Elsaadany, Z., N. E. L. Husseiny, R. A. L. Gamal, A. Gad, N. Momen, and E. A. Elsoud, "The potential risk of certain SNPs in EPHX1, NQO1, and PON1 genes among B-Non-Hodgkin Lymphoma patients: An Egyptian case-control study", Gene Reports, vol. 17, 2019.
Farawela, H., R. Fouad, N. Zahran, B. Madkour, Z. El-Saadany, S. Toimaa, S. Mamdouh, and H. El-Kiat, "Fibronectin gene polymorphisms in HCV related type II mixed cryoglobulinemia: risk of development of B-cell lymphoma", Comparative Clinical Pathology, vol. 27, pp. 1389-1395, 2018.
Hamdy, M. S. A. - D., Z. A. E. - Saadany, M. M. louf Makhlouf, A. I. Salama, N. S. Ibrahim, and A. A. Gad, "TAp73 and ΔNp73 relative expression in Egyptian patients with lymphoid neoplasms", Tumori, vol. 103, issue 3, pp. 268-271, 2017.
Arnaout, H., F. G. Allah, O. Khorshid, Z. Elsaadany, N. Fouad, and M. Amer, TSC gene expression in the newly diagnosed Egyptian acute leukemia patients, , vol. 27, pp. 1199-1204, 2018.
Aboul-Enein, A., A. El-Beshlawy, M. O. N. A. HAMDY, Z. El-Saadany, A. Samir, and H. A. El-Samie, "Peripheral expression of hepcidin gene in Egyptian β-thalassemia major", Gene, vol. 564, issue 2, pp. 206-209, 2015. Peripheral expression of hepcidin gene in Egyptian β-thalassemia major
Hamdy, M. S. E. - D., A. S. Nasr, M. M. Makhlouf, Z. A. El_Saadany, S. M. Khedr, and M. Samir, Impact of Prothrombotic Risk Factors on the Clinical Phenotype in Haemophilia Patients, , Submitted.
El-Danasouri, N. M., S. H. Ragab, M. A. Rasheed, Z. A. El_Saadany, and S. N. A. El-Fattah, "MDM2 SNP309 and p53 codon 72 genetic polymorphisms and risk of AML: An Egyptian study", Annals of clinical and laboratory science, vol. 44, issue 4, pp. 449-454, 2014. Abstract

Background: Acute myeloid leukemia (AML) is a heterogeneous disease with numerous genetic abnormalities corresponding to a variety of subtypes. p53 is involved in multiple cellular pathways including apoptosis, transcriptional control, and cell cycle regulation. Single nucleotide polymorphism (SNP) at codon 72 of the p53 gene is associated with the risk for development of various neoplasms. MDM2 SNP309 is a single nucleotide T to G polymorphism located in the MDM2 gene promoter which enhances the expression of MDM2 protein, thereby leading to attenuation of the p53 stress response. Objective: The current study aimed at defining the role of MDM2 and p53 genetic polymorphisms and risk of AML. Methodology: Genotyping for MDM2 was done by AS-PCR technique while p53 codon 72 genotyping was done by PCR- RFLP for 50 patients and 50 controls. Results: The study did not detect any significant differences regarding MDM2 or p53 polymorphisms in AML cases compared to controls. A borderline significance was found between cases and controls regarding combined MDM2 T/G and p53 genotyping. MDM2 variant genotype was significantly associated with younger age group and lower Hb level while P53 variant was significantly associated with less frequent CD117 expression.

EL-GHANY, H. O. D. A. M. O. H. A. M. E. D. A., Z. A. E. - Saadany, N. E. V. I. E. N. M. O. H. A. M. E. D. BAHAA, N. Y. Ibtahim, and S. M. Hussein, "Stromal Cell Derived Factor-1 (CXCL12) Chemokine Gene Variant in Myeloid Leukemias", Clinical Laboratory, vol. 60, pp. 735-741, 2014. Abstract

Background: Acute and chronic myeloid leukemia are initiated and sustained by a small, self-renewing population
of leukemic stem cells, which produce progeny of a heterogeneous population of progenitor cells. CXCL12, a chemokine
abundantly produced by the bone marrow microenvironment, and its receptor CXCR4 have crucial roles
in malignant cell trafficking. We set out to determine the CXCL12 gene polymorphism at codon G801A and evaluate
its influence on malignant cell dissemination and tissue infiltration in myeloid leukemias.
Methods: Genotyping for CXCL12 was done by restriction PCR-RFLP for 48 myeloid leukemia patients: 38 de
novo AML and 10 CML. Fifty age and sex matched volunteers were evaluated as controls.
Results: Regarding AML patients, the frequency of wild genotype was 50% and the heterozygous genotype was
50%. In CML patients, the frequency of wild genotype was 30% while the heterozygous genotype was 70%. In the
control group, 57.2% had wild genotype while 42.8% had heterozygous genotype with no significant difference detected
between myeloid leukemia patients and the control group. There was a statistically insignificant association
between wild and heterozygous genotypes regarding clinical, laboratory data and extramedullary dissemination.
Conclusions: CXCL12 polymorphism is not associated with either increased myeloid leukemia risk or extramedullary
blast dissemination.

Goda, H. M., Z. A. El_Saadany, N. M. Bahaa, and R. M. salama, "Interleukin 28B polymorphisms and therapy response in Egyptian hepatitis C genotype-4 patients", DNA Cell Bioliogy, vol. 33, issue 9, pp. 642-646, 2014. Abstract

Hepatitis C infection represents a major health problem in Egypt; only 20% of patients undergo
spontaneous clearance of the virus and around 25% of all patients progress to develop cirrhosis. More
than 90% of Egyptian patients have hepatitis C virus (HCV) genotype-4. Combined pegylated
interferon and oral ribavirin are the current standard therapies for HCV-4. The aim of the work is to
evaluate the predictive power of the rs12979860 IL28B SNP and rs12980275 IL28B SNP for treatment
response in Egyptian patients infected with HCV genotype 4. One hundred eleven HCV patients
receiving combined treatment were studied for rs12979860 and rs12980275 polymorphisms by the
restriction fragment length polymorphism technique. The rs12979860 CC and rs12979860 AA
genotypes were significantly associated with sustained virological response (p=0.001). Our results
suggest that studying IL28B polymorphisms contribute to proper prediction of response to standard
therapies in Egyptian patients, optimizing cost effectiveness, and minimizing unneeded adverse effect
of therapy.

Shiba, H., M. A. Kamal, R. Zayed, Z. A. El_Saadany, L. Elmessery, J. Abdelmoniem, D. R. AbdelRahman, and F. Ramadan, "BAFF Promoter Polymorphisms in Egyptian Patients with Systemic Lupus Erythematosus", Annals of Clinical and Laboratory Science, vol. 43, pp. 289-294, 2014.
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