A gain-of-function mutation of JAK2 in myeloproliferative disorders.
By R. Kralovics, F. Passamonti, A. Buser, Soon-Siong Teo, R. Tiedt, J. Passweg, A. Tichelli, M. Cazzola, R. Skoda. New England Journal of Medicine, 2005
3,651 citations recorded by the source corpus.
Subfields: Genetics, Hematology
View Paper: https://www.semanticscholar.org/paper/30c69f34e44abb61a16ca9b34c11a1e91f70c6bc
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In Genetics
- Benjamin M. Neale
- Elaine R. Mardis
- J. O’Shea
- Patrick F. Sullivan
- Benjamin L. Ebert
- Steven A. McCarroll
- Shaun Purcell
- Richard K. Wilson
In Hematology
Citations in the corpus
- Targeting cancer stem cell pathways for cancer therapy (2020, background): “314 Several lines of evidence show that constitutive activation of JAK2 and STAT3 in the absence of any stimulating ligand occurs in polycythemia vera.”
- A dynamic prognostic model to predict survival in primary myelofibrosis: a study by the IWG-MRT (International Working Group for Myeloproliferative Neoplasms Research and Treatment). (2010, methodology): “The inclusion criteria were (1) diagnosis of PMF based on the presence of megakaryocyte proliferation and atypia accompanied by increased reticulin and/or collagen in bone marrow as major criterion, as well as of the JAK2 (V617F) or the MPL mutations if available and 2 criteria among anemia, splenom”
- Deep reinforcement learning for de novo drug design (2017, background): “ytoplasm it also plays an important role in signal transduction (63). Mutations in JAK2 have been implicated in multiple conditions like thrombocythemia, myelofibrosis or myeloproliferative disorders (64). The reward functions in both cases (min and max) were defined as exponential functions of pIC ”
- Mechanisms and consequences of Jak-STAT signaling in the immune system (2017, background): “STAT-binding inhibitory peptides (8), small-molecule STAT inhibitors (9),”
- The 2008 revision of the World Health Organization (WHO) classification of myeloid neoplasms and acute leukemia: rationale and important changes. (2009, background): “It is recommended, however, that the cytogenetic abnormality be included in the diagnostic report, for example, “therapy-related AML with t(9;11)(p22;q23).”
- Mechanisms of fibrosis: therapeutic translation for fibrotic disease (2012, neutral): “Studies are also under way to examine whether a serine/threonine protein kinase inhibitor reduces the number of circulating fibrocytes in individuals with IPF 167 .”