47 research outputs found

    A leggyakoribb nem onkológiai eredetű nőgyógyászati kórképek epigenetikai háttere

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    Epigenetic effects influence the function of genes regulating the main physiological mechanisms. Some of these environmental factors may reduce or inhibit the function of these genes. The environmental effects on gene function may result in a change of the DNA structure leading to non-heritable phenotype changes. Epigenetic factors play an important etiological role in the development of numerous diseases in obstetrics and gynecology. Uterine fibroids probably have a complex etiological background including epigenetic mechanisms. The multifactorial aetiology of endometriosis suggests key roles for immunological and hormonal factors in the development of the diseases. These mechanisms are influenced by epigenetic factors, which may serve as therapeutic targets in the future. The possible in utero origin of polycystic ovary syndrome determines the main directions of research concerning epigenetic factors in the etiological background, with the hope of eventual prevention and/or treatment in the preconceptional period as well as during pregnancy care. Orv. Hetil., 2014, 155(13), 492-499

    A méh leiomyomája = Uterine leiomyoma

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    A leiomyoma, a méh benignus, simaizom-eredetű daganata, a méheltávolítás leggyakoribb javallatát képezi világszerte. A tumor a nők akár 20–25%-ában is kialakulhat, olyan tüneteket okozva, mint vérzészavar, alhasi fájdalom, esetenként infertilitás. A kezelés fő irányát mind a mai napig a sebészi terápia jelenti, ugyanakkor mind több csekély invazivitású eljárás áll rendelkezésre, amelyek a hysterectomia és myomectomia alternatíváját jelentik. Ezen módszerek legnagyobb hátrányát az alkalmazásukat követően a recidívák kialakulása jelenti. Léteznek a gyógyszeres terápia lehetőségei is; ezek használatát azonban korlátozzák a hosszú távú kezelés kapcsán várható mellékhatások. A szerzők tanulmányukkal áttekintést nyújtanak e gyakori nőgyógyászati betegségről, amelynek biológiai-genetikai alapjait jobban megismerve a kezelés új és hatékony lehetőségei válhatnak a klinikusok számára elérhetővé. Orv. Hetil., 2010, 42, 1734–1741. | Uterine fibroids, benign tumors of the human uterus, are the most common indication for hysterectomy. They are clinically apparent in 20–25% of women and cause significant complaints, like prolonged and heavy menstruation, pelvic pressure or pain, sometimes reproductive dysfunction. Though surgery has been the mainstay of fibroid treatment, various minimally invasive procedures have been developed in addition to hysterectomy and abdominal myomectomy. Formation of new leiomyomas after these conservative therapies remains a substantial problem. Also drug-therapy methods are available, but the possible side-effects limit their long-term use. Authors attempt to give an overview of this common gynecological disease, yielding a new insight into the basic biology and genetics of fibroids, with the hope of new and effective methods of therapy in the future. Orv. Hetil., 2010, 42, 1734–1741

    Identification of Galectin-1 as a Critical Factor in Function of Mouse Mesenchymal Stromal Cell-Mediated Tumor Promotion

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    Bone marrow derived mesenchymal stromal cells (MSCs) have recently been implicated as one source of the tumor-associated stroma, which plays essential role in regulating tumor progression. In spite of the intensive research, the individual factors in MSCs controlling tumor progression have not been adequately defined. In the present study we have examined the role of galectin-1 (Gal-1), a protein highly expressed in tumors with poor prognosis, in MSCs in the course of tumor development. Co-transplantation of wild type MSCs with 4T1 mouse breast carcinoma cells enhances the incidence of palpable tumors, growth, vascularization and metastasis. It also reduces survival compared to animals treated with tumor cells alone or in combination with Gal-1 knockout MSCs. In vitro studies show that the absence of Gal-1 in MSCs does not affect the number of migrating MSCs toward the tumor cells, which is supported by the in vivo migration of intravenously injected MSCs into the tumor. Moreover, differentiation of endothelial cells into blood vessel-like structures strongly depends on the expression of Gal-1 in MSCs. Vital role of Gal-1 in MSCs has been further verified in Gal-1 knockout mice. By administering B16F10 melanoma cells into Gal-1 deficient animals, tumor growth is highly reduced compared to wild type animals. Nevertheless, co-injection of wild type but not Gal-1 deficient MSCs results in dramatic tumor growth and development. These results confirm that galectin-1 is one of the critical factors in MSCs regulating tumor progression
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