الفهرس 
CML Overview, incidence, and prevalenceOnly 14 pages are availabe for public view
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Abstract
Background: SET domain containing 2 is an enzyme that in humans is encoded by the SETD2 Gene. The SETD2 gene is located on the short arm of chromosome 3 and has been shown to play a tumor suppressor role inhuman cancer. Depletion of SETD2 increases the frequency of deletion mutations that arise by the alternative DNA repair process of microhomology mediated end joining. SETD2 is a key member of nuclear receptor SET domain-containing (NSD) family and it is the only methyltransferase which can alter the trimethylation status of H3K36 and regulate protein structure as well as its function.
Aim of the Work: Our aim is to measure serum SETD2 in CML patient and to correlate serum SETD2 and outcomes and other prognostic factors.
Patients and Methods: This study was a case control study that were conducted on CML patients who was recruited from clinical hematology department at Ain Shams university hospital in hematology unit at Ain Shams University Hospital including 40 diagnosed chronic myeloid leukemia patients medically free with age range from 18-60 years old.
Results: In this study we demonstrated that there was insignificant difference between both groups as regard age and sex. In this thesis we illustrated that there were 2 accelerated, 38 chronic, 20 with GLIVEC (Imatinib), 20 with TASIGNA (Nilotinib). In this study we found that in case group, there were 11 cases with nausea, 9 with diarrhea, 11 with vomiting, 9 with headache. in study in our hands, we found that there was significant difference between both groups as regard Platelets. In study to assess Role of circulating endothelial cells and platelet microparticles as markers of angiogenesis in chronic myeloid leukemia.
Conclusion: We documented the presence of loss-of-function mutations of the histone methyltransferase SETD2 in the CML patients on TKI treatment.