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Vitiligo is a developed depigmentation disorder consisting of two forms which are segmental vitiligo (SV), affect one side of the body in 50% of individuals and non-segmental vitiligo (NSV) which is more common and affects both side of the body. A studydocumented that vitiligo susceptibility genes that are linked to immune regulation and immune targeting of melanocytes which are Tumor necrosis factor alpha (TNF-α), Interferon gamma (IFN-γ) and interleukin 10 (IL-10), are responsible for the pathogenesis of vitiligo. This study was designed to shed light on cytokinesand oxidative stress which may play a critical role in the pigmentary process of NSV.Fifty NSV patients were collected from dermatology department Baghdad teaching hospital, Baghdad, Iraq. And fifty healthy volunteers' individuals enrolled in this study during the period from November 2018 to May 2019. Some parameters including the concentration of immunological guideline TNF-α, IFN-γ and IL-10, and the level of oxidative stress H2O2 in malondialdehyde (MDA) form and superoxide dismutase SOD were evaluated in sera using ELISA technique.Serum level of TNF-α and IFN-γ were significantly higher in patient as compared to control. While serum IL-10 was significantly lower in vitiligo when compared with healthy.The assayed serum level of oxidative stress MDA and superoxide dismutase was found to be increased in vitiligo.There was an imbalance between pro and anti-inflammatory cytokines. Elevated levels of MDA and SOD suggested that an oxidative stress and antioxidants could play an adjuvant role in the management of vitiligo in addition to specific therapies.

Glioblastoma multiforme is the most aggressive malignant primary brain tumor in humans, with poor prognosis. A new glioblastoma cell line (ANGM5) was established from a cerebral glioblastoma multiforme in a 72-year-old Iraqi man who underwent surgery for an intracranial tumor. This study was carried out to evaluate the antitumor effect of live attenuated measles virus (MV) Schwarz vaccine strain on glioblastoma multiforme tumor cell lines in vitro. Live attenuated MV Schwarz strain was propagated on Vero, human rhabdomyosarcoma, and human glioblastoma-multiform (ANGM5) cell lines. The infected confluent monolayer appeared to be covered with syncytia with granulation and vacuolation, as well as cell rounding, shrinkage, and large empty space with cell debris as a result of cell lysis and death. Cell lines infected with virus have the ability for hemadsorption to human red blood cells after 72 hours of infection, whereas no hemadsorption of uninfected cells is seen. Detection of MV hemagglutinin protein by monoclonal antibodies in infected cells of all cell lines by immunocytochemistry assay gave positive results (brown color) in the cytoplasm of infected cells. Cell viability was measured after 72 hours of infection by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Results showed a significant cytotoxic effect for MV (P≤0.05) on growth of ANGM5 and rhabdomyosarcoma cell lines after 72 hours of infection. Induction of apoptosis by MV was assessed by measuring mitochondrial membrane potentials in tumor cells after 48, 72, and 120 hours of infection. Apoptotic cells were counted, and the mean percentage of dead cells was significantly higher after 48, 72, and 120 hours of infection compared with control cells. This study concludes that live attenuated MV Schwarz vaccine induces the oncolytic effect in Iraqi tumor cell line ANGM5 and in the rhabdomyosarcoma cell line through syncytia in tumor cells, which is one of the causes of cell death. The MV vaccine strain has the ability to insert its hemagglutinin protein into the tumor cell surface, leading to modification of the antigenic surface of tumor cells that may induce an antitumor immune response, MV vaccine strain induced cell killing by direct cytolysis and apoptosis induction. These antitumor features may indicate the use of MV in the treatment of glioblastoma.

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Background: Acute myeloid leukemia (AML) is a hematopoietic disorder in which there are too many immature blood-forming cells accumulating in the bone marrow and interfering with the production of normal blood cells. It has long been recognized that AML is a clinically heterogeneous disease characterized by a multitude of chromosomal abnormalities and gene mutations, which translate to marked differences in responses and survival following chemotherapy. This study aimed to clarify the chromosomal aberrations in early diagnosed and relapsed cases of AML. Materials and methods: Chromosomal changes were studied in thirty Iraqi patient samples diagnosed with acute myeloid leukemia were divided into 9 newly diagnosed and 13 received chemotherapy who were incomplete remission and 8 relapsed subjects. Results: Analysis of all chromosomal aberrations showed complex karyotype for most cells of relapsed AML patients compared with newly diagnosed patients. Conclusions: Chromosomal abnormalities are linked to AML development and high complexity of karyotyping for relapsed group.