malignancy characterized by the proliferation and aberrant differentiation of immature clonal myeloid cells. The prognosis of AML is variable, based on clinical features such as patient age, performance status, and comorbidities, as well as leukemia-specific genetic features including cytogenetics and molecular classification. The modern application of next-generation sequencing technology has uncovered marked heterogeneity and genomic complexity within AML, based on the presence or absence of cooperating mutations within functional categories such as epigenetic regulators, cell signaling and proliferation pathways, and master hematopoietic transcription factors...
December 2, 2016: Hematology—the Education Program of the American Society of Hematology
https://www.readbyqxmd.com/read/27848185/pediatric-intestinal-beh%C3%A3-et-disease-complicated-by-myeloid-malignancies
#9
Kiichiro Kanamitsu, Akira Shimada, Ritsuo Nishiuchi, Tomonari Shigemura, Yozo Nakazawa, Kenichi Koike, Yuichi Kodama, Yuichi Shinkoda, Yoshifumi Kawano, Kozo Yasui, Koji Sasaki, Ryosuke Kajiwara, Hirokazu Tsukahara, Atsushi Manabe
Behçet disease (BD) is rarely seen in children. Its clinical manifestations are believed to differ between pediatric and adult patients. The characteristics of BD complicated by myelodysplastic syndrome (MDS) are well established for adult patients; however, because only a few cases of pediatric-onset BD complicated by MDS have been reported, its clinical characteristics remain unknown. We here retrospectively review pediatric-onset BD complicated by myeloid malignancies in Japan, having identified five such patients...
November 15, 2016: International Journal of Hematology
https://www.readbyqxmd.com/read/27756750/the-emt-regulator-zeb2-is-a-novel-dependency-of-human-and-murine-acute-myeloid-leukemia
#10
Hubo Li, Brenton G Mar, Huadi Zhang, Rishi V Puram, Francisca Vazquez, Barbara A Weir, William C Hahn, Benjamin Ebert, David Pellman
Acute myeloid leukemia (AML) is a heterogeneous disease with complex molecular pathophysiology. To systematically characterize AML's genetic dependencies, we conducted genome-scale short hairpin RNA screens in 17 AML cell lines and analyzed dependencies relative to parallel screens in 199 cell lines of other cancer types. We identified 353 genes specifically required for AML cell proliferation. To validate the in vivo relevance of genetic dependencies observed in human cell lines, we performed a secondary screen in a syngeneic murine AML model driven by the MLL-AF9 oncogenic fusion protein...
January 26, 2017: Blood
https://www.readbyqxmd.com/read/27752467/novel-therapeutic-options-in-acute-myeloid-leukemia
#11
REVIEW
Michael Medinger, Claudia Lengerke, Jakob Passweg
Acute myeloid leukemia (AML) is a biologically complex and molecularly and clinically heterogeneous disease, and its incidence is increasing as the population ages. Cytogenetic anomalies and mutation testing remain important prognostic tools for tailoring treatment after induction therapy. Despite major advances in understanding the genetic landscape of AML and its impact on the pathophysiology and biology of the disease, as well as the rapid development of new drugs, standard treatment options have not experienced major changes during the past three decades...
2016: Leukemia Research Reports
https://www.readbyqxmd.com/read/27725595/pathophysiology-of-mds-genomic-aberrations
#12
Motoshi Ichikawa
Myelodysplastic syndromes (MDS) are characterized by clonal proliferation of hematopoietic stem/progenitor cells and their apoptosis, and show a propensity to progress to acute myelogenous leukemia (AML). Although MDS are recognized as neoplastic diseases caused by genomic aberrations of hematopoietic cells, the details of the genetic abnormalities underlying disease development have not as yet been fully elucidated due to difficulties in analyzing chromosomal abnormalities. Recent advances in comprehensive analyses of disease genomes including whole-genome sequencing technologies have revealed the genomic abnormalities in MDS...
2016: [Rinshō Ketsueki] the Japanese Journal of Clinical Hematology
https://www.readbyqxmd.com/read/27697023/genetic-and-epigenetic-drug-targets-in-myelodysplastic-syndromes
#13
Karmen Stankov, Sunčica Stankov, Jasmina Katanić
BACKGROUND: Myelodysplastic syndromes (MDS) represent a heterogeneous group of clonal disorders of hematopoietic system, characterized by genetic, epigenetic or microenvironmental alterations of aging hematopoietic stem cells. Pathophysiology of MDS comprises the suppression of normal hematopoiesis and reduced myeloid progenitor cells differentiation, with the main consequence of peripheral cytopenias and increased risk to evolution in acute myeloid leukemia (AML). METHOD: This review summarizes the evolving understanding of the role of genetic and epigenetic alterations involved in pathogenesis and current and future strategies for therapeutic targeting in myelodysplastic syndromes...
October 3, 2016: Current Pharmaceutical Design
https://www.readbyqxmd.com/read/27639498/molecular-biomarkers-in-acute-myeloid-leukemia
#14
REVIEW
Jeanette Prada-Arismendy, Johanna C Arroyave, Sarah Röthlisberger
Acute myeloid leukemia (AML) is the most common acute leukemia in adults. The pathophysiology of this disease is just beginning to be understood at the cellular and molecular level, and currently cytogenetic markers are the most important for risk stratification and treatment of AML patients. However, with the advent of new technologies, the detection of other molecular markers such as point mutations and characterization of epigenetic and proteomic profiles, have begun to play an important role in how the disease is approached...
January 2017: Blood Reviews
https://www.readbyqxmd.com/read/27622049/the-immune-receptor-tim-3-acts-as-a-trafficker-in-a-tim-3-galectin-9-autocrine-loop-in-human-myeloid-leukemia-cells
#15
Isabel Gonçalves Silva, Laura Rüegg, Bernhard F Gibbs, Marco Bardelli, Alexander Fruehwirth, Luca Varani, Steffen M Berger, Elizaveta Fasler-Kan, Vadim V Sumbayev
The immune receptor Tim-3 is often highly expressed in human acute myeloid leukemia (AML) cells where it acts as a growth factor and inflammatory receptor. Recently, it has been demonstrated that Tim-3 forms an autocrine loop with its natural ligand galectin-9 in human AML cells. However, the pathophysiological functions of Tim-3 in human AML cells remain unclear. Here, we report for the first time that Tim-3 is required for galectin-9 secretion in human AML cells. However, this effect is cell-type specific and was found so far to be applicable only to myeloid (and not, for example, lymphoid) leukemia cells...
July 2016: Oncoimmunology
https://www.readbyqxmd.com/read/27595359/leukemia
#16
Gunnar Juliusson, Rachael Hough
Leukemias are a group of life threatening malignant disorders of the blood and bone marrow. In the adolescent and young adult (AYA) population, the acute leukemias are most prevalent, with chronic myeloid leukemia being infrequently seen. Factors associated with more aggressive disease biology tend to increase in frequency with increasing age, whilst tolerability of treatment strategies decreases. There are also challenges regarding the effective delivery of therapy specific to the AYA group, consequences on the unique psychosocial needs of this age group, including compliance...
2016: Progress in Tumor Research
https://www.readbyqxmd.com/read/27566651/novel-prognostic-and-therapeutic-mutations-in-acute-myeloid-leukemia
#17
REVIEW
Michael Medinger, Claudia Lengerke, Jakob Passweg
Acute myeloid leukemia (AML) is a biologically complex and molecularly and clinically heterogeneous disease, and its incidence increases with age. Cytogenetics and mutation testing remain important prognostic tools for treatment after induction therapy. The post-induction treatment is dependent on risk stratification. Despite rapid advances in determination of gene mutations involved in the pathophysiology and biology of AML, and the rapid development of new drugs, treatment improvements changed slowly over the past 30 years, with the majority of patients eventually experiencing relapse and dying of their disease...
September 2016: Cancer Genomics & Proteomics
https://www.readbyqxmd.com/read/27556667/diffuse-alveolar-hemorrhage-in-acute-myeloid-leukemia
#18
Sowmya Nanjappa, Daniel K Jeong, Manjunath Muddaraju, Katherine Jeong, Ebone D Hill, John N Greene
Diffuse alveolar hemorrhage is a potentially fatal pulmonary disease syndrome that affects individuals with hematological and nonhematological malignancies. The range of inciting factors is wide for this syndrome and includes thrombocytopenia, underlying infection, coagulopathy, and the frequent use of anticoagulants, given the high incidence of venous thrombosis in this population. Dyspnea, fever, and cough are commonly presenting symptoms. However, clinical manifestations can be variable. Obvious bleeding (hemoptysis) is not always present and can pose a potential diagnostic challenge...
July 2016: Cancer Control: Journal of the Moffitt Cancer Center
https://www.readbyqxmd.com/read/27556501/ralb-provides-critical-survival-signals-downstream-of-ras-in-acute-myeloid-leukemia
#19
Craig E Eckfeldt, Emily J Pomeroy, Robin D W Lee, Katherine S Hazen, Lindsey A Lee, Branden S Moriarity, David A Largaespada
Mutations that activate RAS proto-oncogenes and their effectors are common in acute myeloid leukemia (AML); however, efforts to therapeutically target Ras or its effectors have been unsuccessful, and have been hampered by an incomplete understanding of which effectors are required for AML proliferation and survival. We investigated the role of Ras effector pathways in AML using murine and human AML models. Whereas genetic disruption of NRAS(V12) expression in an NRAS(V12) and Mll-AF9-driven murine AML induced apoptosis of leukemic cells, inhibition of phosphatidylinositol-3-kinase (PI3K) and/or mitogen-activated protein kinase (MAPK) signaling did not reproduce this effect...
4, 2016: Oncotarget
https://www.readbyqxmd.com/read/27531677/hyperfibrinolysis-increases-blood-brain-barrier-permeability-by-a-plasmin-and-bradykinin-dependent-mechanism
#20
Oscar A Marcos-Contreras, Sara Martinez de Lizarrondo, Isabelle Bardou, Cyrille Orset, Mathilde Pruvost, Antoine Anfray, Yvann Frigout, Yannick Hommet, Laurent Lebouvier, Joan Montaner, Denis Vivien, Maxime Gauberti
Hyperfibrinolysis is a systemic condition occurring in various clinical disorders such as trauma, liver cirrhosis, and leukemia. Apart from increased bleeding tendency, the pathophysiological consequences of hyperfibrinolysis remain largely unknown. Our aim was to develop an experimental model of hyperfibrinolysis and to study its effects on the homeostasis of the blood-brain barrier (BBB). We induced a sustained hyperfibrinolytic state in mice by hydrodynamic transfection of a plasmid encoding for tissue-type plasminogen activator (tPA)...
November 17, 2016: Blood
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