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and - Hanaa Hamed Arnaout1, Mervat Mamdooh Khorshied1, O. R. K. 2* M. H. E. - N. M., "Association of Caspase 8 and Caspase 10 Genetic Polymorphisms with B-cell Non Hodgkin’s Lymphoma in Egypt: A Case-Control Study.", J Cancer Sci Ther , vol. 4, issue 9, pp. 249-253 , 2012. AbstractCU-PDF

Background and purpose: Non-Hodgkin lymphomas are closely related diseases with distinctive morphologic, immunophenotypic, genetic, and clinical features. Genetic susceptibility studies of NHL are mandatory to identify at risk populations and to clarify important disease mechanisms. Caspase genes play a key role in regulation of apoptotic cell death, and dysregulation of this signaling pathway has been shown to participate in tumorigenesis. The current study aimed at defining the role of Caspase 8-D302H, Caspase 8-652 6N ins/del and Caspase 10-I522L genetic polymorphisms as risk factors for NHL and their possible role as genetic prognostic markers.

Methods: The present study included 100 Egyptian B-cell NHL patients and 100 healthy controls. Genotyping of the studied genes was performed by polymerase chain reaction-restriction fragment length polymorphism (PCRRFLP) technique. Data was analyzed using SPSS statistical package version 15.

Results: The study revealed that CASP8-D302H mutant genotypes were significantly higher in NHL patients when compared to the controls and conferred increased risk of NHL. For CASP8-652 6N ins/del and Casp10- I522L, there was no statistical difference in the distribution of the different genotypes between NHL cases and the controls. Furthermore, there were no statistical differences between NHL patients harboring the wild or mutant genotypes of the studied genes as regards their response to therapy.

Conclusions: CASP8-D302H genetic polymorphism represents a genetic risk factor for NHL in Egyptian population. Hopefully, better understanding of the functional consequences of caspase genes polymorphism would provide a foundation for future studies of the possible role of these genes in lymphomagenesis.

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A, I., A. R. H, K. M, S. R, N. N, and K. O, "Tumor necrosis factor alpha-308 and Lymphotoxin alpha+252 genetic polymorphisms and the susceptibility to non-Hodgkin lymphoma in Egypt.", Leuk Res. , vol. 36, issue 6, pp. 694-698, 2012. AbstractCU-PDF

Genetic polymorphism within the regulatory regions of tumor necrosis factor-alpha (TNF-α) and Lymphotoxin-alpha (LT-α) may be involved in the development of lymphoid malignancies. The aim of the current study was to investigate the effect of TNFα−308 and LTα+252 genetic polymorphism on susceptibility to non-Hodgkin lymphoma (NHL) in Egypt. Genotyping of the studied genes by restriction fragment length polymorphism polymerase chain reaction was conducted on 84 NHL and 100 healthy controls and revealed that TNFα−308 homotype (AA) was significantly higher in NHL patients and conferred sixfold increased risk of NHL (OR = 5.9, 95%CI = 2.3–16.1). Moreover, TNFα/LTα high-producer haplotypes were significantly higher in NHL patients and conferred increased risk of NHL (OR = 4.59, 95%CI = 2.19–9.42).

A.M.Khattab, R., M. M.A.Khorshied, S. S. A. Shafy, M. S. E. Ansary, and S. M. Moukhtar., "In vitro transdifferentiation of umbilical cord stem cells into cardiac myocytes: Role of growth factors", The Egyptian Journal of Critical Care Medicine , vol. 1, pp. 43–50, 2013.
AA, M., I. AM, E. - M. MW, M. IM, K. MM, G. HM, and R. RM., "Ex vivo expansion of stem cells: defining optimum conditions using various cytokines", Lab Hematol., vol. 12, issue 2, pp. 86-93, 2006.
AA, M., I. AM, E. - M. MW, M. IM, K. MA, G. HM, and R. RM., "Ex vivo expansion of stem cells: defining optimum conditions using various cytokines", Lab Hematol., vol. 12, issue 2, pp. 86-93, 2006.
Abdel Rahman HA, Khorshied MM, E. H. H. K. O. M., "The link between genetic polymorphism of glutathione-S-transferases, GSTM1, and GSTT1 and diffuse large B-cell lymphoma in Egypt.", J Cancer Res Clin Oncol. , vol. 138, issue 8, pp. 1363-8., 2012.
Arnaout, H. H., M. M. Khorshied, O. R. M. Khorshid, and M. H. El-Nagdy, "Association of Caspase 8 and Caspase 10 Genetic Polymorphisms with B-cell Non Hodgkin’s Lymphoma in Egypt: A Case-Control Study", J Cancer Sci Ther , vol. 4, issue 9, pp. 249-253 , 2012. association_of_caspase_8_and_caspase_10-nhl-ours-2012pdf.pdf
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B, E. - Z., B. D, H. R, G. H, S. S, K. MM, and S. MA, "Rituximab treatment in pemphigus vulgaris: effect on circulating Tregs.", Arch Dermatol Res. 2017, 2017.
Bakr, S., M. Khorshied, N. Talha, K. Y. Jaffer, N. Soliman, K. Eid, and M. El-Ghamrawy, "Implication of HMOX1 and CCR5 genotypes on clinical phenotype of Egyptian patients with sickle cell anemia.", Annals of hematology, vol. 98, issue 8, pp. 1805-1812, 2019. Abstract

Sickle cell disease (SCD) is a relatively common inherited hemolytic anemia among individuals of African descent. Genetic factors might clarify clinical diversity of the disease and variations in treatment response. Some researchers investigated heme oxygenase-1 (HMOX1) or chemokine receptor 5 (CCR5Δ32) genotypes among SCD patients and their correlation with fetal hemoglobin (HbF) and disease severity. However, there are no such records among Arab nations. We aimed to estimate the prevalence of the HMOX1-413 A>T (rs2071746) and CCR5Δ32 (rs333) polymorphisms, and to assess their effect on SCD phenotype and HbF level among Egyptian patients. Polymerase chain reaction assay was used to determine these polymorphisms among 100 SCD patients and 100 healthy controls. Though not statistically significant, the frequency of individual carrying HMOX-1 polymorphic AT and TT genotypes in both patient and control groups was 92% and 85% respectively. Regarding CCR5Δ32 polymorphisms, all SCD patients harbored the wild genotype (100%), while the heteromutant genotype was encountered in 2% of our controls. Patients harboring mutant HMOX-1 had a less frequent vaso-occlusive crisis (VOC)/lifetime, less VOC in the last year, less incidence of stroke, less frequency of hospitalization, and responded more frequently to hydroxyurea with statistically significant differences (p = 0.028, 0.007, 0.046, 0.007, and 0.011 respectively). No significant associations with HbF level or other hematologic parameters were encountered among our cohort. Our study results suggest a protective effect of mutant HMOX-1 genotypes in ameliorating the phenotypic severity of the disease. HMOX1-413 A>T (rs2071746) polymorphisms might prove to be a prognostic marker among Egyptian SCD, but not CCR5Δ32 (rs333) polymorphisms.

Bakr, S., M. Khorshied, N. Talha, K. Y. Jaffer, N. Soliman, K. Eid, and M. El-Ghamrawy, "Implication of HMOX1 and CCR5 genotypes on clinical phenotype of Egyptian patients with sickle cell anemia.", Annals of hematology, vol. 98, issue 8, pp. 1805-1812, 2019. Abstract

Sickle cell disease (SCD) is a relatively common inherited hemolytic anemia among individuals of African descent. Genetic factors might clarify clinical diversity of the disease and variations in treatment response. Some researchers investigated heme oxygenase-1 (HMOX1) or chemokine receptor 5 (CCR5Δ32) genotypes among SCD patients and their correlation with fetal hemoglobin (HbF) and disease severity. However, there are no such records among Arab nations. We aimed to estimate the prevalence of the HMOX1-413 A>T (rs2071746) and CCR5Δ32 (rs333) polymorphisms, and to assess their effect on SCD phenotype and HbF level among Egyptian patients. Polymerase chain reaction assay was used to determine these polymorphisms among 100 SCD patients and 100 healthy controls. Though not statistically significant, the frequency of individual carrying HMOX-1 polymorphic AT and TT genotypes in both patient and control groups was 92% and 85% respectively. Regarding CCR5Δ32 polymorphisms, all SCD patients harbored the wild genotype (100%), while the heteromutant genotype was encountered in 2% of our controls. Patients harboring mutant HMOX-1 had a less frequent vaso-occlusive crisis (VOC)/lifetime, less VOC in the last year, less incidence of stroke, less frequency of hospitalization, and responded more frequently to hydroxyurea with statistically significant differences (p = 0.028, 0.007, 0.046, 0.007, and 0.011 respectively). No significant associations with HbF level or other hematologic parameters were encountered among our cohort. Our study results suggest a protective effect of mutant HMOX-1 genotypes in ameliorating the phenotypic severity of the disease. HMOX1-413 A>T (rs2071746) polymorphisms might prove to be a prognostic marker among Egyptian SCD, but not CCR5Δ32 (rs333) polymorphisms.

BM, E. - Z., E. S, B. D, Z. NS, Z. NS, S. R, S. MA, A. - H. D, G. H, H. R, et al., "Effect of Procedural-Related Variables on Melanocyte-Keratinocyte Suspension Transplantation in Nonsegmental Stable Vitiligo: A Clinical and Immunocytochemical Study.", Dermatol Surg., vol. 43, issue 2, pp. 226-235, 2017.
BM, E. - Z., A. OA, Z. NS, A. - R. HM, B. DA, and K. MM, "PTPN22 gene polymorphism in Egyptian alopecia areata patients and its impact on response to diphencyprone immunotherapy.", Gene, vol. Epub ahead of print, 2013. Abstract

PTPN22 1858C>T gene polymorphism has been associated with several autoimmune disorders including alopecia areata. The aim of the current study was to investigate the effect of the inherited genetic polymorphism 1858C>T of PTPN22 gene on the predisposition to severe forms of alopecia areata and its effect on the response to DPC treatment. To achieve our aim, PTPN22 1858C>T genotyping was performed by PCR-based restricted fragment length polymorphism (PCR-RFLP) analysis. The study included 103 Egyptian patients with extensive alopecia areata treated by DPC. Hundred healthy age and sex matched blood donors were included in the current study as a control group. Results of genotyping showed that PTPN22 CT and TT mutant genotypes were significantly higher in AA patients compared to controls and conferred increase risk of AA (OR = 2.601, 95% CI = 1.081–6.255). Statistical comparison between AA patients with wild and mutant genotypes revealed that the duration of the illness was significantly longer in those harboring the mutant genotypes. Moreover, the association of other autoimmune diseases as atopy and diabetes mellitus was higher in patients with mutant genotypes. Furthermore, PTPN22 1858C>T genetic polymorphism did not affect the patients' response to DPC immunotherapy.

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and DA, - K. M. M. B., "Glutathione S-transferase M1 and T1 genetic polymorphism in Egyptian patients with nonsegmental vitiligo. ", Clinical and Experimental Dermatology, vol. 38, issue 2, pp. 160-3. , 2012.
Deen, M. A. K. E., M. M. Khorshied, Z. A. E. Sadani, Y. M. Amrousy, and N. M. Galal, "Mannose-binding lectin (MBL2) gene polymorphism in sickle cell anemia: an Egyptian study", Comparative Clinical Pathology , vol. 22, issue 3, pp. 387-394, 2013.
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El-Masry, M. W., M. M. Khorshied, I. A. Shaheen, N. N. Abulata, and T. A. Hashem, "Flow cytometric detection of leukemic stem cells (LSCs) in Egyptian pediatric B-acute lymphoblastic leukemia", Comparative Clinical Pathology, vol. 21, issue 5, pp. 993–997, 2012.
Enein, A. A. A., I. A. A. Khaled, M. M. Khorshied, A. O. A. El-Aziz, N. Zahran, A. M. El Saeed, H. I. Shousha, and H. A. L. A. Rahman, "Genetic variations in DNA-repair genes (XRCC1, 3, and 7) and the susceptibility to hepatocellular carcinoma in a cohort of Egyptians.", Journal of medical virology, vol. 92, pp. 3609–3616, 2020. Abstract

Chronic hepatitis C (CHC) is a worldwide etiology of chronic hepatic insult particularly in Egypt. DNA-repair systems are responsible for maintaining genomic integrity by countering threats posed by DNA lesions. Deficiency in the repair capacity due to genetic alterations in DNA-repair genes can lead to genomic instability and increased risk of cancer development. The present work aimed at studying the possible association between XRCC1-G28152A (rs25487), XRCC3-C18067T (rs861539), and XRCC7-G6721T (rs7003908) single nucleotide polymorphisms (SNPs) and the susceptibility to hepatocellular carcinoma (HCC) in Egyptian population. The study was conducted on 100 newly diagnosed HCC patients and 100 age- and sex-matched healthy controls. Laboratory workup revealed that all HCC patients have chronic hepatitis C viral infection. Genotyping of the studied SNPs was performed by real-time PCR. The heteromutant genotype of XRCC1 (GA) conferred an almost two-fold increased risk of HCC (OR ,  2.35; 95% CI, 1.33-4.04). Regarding XRCC7, the heteromutant (TG) genotype conferred a two-fold increased risk of HCC (OR ,  2.17; 95% CI, 1.23-3.82). Coinheritance of the polymorphic genotypes of XRCC1 and 7 was significantly higher in HCC cases than controls and was associated with an 11-fold increased risk of HCC (OR , 11.66; 95% CI,  2.77-49.13). The frequency of XRCC3 polymorphic genotypes in HCC patients was close to that of the controls.

Esmat, S., D. Bassiouny, M. A. Saleh, D. abd el halim, R. Hegazy, M. El Hawary, H. E. B. A. GAWDAT, H. Gouda, M. Khorshied, and N. E. S. R. I. N. SAMIR, "Studying the effect of adding growth factors to the autologous melanocyte keratinocyte suspension in segmental vitiligo.", Dermatologic therapy, vol. 33, issue 3, pp. e13368, 2020. Abstract

Addition of different growth factors to the medium used in autologous melanocyte-keratinocyte transplantation procedure (MKTP) was reported in the literature. The aim of the current study was comparison of response to MKTP in segmental vitiligo (SV) with and without adding growth factors to the suspension medium. Eighteen cases with SV were randomly divided into two groups. In group A: Ham F12 medium was used for suspension and in group B: 5 ng/mL recombinant basic fibroblast growth factor (bFGF) and 25 mg/500 mL 3'5' cyclic adenosine monophosphate (cAMP) were added to the medium. All cases received NB-UVB twice weekly for 24 weeks. The area of vitiligo lesions was measured before and after therapy by point-counting technique and complications were recorded. Excellent response (90%-100% repigmentation) occurred in 5/9 cases (56%) in group A and 7/9 cases (78%) in group B (with growth factors). A significant decrease in the area of treated lesions before and after therapy was found in both groups A and B (P = .0012 and .0004, respectively), however, a higher percentage of reduction in area of vitiligo was seen in group B cases (70% in group A vs 90% in group B; P value: .028). Marginal halo was seen in five cases in group A and six in group B. In conclusion addition of bFGF and cAMP to MKTP medium improved the results of the procedure. It could be considered if economically feasible.

Eyada, T. K., K. MM, M. A. K. E. Din, R. A. Zayed, A. Soliman, and D. O. Darwish, "PRAME and WT1 Genes expression in Chronic Myeloid Leukemia Patients: Clinical importance and future prospects", Pan Arab Journal of Oncology, vol. 1, issue 1, pp. 99-108, 2009.
Eyada TK, Farawela HM, K. M. M. S. I. A. S. N. M. K. I. A., "FcγRIIa and FcγRIIIa genetic polymorphisms in a group of pediatric immune thrombocytopenic purpura in Egypt.", Blood Coagul Fibrinolysis. , vol. 23, issue 1, pp. 64-8. , 2012.
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Farawela, H. M., M. M. Khorshied, H. M. Zawam, N. M. Kassem, and H. A. Kassem, "The clinical relevance and prognostic significance of adenosine triphosphate ATP-binding cassette (ABCB5) and multidrug resistance (MDR1) genes expression in acute leukemia: an Egyptian study.", J Cancer Res Clin Oncol. , vol. 140, issue 8, pp. 1323-30, 2014.
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Ghobrial, E. E., H. M. Marzouk, M. M. Khorshied, and M. G. Sayed, "Level of Interleukin 37 (IL-37) in Children with Systemic Lupus Erythematosus and Its Correlation with Disease Activity", Iranian Journal of Pediatrics 28 , vol. 28, issue 1, 2018.
Gouda, H. M., M. M. Khorshied, I. A. Shaheen, M. E. H. Sissy, and M. A. Mohsen, "Association between matrix metalloproteinase 2 (MMP2) promoter polymorphisms and the susceptibility to non-Hodgkin's lymphoma in Egyptians.", Ann Hematol. , vol. 93, issue 8, pp. 1313-8, 2014.
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H, F., K. M, S. I, Gouda H, N. A, A. N, M. HA, Z. HM, and M. SM., "The association between hepatitis C virus infection, genetic polymorphisms of oxidative stress genes and B-cell non-Hodgkin's lymphoma risk in Egypt.", Infect Genet Evol. , vol. 12, issue 6, pp. 1189–1194, 2012. AbstractCU-PDF

Hepatitis C virus (HCV) has been postulated to be an etiological agent for lymphoid malignancies. Polymorphisms in oxidative stress genes as; superoxide dismutase (SOD2), glutathione peroxidase (GPX1), catalase (CAT), myeloperoxidase (MPO) and nitric oxide synthase (NOS2) may influence non-Hodgkin’s lymphoma (NHL) risk. HCV screening and polymorphisms in these five genes coding for antioxidant enzymes were studied in 100 Egyptian patients with B cell-NHL and 100 controls to clarify the association between HCV infection, oxidative stress genes polymorphisms and B cell-NHL risk. A significantly higher prevalence of HCV infection was detected among NHL patients relative to controls and this carried a 14-fold increased NHL risk (odds ratio (OR) = 14.3, 95% confidence interval (CI) = 5.4–38.3, p < 0.0001). GPX1 and MPO genetic polymorphisms conveyed increase in B-NHL risk (OR = 3.3, 95% CI = 1.4–7.4, p = 0.004 and OR = 4.4, 95% CI = 1.3–14.2, p = 0.009 respectively). Further analyses stratified by HCV infection revealed that concomitant HCV infection and GPX1 gene polymorphism had a synergetic effect on NHL risk with an OR of 15 (95%CI = 2.2–69.6, p < 0.0001). In addition, combined HCV infection and MPO gene polymorphisms had a pronounced NHL risk (OR = 9.2, 95%CI = 2.5–33.9, p < 0.0001). SOD2, CAT and NOS2 genetic polymorphisms were not found to confer increased NHL risk. This study revealed that HCV infection is a risk factor for NHL in Egypt. Polymorphisms in GPX1 and MPO genes may influence NHL risk in HCV infected Egyptian patients. Larger scale studies are warranted to establish this genetic susceptibility for NHL.

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