Molecular genetic alterations

Ang SO, Chen H, Gordeuk VR et al. (2002) Endemic polycythemia in Russia: mutation in the VHL gene. Blood Cells Molecules & Diseases, 28, 57-62.

Asimakopoulos FA, Hinshelwood S, Gilbert JGR et al. (1997) The gene encoding hematopoietic cell phosphatase (SHP-1) is structurally and transcriptionally intact in polycythemia vera. Oncogene, 14, 12151222.

Axelrad AA, Eskinazi D, Correa PN et al. (2000) Hypersensitivity of circulating progenitor cells to megakaryocyte growth and development factor (PEG-rHu MGDF) in essential thrombocythemia. Blood, 96, 3310-3321.

Correa, PN, Eskinazi D, Axelrad AA. (1994) Circulating erythroid progenitors in polycythemia vera are hypersensitive to insulin-like growth factor-1 in vitro: studies in an improved serum-free medium. Blood, 83, 99-112.

Gregg XT, Prchal JT. (1997) Erythropoietin receptor mutations and human disease. Seminars in Hematology, 34, 70-76.

Hinshelwood S, Bench AJ, Green AR. (1997) Pathogenesis of polycythae-mia vera. Blood Reviews, 11, 224-232.

Horikawa Y, Matsumura I, Hashimoto K et al. (1997) Markedly reduced expression of platelet c-mpl receptor in essential thrombocythemia. Blood, 90, 4031-4038.

Mesa RA, Hanson CA, Li C et al. (2002) Diagnostic and prognostic value of bone marrow angiogenesis and megakaryocyte c-Mpl expression in essential thrombocythaemia. Blood, 99, 4131-4137.

Moliterno AR, Hankins WD, Spivak JL. (1998) Impaired expression of the thrombopoietin receptor by platelets from patients with poly-cythemia vera. New England Journal of Medicine, 338, 572-580.

Moliterno AR, Spivak JL. (1999) Posttranslational processing of the thrombopoietin receptor is impaired in polycythemia vera. Blood, 94, 2555-2561.

Prchal JF, Axelrad AA. (1974) Bone marrow responses in polycythemia vera. New England Journal of Medicine, 290, 1382.

Temerinac S, Klippel S, Strunck E et al. (2000) Cloning of PRV-1, a novel member of the uPAR receptor superfamily, which is overexpressed in polycythemia rubra vera. Blood, 95, 2569-2576.

Wiestner A, Schlemper RJ, van der Maas APC et al. (1998) An activating splice donor mutation in the thrombopoietin gene causes hereditary thrombocythaemia. Nature Genetics, 18, 49-52.

Diabetes 2

Diabetes 2

Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...

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