Molecular Defects in Chronic Myeloproliferative Disorders

Albitar, Mäher; Freireich, Emil J.

doi:10.1007/bf03401794

Cited by 9 publications

(2 citation statements)

References 105 publications

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“…3B). Neutrophilia can be the consequence of hematological neoplasias, such as chronic myeloproliferative disorders [17]. Myeloproliferative neoplasia are characterized by an increase in myelopoiesis.…”

Section: Altered Myeloid Homeostasis and Fatal Inflammatory Disorder mentioning

confidence: 99%

Massive inflammatory syndrome and lymphocytic immunodeficiency in KARAP/DAP12-transgenic mice

Lucas

Daniel²,

Tomasello

et al. 2002

Eur. J. Immunol.

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KARAP/DAP12 is a broadly distributed transmembrane signaling polypeptide with an immunoreceptor tyrosine‐based activation motif, and is non‐covalently associated with a variety of activating surface receptors. We report here the characterization of transgenic mice that overexpress KARAP/DAP12 polypeptides in both myeloid and lymphoid compartments. KARAP/DAP12‐transgenic mice present, in a transgene dose‐dependent manner, a complex phenotype characterized by two independent and spontaneous hematological abnormalities: (i) a severe lymphopenia and (ii) a massive inflammatory syndromeassociated with neutrophilia and lung infiltration by multinucleated macrophages. These myeloid abnormalities observed in KARAP/DAP12‐transgenic mice indicate that KARAP/DAP12‐driven signals are critically involved in inflammation, and constitute an essential target to control the resolution of inflammatory disorders based on monocytes/macrophages and neutrophils.

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Section: Altered Myeloid Homeostasis and Fatal Inflammatory Disorder mentioning

confidence: 99%

Massive inflammatory syndrome and lymphocytic immunodeficiency in KARAP/DAP12-transgenic mice

Lucas

Daniel²,

Tomasello

et al. 2002

Eur. J. Immunol.

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“…Alternatively, about 10% of AML cases without cytogenetic evidence of 11q23 rearrangements show internal tandem duplication of MLL, often in association with trisomy 11 (87,88). In addition, more than 20% of patients with intragenic aberrations of MLL demonstrate a mutation/deletion involving FLT3 (CD135), but this occurs in only about 10% of AML cases with MLL translocations and only in 5% of adult AML with normal MLL status (89).…”

Section: Aml With 11q23 Abnormalitiesmentioning

confidence: 99%

Cytogenetic biomarkers for human cancer

Keen-Kim

Nooraie²,

Pn³

2008

Front Biosci

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Human cancer cytogenetics is the study of chromosomal rearrangements and numerical abnormalities in malignant tissue. Since the 1960s and the discovery of the Philadelphia chromosome, hundreds of common and characteristic chromosomal aberrations have been observed in various neoplasias. Because these cytogenetic aberrations provide diagnostic, prognostic, and treatment-related information for the associated cancers, they are considered biomarkers for disease. Here we describe many of the best-known chromosome rearrangements and variant rearrangements in hematologic disease and solid tumors, indicate the genes and underlying molecular mechanisms known to be involved in development and progression of disease, and describe the newer molecular cytogenetic technologies and how they are currently being used in cancer diagnostics. We also highlight many important pit-falls in obtaining, transporting, and analyzing neoplastic samples which can compromise cytogenetic studies and preclude its use as a diagnostic tool.

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