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ORIGINAL ARTICLE
Year : 2012  |  Volume : 37  |  Issue : 2  |  Page : 91-95

Detection of Cx43 and P27 in acute myeloid leukemia patients with t(8;21)


1 Department of Clinical Pathology, Faculty of Medicine, Zagazig University, Zagazig, Egypt
2 Department of Biochemistry, Faculty of Medicine, EL_Minia University, EL_Minia, Egypt
3 Department of Medical Oncology, Faculty of Medicine, Zagazig University, Zagazig, Egypt

Correspondence Address:
Samy B.M. El-Hady
Department of Clinical Pathology, Faculty of Medicine, Zagazig University, Zagazig
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.7123/01.EJH.0000415083.42211.0a

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Background

Connexin 43 (Cx43) inhibits cell proliferation in gap junction-dependent and gap junction-independent mechanisms and contributes to the pathogenesis of many diseases. The aim of this study was to assess Cx43 expression in acute myeloid leukemia (AML) patients with t(8;21) compared with patients without this translocation and correlate this expression with the cyclin-dependent kinase inhibitor P27.

Patients and methods

Group I comprised 21 patients with de-novo M2 who were positive for t(8;21). Group II comprised 29 patients with de-novo M2 who were negative for t(8;21). Group III comprised 25 apparently normal individuals, with matched age and sex, which served as the control group. In addition to routine laboratory investigations, detection of Cx43 expression on bone marrow mononuclear cells (MNCs) and P27 in MNC lysate was carried out for all patients.

Results

In this study, we found increased expression of Cx43 on leukemic cells carrying t(8;21) compared with leukemic cells without t(8;21). Compared with normal cells, there was decreased expression of Cx43 on leukemic cells carrying t(8;21). Furthermore, we found significant negative correlation between the count of leukemic cells and Cx43 expression. We found increased levels of P27kip1 protein in MNCs extracted from leukemic patients with positive t(8;21) compared with leukemic patients without this translocation. In addition, we found significant positive correlation between Cx43 expression and P27kip1 protein level.

Conclusion

Our experiments show that Cx43 expression increases in M2 with t(8;21) and may contribute to the growth-arresting effect of leukemogenic AML1–eight-twenty one (ETO) fusion protein, possibly by causing the accumulation of P27kip1 protein. These novel discoveries have shed new light on the mechanisms of AML1–ETO-induced growth arrest and have provided a foundation for exploring additional mutagenic ‘hits’ for AML1–ETO-associated AML. We recommend the use of drugs that improve Cx43 expression in treating M2.



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