With a high rate of Ras mutation in<unk> , deregulation of this signalling pathway has been linked to the pathogenesis of the disease. Tumour necrosis factor, GM-CSF, interleukin-3, interleukin-4, interleukin-6, and interleukin-10 may have a role in hyperproliferative<unk>  cells. These cytokines can stimulate the growth of<unk>  in vitro. Hypermethylation of cytosine residues (usually in the promoter regions of genes) occurs in many malignancies to regulate gene expression. One commonly hypermethylated gene in<unk>  is p15INK4b, a gene involved in cell cycle regulation. Genetic mutations Clonal genetic abnormalities are common in<unk>  but they are not specific for diagnosis of the disease. The most common found are the 8+, −7/del (7q) and structural 12p abnormalities. KRAS and NRAS are mutated in 25–40% of the cases of<unk> . The Jak2 V617F mutation is found in 10% of cases. Mutations in transcription factors such as RUNX1, CEBPA, NPM1 and WT1 have been found in up to 30% of cases. Mutations of CBL are found in approximately 5–18% of cases. Mutations in the TET2 gene are found in approximately 40–50% of<unk> . Inactivating mutations in one of the two parental GATA2 genes lead to a reduction, i.e. a haploinsufficiency, in the cellular levels of the gene's product, the GATA2 transcription factor, and thereby to a rare autosomal dominant genetic disease, GATA2 deficiency. This disease is associated with a highly variable set of disorders including the myelodysplastic syndrome, acute myeloid leukemia, and<unk> . GATA2-deficiency-induced<unk> , like other types of<unk> , is commonly preceded by monocytosis.
Chronic myelomonocytic leukemia
Prolymphocytic leukemia
Large granular lymphocytic leukemia
Chronic neutrophilic leukemia
Acute myelomonocytic leukemia
Mixed-phenotype acute leukemia
Atypical chronic myeloid leukemia
Acute myeloblastic leukemia with maturation