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Epigenesis of Carcinogenesis as Inflammatory Cytokine Mechanics

机译:表观遗传学作为炎症细胞因子的机制。

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Epigenesis in malignant evolution would transform mechanics of development of genetic mutationin terms of failure of DNA repair pathways. Genetic instability would be an expressed result of the developmentof mutagenesis that includes such failed DNA repair mechanisms. The cytokine/chemokine axis of influencein terms of carcinogenesis might particularly implicate proliferation of cells and infiltration of stroma involvingalso targeted action of trophic factors. Epigenesis would be an expression of a malignant transformation eventthat incorporates various modes of evolution in DNA mutagenesis. DNA mutations that develop as multiplepathways of impaired subsequent mutational repair mechanisms would both account for and extend theinfluence of genetic instability systems in carcinogenesis. One might recognize a full array of mechanisticevents inherent to a concept of transformational processes both originating and subsequently promotingvarious systems of tropism and trophism even as the cellular clonality is itself extended beyond the initialcarcinogenetic focus.
机译:就DNA修复途径的失败而言,恶性进化中的表观遗传学将改变遗传突变的发展机制。遗传不稳定性将是诱变发展的表达结果,其中包括这种失败的DNA修复机制。就致癌作用而言,影响的细胞因子/趋化因子轴可能特别暗示细胞增殖和基质浸润,其中还涉及营养因子的靶向作用。表观遗传学将是恶性转化事件的一种表达,在DNA诱变中结合了多种进化模式。作为受损的后续突变修复机制的多种途径而发展的DNA突变将解释并扩展遗传不稳定系统在致癌中的影响。人们可能会认识到转化过程概念固有的一整套机制事件,这些转化过程既起源于又促进了各种向心性和营养性系统,即使细胞克隆性本身已超出了最初的致癌重点。

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