scholarly journals Molecular stratifications of Myeloproliferative Neoplasms according to WHO 2008 classification for hematopoietic and lymphoid tissues (experience from Qatar).

2016 ◽  
Vol 13 (2) ◽  
Author(s):  
Mohamed A Yassin
Keyword(s):  
Myeloproliferative Neoplasms ◽  
Lymphoid Tissues ◽  
Who 2008

Myelodysplastic/Myeloproliferative Neoplasms

Hematology ◽  
2011 ◽  
Vol 2011 (1) ◽  
pp. 264-272 ◽  
Author(s):  
Mario Cazzola ◽  
Luca Malcovati ◽  
Rosangela Invernizzi
Keyword(s):  
Clinical Laboratory ◽  
Myeloproliferative Neoplasms ◽  
Chronic Myelomonocytic Leukemia ◽  
World Health ◽  
Refractory Anemia ◽  
Molecular Diagnostic ◽  
Juvenile Myelomonocytic Leukemia ◽  
Lymphoid Tissues ◽  
Ring Sideroblasts ◽  
Myelomonocytic Leukemia

Abstract According to the World Health Organization (WHO) classification of tumors of hematopoietic and lymphoid tissues, myelodysplastic/myeloproliferative neoplasms are clonal myeloid neoplasms that have some clinical, laboratory, or morphologic findings that support a diagnosis of myelodysplastic syndrome, and other findings that are more consistent with myeloproliferative neoplasms. These disorders include chronic myelomonocytic leukemia, atypical chronic myeloid leukemia (BCR-ABL1 negative), juvenile myelomonocytic leukemia, and myelodysplastic/myeloproliferative neoplasms, unclassifiable. The best characterized of these latter unclassifiable conditions is the provisional entity defined as refractory anemia with ring sideroblasts associated with marked thrombocytosis. This article focuses on myelodysplastic/myeloproliferative neoplasms of adulthood, with particular emphasis on chronic myelomonocytic leukemia and refractory anemia with ring sideroblasts associated with marked thrombocytosis. Recent studies have partly clarified the molecular basis of these disorders, laying the groundwork for the development of molecular diagnostic and prognostic tools. It is hoped that these advances will soon translate into improved therapeutic approaches.

scholarly journals Atypical chronic myeloid leukemia is clinically distinct from unclassifiable myelodysplastic/myeloproliferative neoplasms

Blood ◽  
2014 ◽  
Vol 123 (17) ◽  
pp. 2645-2651 ◽  
Author(s):  
Sa A. Wang ◽  
Robert P. Hasserjian ◽  
Patricia S. Fox ◽  
Heesun J. Rogers ◽  
Julia T. Geyer ◽  
...  
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Clinical Features ◽  
Myeloid Leukemia ◽  
Myeloproliferative Neoplasms ◽  
Clinicopathological Parameters ◽  
Patient Risk ◽  
Key Points ◽  
Atypical Chronic Myeloid Leukemia ◽  
Who 2008

Key Points Within MDS/MPN, the WHO 2008 criteria for aCML identify a subgroup of patients with aggressive clinical features distinct from MDS/MPN-U. The MDS/MPN-U category is heterogeneous, and patient risk can be further stratified by a number of clinicopathological parameters.

scholarly journals Diagnosis, risk stratification, and response evaluation in classical myeloproliferative neoplasms

Blood ◽  
2017 ◽  
Vol 129 (6) ◽  
pp. 680-692 ◽  
Author(s):  
Elisa Rumi ◽  
Mario Cazzola
Keyword(s):  
Bone Marrow ◽  
Diagnostic Criteria ◽  
Myeloproliferative Neoplasms ◽  
Phenotypic Variability ◽  
Vascular Complications ◽  
Prognostic Models ◽  
Lymphoid Tissues ◽  
Driver Genes ◽  
Jak2 Mutation ◽  
Endogenous Erythropoietin

Abstract Philadelphia-negative classical myeloproliferative neoplasms (MPNs) include polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF). The 2016 revision of the WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues includes new criteria for the diagnosis of these disorders. Somatic mutations in the 3 driver genes, that is, JAK2, CALR, and MPL, represent major diagnostic criteria in combination with hematologic and morphological abnormalities. PV is characterized by erythrocytosis with suppressed endogenous erythropoietin production, bone marrow panmyelosis, and JAK2 mutation. Thrombocytosis, bone marrow megakaryocytic proliferation, and presence of JAK2, CALR, or MPL mutation are the main diagnostic criteria for ET. PMF is characterized by bone marrow megakaryocytic proliferation, reticulin and/or collagen fibrosis, and presence of JAK2, CALR, or MPL mutation. Prefibrotic myelofibrosis represents an early phase of myelofibrosis, and is characterized by granulocytic/megakaryocytic proliferation and lack of reticulin fibrosis in the bone marrow. The genomic landscape of MPNs is more complex than initially thought and involves several mutant genes beyond the 3 drivers. Comutated, myeloid tumor-suppressor genes contribute to phenotypic variability, phenotypic shifts, and progression to more aggressive disorders. Patients with myeloid neoplasms are at variable risk of vascular complications, including arterial or venous thrombosis and bleeding. Current prognostic models are mainly based on clinical and hematologic parameters, but innovative models that include genetic data are being developed for both clinical and trial settings. In perspective, molecular profiling of MPNs might also allow for accurate evaluation and monitoring of response to innovative drugs that target the mutant clone.

Myeloproliferative Neoplasms – Classification, Diagnostic and Therapeutic Options in the Light of Molecular Findings

2009 ◽  
Vol 03 (01) ◽  
pp. 57 ◽  
Author(s):  
Andrzej Hellmann ◽  
Maria Bieniaszewska ◽  
◽  
Keyword(s):  
Tyrosine Kinase ◽  
Kinase Inhibitors ◽  
Myeloproliferative Neoplasms ◽  
Target Therapy ◽  
Diagnostic Procedures ◽  
Myeloproliferative Disorders ◽  
World Health ◽  
Lymphoid Tissues ◽  
Health Organization ◽  
Molecular Aberrations

The discovery of specific molecular aberrations (gene fusions or mutations) has had a profound effect on the understanding and management of myeloproliferative disorders (MPDs). First, it has provided clear evidence that all of these disorders are of neoplastic origin. This fact resulted in the change of the nomenclature proposed in the World Health Organization (WHO) Classification of Tumours of Haematopoietic and Lymphoid Tissues 2008, where the term MPDs was replaced by myeloproliferative neoplasms (MPNs). Second, useful tools for diagnostic procedures were developed, i.e. polymerase chain reaction (PCR) or other molecular assays. Thanks to this, previous complicated diagnostic algorithms could be simplified and the numerical value requirements could be lowered, making the diagnosis simpler and quicker. The other implication of the molecular findings in myeloproliferative neoplasms is derived from the fact that all discovered mutations result in translation of proteins with tyrosine kinase activity. So, nowadays the majority of myeloproliferative neoplasms can be treated with target therapy using tyrosine kinase inhibitors.

Role of JAK2 V617F mutation and aberrant expression of microRNA-143 in myeloproliferative neoplasms

2015 ◽  
Vol 53 (7) ◽  
Author(s):  
Marco Benati ◽  
Martina Montagnana ◽  
Elisa Danese ◽  
Giovanna De Matteis ◽  
Dino Veneri ◽  
...  
Keyword(s):  
Polycythemia Vera ◽  
Essential Thrombocythemia ◽  
Blood Cells ◽  
Healthy Subjects ◽  
Myeloproliferative Neoplasms ◽  
Jak2 V617f ◽  
Idiopathic Myelofibrosis ◽  
Aberrant Expression ◽  
Who 2008

AbstractMyeloproliferative neoplasms (MPNs) are clonal myeloid disorders characterized by the overproduction of mature blood cells. The pathogenetic hallmark of MPNs is the dysregulation of JAK-STAT signaling, usually associated with theIn total 78 patients with a clinical diagnosis of polycythemia vera (PV), essential thrombocythemia (ET) and idiopathic myelofibrosis (IM), made according to the WHO 2008 criteria, were included in the study. Twenty healthy subjects were checked as controls. Quantification ofThe miR-143 expression in MPNs patients was 2.97-fold higher than in controls.Our findings of aberrant miR-143 expression support the concept that factors other than

Fine Structural Alterations in Thyroid Follicular Cells (FC) and Changes in Serum Thyroxine Produced by Feeding Polychlorinated Biphenyl (PCB) to Rats

1977 ◽  
Vol 35 ◽  
pp. 498-499
Author(s):  
W.T. Collins ◽  
Charles C. Capen ◽  
Louis Kasza
Keyword(s):  
Feed Efficiency ◽  
Polychlorinated Biphenyl ◽  
Serum Proteins ◽  
Skin Lesions ◽  
Hepatic Necrosis ◽  
Ultrastructural Changes ◽  
Lymphoid Tissues ◽  
Heat Transfer Fluids ◽  
Thyroid Follicular Cells ◽  
Peripheral Metabolism

The widespread contamination of the environment with PCB, a compound used extensively by industry in hydraulic and heat transfer fluids as well as plasticizers and solvents in adhesives and sealants, has resulted in detectable tissue levels in a large portion of the human population, domestic animals, and wildlife. Intoxication with PCB produces severe hepatic necrosis, degeneration of lymphoid tissues and kidney, skin lesions, decreased reproductive performance, reduced feed efficiency, and decreased weight gain. PCB also has been reported to reduce the binding of thyroid hormone to serum proteins and enhance the peripheral metabolism of thyroxine with increased excretion of thyroxine-glucuronide in the bile (Bastomsky, Endocrinology 95: 1150-1155, 1974).The objectives of this investigation were (1) to investigate the histopathologic, histochemical, and ultrastructural changes in thyroid FC produced by the acute (4 week) and chronic (12 week) administration of low (50 ppm) and high (500 ppm) doses of PCB to rats, (2) to correlate these alterations to changes in serum immunoreactive thyroxine concentration, and (3) to investigate the persistence of the effects of PCB on the thyroid gland.

Sign in / Sign up

Export Citation Format

Share Document