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Hui Hao-Shen

Researcher at University Hospital of Basel

Publications -  36
Citations -  2604

Hui Hao-Shen is an academic researcher from University Hospital of Basel. The author has contributed to research in topics: Haematopoiesis & Bone marrow. The author has an hindex of 17, co-authored 29 publications receiving 2289 citations.

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Clonal evolution and clinical correlates of somatic mutations in myeloproliferative neoplasms

TL;DR: Surprisingly, the number of mutations between early and late patient samples did not significantly change, and during a total follow-up of 133 patient years, only 2 new mutations appeared, suggesting that the mutation rate in MPN is rather low.
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Ratio of mutant JAK2-V617F to wild-type Jak2 determines the MPD phenotypes in transgenic mice

TL;DR: Higher levels of JAK2-V617F in mouse bone marrow by retroviral transduction caused a PV-like phenotype without thrombocytosis, consistent with the hypothesis that the ratio of mutant to wild-type JAK1 is critical for the phenotypic manifestation.
Journal Article

Ratio of mutant JAK2-V617F to wild-type Jak2 determines the MPD phenotypes in transgenic mice. Commentary

TL;DR: In this article, the authors generated JAK2-V617F transgenic mice with the sequences encoding the kinase domain placed in the inverse orientation and flanked by antiparallel loxP sites.
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Pf4-Cre transgenic mice allow the generation of lineage-restricted gene knockouts for studying megakaryocyte and platelet function in vivo

TL;DR: To generate transgenic mice that express Cre-recombinase exclusively in the megakaryocytic lineage, a mouse bacterial artificial chromosome clone is modified and the first exon of the platelet factor 4 (Pf4), also called CXCL4, is replaced with a codon-improved Cre cDNA.
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Clonal analysis of TET2 and JAK2 mutations suggests that TET2 can be a late event in the progression of myeloproliferative neoplasms.

TL;DR: In 4 of 8 myeloproliferative neoplasm patients, it was found that some colonies with mutated TET2 carried wild-type JAK2, whereas others wereJAK2-V617F positive, indicating that TET1 occurred before JAK1-V615F, and the lack of a strict temporal order of occurrence makes it unlikely that mutations in TET3 represent a predisposing event for acquiring mutations in JAK3.