Figure 3

Novel European Asiatic Clinical, Laboratory, Molecular and Pathobiological (2015-2020 CLMP) criteria for JAK2V617F trilinear polycythemia vera (PV), JAK2exon12 PV and JAK2V617F, CALR and MPL515 thrombocythemias: From Dameshek to Constantinescu-Vainchenker, Kralovics and Michiels

Jan Jacques Michiels*, King H Lam, Fibo Ten Kate, Dong-Wook Kim, Myungshin Kim, Vasily Shuvaev, Francisca Valster, Vincent Potters, Wilfried Schroyens, Mihaela Andreescu, Adrian Trifa, Achille Pich and Hendrik De Raeve

Published: 03 April, 2020 | Volume 3 - Issue 1 | Pages: 001-020


Figure 3:

According to Constantinescu-Vainchenker low V617F constitutional kinase activity in heterozygous mutated JAK2V617F mutated patients is enough to produce the ET phenotype via the MPL signalling pathway and that higher V617F constitutional kinase activity in JAK2V617F mutated, heterozygous/homozygous or homozygous mutated patients is needed to produce the sequential stages of prodromal, classical and advanced (masked) PV phenotypes via activation of both the EPO and pathways of hematopietic progenitors cells (Table 1). The JAK2V617F dosage hypothesis has been confirmed at the bone marrow haematopoietic stem cell level by the demonstration that endogenous erythroid colonies (EEC) from ET patients are mainly heterozygous for the JAK2V617F mutation, whereas all PV patients are either hetero/homozygous or mainly homozygous for the JAK2V617F mutation (Figure 8).

Read Full Article HTML DOI: 10.29328/journal.ijbmr.1001011 Cite this Article Read Full Article PDF

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