G Hayri Özsan

Dokuz Eylul University, İzmir, Izmir, Turkey

Are you G Hayri Özsan?

Claim your profile

Publications (9)5.43 Total impact

  • Deri Hastaliklari ve Frengi Arsivi 09/2013; 47(3):176-179. DOI:10.4274/turkderm.86094 · 0.05 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Therapy-related leukemias are 10-20% of all acute leukemia cases. Therapy-related acute lymphoblastic leukemia (ALL) is less frequent than therapy-related acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS). In this paper, we present a patient with Ewing's sarcoma (ES) in the soft tissue of his right breast cured by chemotherapy and radiotherapy. He developed Philadelphia negative (Ph(-)) ALL four years following the therapy. (Marmara Medical Journal 2012;25:100-2) Key Words: Ph(-) ALL, Secondary leukemia, Ewing's sarcoma
    Marmara Medical Journal 01/2012; DOI:10.5472/MMJ.2012.02158.1
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Fludarabine-containing combinations have additive cell killing against leukemic blasts in vitro. It has also been shown that imatinib mesylate combined with fludarabine or cladribine had an additive effect on CML CFU-GM cells. In this regard, we aimed to investigate the effect of fludarabine-imatinib mesylate combination against CML blastic phase cell lines K562 and Meg-01. XTT test was performed for proliferation and inhibition assay. According to ob-tained data, five different effective concentrations of each drug in 25 different combinations were tested. Results of the combination studies were analyzed with isobologram. At IC 20 , imatinib mesylate and fludarabine combination showed synergism and strong synergism in K562 and Meg-01 cells, respectively. At IC 50 and IC 75 , combination indexes (CI) indicated strong synergism and synergism. Based on our results, the fludarabine-based chemotherapy regimens can be used for those patients with CML blastic phase in combination with imatinib mesylate. ÖZET İmatinib mesilat ve fludarabin kombinasyonunun Filadelfiya kromozomu pozitif kronik myeloid lösemi hücre serileri üzerindeki sinerjistik etkisi In vitro koşullarda fludarabin içeren kombinasyonların lösemik blastlar üzerinde ve fludarabin ya da kladribinin imatinib mesilat ile kombinasyonlarının KML CFU-GM hücrelerine karşı aditif etkinliğe sahip oldukları gösterilmiştir. Bu gözlemlere dayanarak biz de fludarabin ve imatinib mesilat kombinasyonunun KML blastik faz hücre serileri K562 ve Meg-01 üzerine olan etkinliğini araştırmayı planladık. Proliferasyon ve inhibisyon göstergesi olarak XTT testini kul-landık. Elde edilen verilere göre, her ilacın beş farklı etkin konsantrasyonu 25 farklı kombinasyon halinde test edildi. Kombinasyon çalışmalarının sonuçları izobologram ile analiz edildi. İmatinib mesilat ve fludarabinin kombinasyonunun K562 ve Meg-01 hücre serileri için IC 20 kombinasyon indeksi değerleri sırası ile sinerjistik ve güçlü sinerjistik, IC 50 ve IC 75 değerlerinde de güçlü sinerjistik ve sinerjistik etkinliği göstermekte idi. Bu sonuçlar KML blastik fazdaki hastalar için imatinib mesilat ile kombine edilen fludarabin bazlı rejimlerin kullanılabileceğini göstermektedir.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: ZET Polisitemia veralı hastalarda farklı sitokinler varlığında eritroid koloni gelişimi üzerine imatinib mesylate'ın etkisi Kronik myeloid lösemi tedavisinde kullanılan imatinib mesilat aynı zamanda kök hücre faktörünü de inhibe etmektedir. Imatinib mesilatın bazı polistemia veralı hastalarda otonom eritroid koloni gelişimini inhibe ettiği ve flebotomi ihtiyacını azalttığı da gösterilmiştir. Bu çalışmada, imatinib mesilat varlığında, polistemia veralı üç hasta ile sağlıklı dört kontrol-den elde edilen periferik kan eritroid öncül hücreleri üzerine yarı-katı ortamda insülin benzeri büyüme faktörü-l (IGF-l), kök hücre faktörü (SCF) ve eritropoietin (EPO) ile interlökin-3 (IL-3), granülosit-koloni stimule edici faktörün (GM-CSF) ve granülosit-koloni stimule edici faktörünün (G-CSF) etkisi araştırıldı. Sağlıklı kontrollerden elde edilen hematopoietik öncü hücrelerden eritroid koloni gelişimi sadece tüm sitokinlerin varlığında gözlendi. Bununla birlikte eritroid kolonile-rin sayısı polistemia veralı hastalardan elde edilen sayılara ulaşamadı. Imatinib mesilatın eritroid koloni gelişimi üzerin-deki inhibe edici etkisi belirgindi. Polistemia veralı hastaların hematopoietik öncüllerinden iki tip eritroid koloni gelişimi gözlendi; ilki eksojen sitokinlerden bağımsız ve sitokinlere aşırı duyarlılık gösteren, ikincisi ise eksojen sitokinlere aşırı duyarlılık gösteren tip idi. Her iki tipte de IL-3, GM-CSF ve EPO de dahil olmak üzere, sitokinlerin varlığında imatinib mesilatın inhibe edici etkisi belirgindi. Imatinib mesilatın bu etkisinin IL-3, G-CSF, GM-CSF, EPO ve IGF-l üzerine olduğu-nu söylemek için henüz yeterli kanıt yoktur. Bu çalışmanın sonuçları daha önceki çalışmalardan elde edilen bilgilerle birlikte değerlendirildiğinde, imatinib mesilatın eritroid koloni gelişimini inhibe edici etkisinin kök hücre faktörünün ve reseptörlerinin rol aldığı sinyal ileti yolları üzerinden olduğu söylenebilir. ABSTRACT It has been shown that imatinib mesylate, a drug used in the treatment of chronic myelogenous leukemia, inhibits the effect of stem cell factor, which has a central role in erythropoiesis. In some polycythemia vera (PV) patients, it has inhibited autonomous erythroid colony growth in vitro and decreased the need for phlebotomy. In this study we have investigated the effect of insulin like growth factor (IGF)-I, stem cell factor (SCF) and erythropoietin (Epo) with interleukin (IL)-3, granulocyte macrophage-colony stimulating factor (GM-CSF) and granulocyte-colony stimulating factor (G-CSF) in the presence of imatinib mesylate on the erythroid progenitors derived from peripheral blood mononuclear cells of three patients with PV and four healthy controls in semisolid medium. Erythroid colony formation from hematopoietic progenitors obtained from healthy controls was observed only in the presence of all cytokines. However, the number of erythroid colonies could not reach that of patients with PV. Inhibition of imatinib mesylate on erythroid colony growth was evident. Hematopoietic progenitors of patients with PV displayed two types of colony formation: the first type was exogenous cytokine-independent and was hypersensitive to current cytokines, and the second displayed hypersensitiv-ity to current exogenous cytokines, but was exogenous cytokine-dependent. For both types, the inhibitory effect of ima-tinib mesylate was striking in the presence of all cytokines including IL-3, GM-CSF and Epo. There is no direct evidence yet that imatinib mesylate could inhibit the effect of IL-3, G-CSF, GM-CSF, Epo and IGF-I on erythropoiesis. Considering former studies together with results of this study, it can be argued that imatinib mesylate is effective in PV on the inter-secting signal transduction mechanisms in which stem cell factor and its receptor may have a part.
  • Leukemia Research 04/1997; 21(1). DOI:10.1016/S0145-2126(97)81251-9 · 2.69 Impact Factor
  • Leukemia Research 04/1997; 21(1). DOI:10.1016/S0145-2126(97)81254-4 · 2.69 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Materials and Methods: Twenty-three patients with BD (mean age: 38.3 ± 10.83, M/F: 5/18) diagnosed according to the criteria of the International Study Group and 20 healthy volunteers (mean age: 38.05 ± 6.29, M/F: 9/11) were enrolled in this study. Patients with liver or renal disease, diabetes mellitus, coronary artery disease, hemophilia, antiphospholipid antibody positivity or using oral contraceptive drugs were excluded from the study. Plasma TAFI levels were determined by using an ELISA test. Results: The mean TAFI antigen levels were 8.40 ± 1.81µg/ml in BD patients and 7.30 ± 0.64 µg/ml in healthy volunteers. A statistically significant difference was found between TAFI antigen levels of these two groups (P = 0.01). Conclusions: TAFI antigen levels were found to be increased in BD, regardless of thrombotic events. To clarify the exact role of TAFI in thrombotic complications of the disease, future studies including more patients with and without thrombosis are needed.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The effect of interleukin-1 (IL-1) as an autocrine growth factor on the proliferation of the acute mye-loblastic leukemia (AML) blasts was studied. Bone marrow specimens were obtained from nine patients with different subgroups of AML. IL-1 receptor antagonist (IL-1RA) and IL-1 ß neutralizing antibody (IL-1ß NA) alone or in combination were added to the culture mediums of the AML blast cultures for the de-tection of their inhibitory effect on AML blast cell proliferation and colony formation. Average colony num-bers in the IL-RA, IL-ßNA, and IL-IRA plus IL-IßNA included culture flasks, were 63.7 ± 21.5 %, 69.5 ± 19 %, 53.4 ± 23.7 %, respectively, as compared to those of the control (p < 0.01). Inhibition of colony for-mation by IL-IRA plus IL-IßNA was more prominent than by IL-IßNA alone (p < 0.01). No correlation bet-ween the inhibition of AML blast colony formation and FAB AML subgroups was seen. Result: Both IL-1RA or IL-IßNA or in combination induced varying degrees of inhibition on blast co-lony formation. IL-I inhibitory molecules could be considered as an alternative therapy for AML in pati-ents whose blast cells are sensitive to IL-1 inhibition.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Myelomatous pleural effusion is extremely rare and cases with cavitary involvement are mostly IgA type myeloma. The effusion is thought as a late manifestation in the natural history of multiple myeloma or an expression of the aggressive behaviour of the disease and a very aggressive treatment is indicated. A case of myelomatous effusion pre-senting as plasma-cell leukemia two years after initial diagnosis of IgG type multiple myeloma is described. ÖZET Plazma Hücreli Lösemi ve Myelomatöz Efüzyon: Olgu Sunumu Myelomatöz efüzyon oldukça nadir görülmekte olup, olgularda kaviter tutulum sıklıkla IgA tip multiple myeloma ile birliktelik göstermektedir. Efüzyon hastalığın doğal sürecinde geç dönemde ortaya çıkan bir bulgu olmakla birlikte, hastalığın saldırgan özelliğinin bir sonucu da olabilir ve agresif bir tedavi yaklaşımı gerektirir. İki yıl önce IgG tip mul-tiple myelom tanısı alarak, myelomatöz plevral efüzyon olarak değerlendirilen ve plazma hücreli lösemi olduğu tesbit edilen olgu literatür eşliğinde sunuldu.