الفهرس 
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Abstract
Acute myeloid leukemia is a heterogeneous group of diseases representing clonal proliferations of immature, myeloid, bone marrow–derived cells that most often involve the BM and PB and may present in extramedullary tissues.
The development of AML has been associated with several risk factors. These include age, antecedent hematologic disease, genetic disorders, exposure to radiation, chemicals, or other occupational hazards and previous chemotherapy.
Condensins are multi-subunit protein complexes that play a central role in mitotic chromosome assembly and segregation. Most eukaryotes possess two condensin complexes, named condensin I and condensin II which share the SMC2/SMC4 heterodimer but associated with two different sets of three non-SMC subunits; CAP-H, CAP-G and CAP-D2 for condensin I and CAP-H2, CAP-G2 and CAP-D3 for condensin II.
chromosome condensation and segregation play an essential role in ensuring the fidelity of genetic information transfer during mitosis. Cells that are defective for either chromosome compaction or resolution fail to faithfully segregate replicated chromosomes and become aneuploid, which induces genome instability and subsequent malignant transformation.
The current study involved 55 individuals classified into two groups; group I included 15 apparently healthy individuals as control group and group II included 40 newly diagnosed AML patients who recruited from clinica hematology department at Assiut University Hospital and oncology department at South Egypt Cancer Institute, after BMA and immunophenotyping in the period from May 2017 to May 2019.
All Participants were subjected to the following:
I- Medical History Taking: (age, sex, fever, bleeding, therapeutic history and blood transfusion).
II- Clinical Examination: with stress on hepatomegaly, splenomegaly and lymphadenopathy assessment.
III- Laboratory Investigations:
a. Complete blood counting, examination of Leishman stained peripheral blood films and manual reticulocytic count were done.
b. Erythrocyte sedimentation rate and prothrombin time and concentration.
c. Liver function tests, kidney function tests, serum LDH enzyme, calcium and uric acid levels were performed.
d. Examination of Leishman stained BMA smears, cytochemical staining as directed by morphological features and flow cytometric immunophenotypic analysis of BMA samples were done only for the patients.
e. Specific investigations: multiplex reverse transcription–polymerase chain reaction (RT- PCR) to examine the expression status of condensin genes.
f. Follow up of patient after 6 months by BM blast cell count to predict outcome and prognosis of disease after induction and consolidation therapy.
The current study revealed the following findings:
Patients group showed a significantly lower Hb levels and platelets counts and higher leukocytic count than the control group.
The median of PB and BM blast cells count in patients group were (52%) and (57.5%) respectively. AML-M4 was the most frequent subtype followed by AML-M2 and M3. AML-M6 was the least frequent subtype in this study.
Two of condensin genes, SMC4 and NCAPG, were not detectable in both control and AML cases, while the rest of condensin genes (SMC2, NCAPH NCAPH2, NCAPD2, NCAPD3 and NCAPG2) showed highly statistical significant decrease in AML cases when compared with control group.
There was a statistically significant difference and negative moderate correlation between SMC2, NCAPH2, NCAPD2, NCAPD3 and NCAPG2 genes expression and both of PB and BM blast cells count in patients. NCAPH gene expression showed only negative moderate correlation with BM blast cells count.
On the other hand, condensin genes were all positively correlated to each other in a correlation matrix study, but no association between their expression and the outcome of the disease state has been observed.
Examination of the expression pattern of SMC4 revealed that a truncated transcript of 322 bp was amplified instead of the expected 639 bp PCR amplicon in ten AML samples (25%). This truncated amplicon is most probably produced from RNA with deleted exons 17 and 18. The explanation of these findings were discussed.