ReviewCurrent hematologic malignancy reports2015
Oncogenic Drivers in Myeloproliferative Neoplasms: From JAK2 to Calreticulin Mutations.
Review in Current hematologic malignancy reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 24 citations in OpenAlex.
- Article
- Thiophene derivative inflicts cytotoxicity via an intrinsic apoptotic pathway on human acute lymphoblastic leukemia cells.PloS one · 2023Article
- STAT5b: A master regulator of key biological pathways.Frontiers in immunology · 2022Review
- Novel prognostic genes and subclasses of acute myeloid leukemia revealed by survival analysis of gene expression data.BMC medical genomics · 2021Article
- Direct Targeting Options for STAT3 and STAT5 in Cancer.Cancers · 2019Review
- Increased Dkk-1 plasma levels may discriminate disease subtypes in myeloproliferative neoplasms.Journal of cellular and molecular medicine · 2018Article
- Exploring the Mechanism of Danshen against Myelofibrosis by Network Pharmacology and Molecular Docking.Evidence-based complementary and alternative medicine : eCAM · 2018Article
- Essential thrombocytemia following immune thrombocytopenia with JAK2V617F mutation.Leukemia research reports · 2018Article
- Increased B cell activation is present in JAK2V617F-mutated, CALR-mutated and triple-negative essential thrombocythemia.Oncotarget · 2017Article
- Austrian recommendations for the management of primary myelofibrosis, post-polycythemia vera myelofibrosis and post-essential thrombocythemia myelofibrosis: an expert statement.Wiener klinische Wochenschrift · 2017Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During the past 10 years, major progress has been accomplished with the discovery of activating mutations that are associated with the vast majority of BCR-ABL negative human myeloproliferative neoplasms (MPNs). The identification in 2005 of JAK2 V617F triggered great interest in the JAK2-STAT5/STAT3 pathway. Discovery in 2006 of mutants of thrombopoietin receptor (TPO-R/MPL) and later on of mutants in negative regulators of JAK-STAT pathway led to the notion that persistent JAK2 activation is a hallmark of MPNs. In 2013, mutations in the gene coding for the chaperone calreticulin were reported in 20-30% of essential thrombocythemia and primary myelofibrosis patients. Here, we will address the question: what do we know about calreticulin that could help us understand its role in MPNs? In addition to oncogenic driver mutations, certain MPNs also exhibit epigenetic mutations. Targeting of both oncogenic drivers and epigenetic defects could be required for effective therapy.
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