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A decrease in degradation and an increase in the level of the HIF-1 factor is caused by defects in the VHL gene (for example, representatives of the population of Chuvashia are characterized by a homozygous mutation of this gene). Polycythemia vera can be caused by abnormalities of chromosome 9, but the most common is a deletion of the long arm of chromosome 20.


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In 2005, a point mutation in exon 14 of the Jak2 kinase gene (mutation JAK2V617F) was identified, which causes the replacement of the amino acid valine with phenylalanine in the pseudokinase domain JH2 of the JAK2 protein at position 617.

The JAK2V617F mutation in hematopoietic precursor cells in erythremia is presented in a homozygous form (the formation of the homozygous form is affected by mitotic recombination and duplication of the mutant allele). When JAK2V617F and STAT5 are active, the level of reactive oxygen species increases, resulting in a transition of the cell cycle from the G1 to S phase. The adapter protein STAT5 and reactive oxygen species transmit a regulatory signal from JAK2V617F to the cyclin D2 and p27kip genes, which causes an accelerated transition of the cell cycle from phase G1 to S. As a result, the proliferation of erythroid cells that carry a mutant form of the JAK2 gene increases.

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In JAK2V617F-positive patients, this mutation is detected in myeloid cells, B- and T-lymphocytes and natural killer cells, which proves the proliferative advantage of defective cells compared to the norm. Polycythemia vera in most cases is characterized by a fairly low ratio of clarinex to normal allele in mature myeloid cells and early precursors. In the presence of clonal dominance, patients have a more severe clinical picture compared to patients without this defect.