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Antican Res & Epigenom:揭示隐藏在癌症背后的表观遗传学“开关”机制

  1. “开关”机制
  2. 癌症
  3. 表观遗传学

来源:生物谷 2014-06-04 10:09

近日,刊登在国际杂志Anticancer Research和Epigenomics上的两篇研究报告中,来自波士顿大学医学院的研究人员通过研究表明,表观遗传开关的开启或关闭或许是隐藏在许多类型癌症发生背后的机制;表观遗传是一种现象,即遗传上均一的细胞会表达不同的基因,最终引发不同的物理学特性。

2014年6月4日讯 /生物谷BIOON/ --近日,刊登在国际杂志Anticancer ResearchEpigenomics上的两篇研究报告中,来自波士顿大学医学院的研究人员通过研究表明,表观遗传开关的开启或关闭或许是隐藏在许多类型癌症发生背后的机制;表观遗传是一种现象,即遗传上均一的细胞会表达不同的基因,最终引发不同的物理学特性。

当前癌症发生的原因归结于环境因素和机体自身的遗传改变,进一步将就是机体癌症的发生都来自于遗传突变、暴露于毒性物质中或者激素的失衡等;癌症的发生极其复杂,很多人都知道新的突变以及许多癌症引发基因的激活都会在癌症的发生和发展过程中出现。

研究者Sibaji Sarkar教授表示,如果我们认为自然界中的万物都是以一种有组织的形式发生的,那么假设癌症的发生并不是杂乱无章的理论也是合乎逻辑的,而引发癌症的一般机制也是必然存在的。肿瘤可以通过不同阶段来发展间接地支撑了表观遗传学开关存在的理论,当癌症发生过程中癌细胞会快速生长,其会在当前的阶段非常稳定,而且其特性也不会轻易改变。

Sarkar说道,如果我们认为所有不可逆转的改变、突变以及致癌物的效应会促使细胞快速生长,那么使得细胞停止生长的机制就显得尤为重要,研究癌症的发展是揭示癌细胞不断生长分化的重要阶段,在癌症发展过程中存在细胞快速生长和分化的不同阶段,而允许生长和分化的开关控制仅仅是通过不可逆转的机制来实现的,比如表观遗传改变。

此前研究者认为表观遗传改变涉及癌症祖细胞的形成以及癌症的发展,而且研究者也认为表观遗传的改变可以控制癌细胞的快速生长以及其特性的改变。最后研究者表示,当调节遗传改变的表观遗传代码不能够被识别时,揭示癌症祖细胞的不可逆及千变万化的改变就变得相当有趣了,未来研究者们将通过进行更为深入的表观遗传学研究来为开发新型杀灭癌症祖细胞的药物以及新型疗法提供一定的思路和希望,同时也为减少癌症复发和降低癌细胞耐药提供研究数据。(生物谷Bioon.com)

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Genetic and Epigenetic Aspects of Breast Cancer Progression and Therapy

SHANNON BYLER, SARAH GOLDGAR, SARAH HEERBOTH, MEGHAN LEARY, GENEVIEVE HOUSMAN*, KIMBERLY MOULTON and SIBAJI SARKAR⇑

Although breast cancer is a heterogeneous disease that is challenging to characterize and treat, the recent explosion of genetic and epigenetic research may help improve these endeavors. In the present review, we use genetic diversity to characterize and classify different types of breast cancer. We also discuss genetic and epigenetic changes that are involved in the development of different breast cancer types and examine how these changes affect prognosis. It appears that while a combination of mutations and copy number changes determine the type of breast cancer, epigenetic alterations may be the primary initiators of cancer development. Understanding these critical biomarkers and molecular changes will advance our ability to effectively treat breast cancer. Next, we examine potential drug therapies directed at epigenetic changes, as such epigenetic drug treatments may prove useful for treating patient-specific tumors, breast cancer progenitor cells, and drug-resistant cells. Lastly, we discuss on mechanisms of carcinogenesis, including a novel hypothesis outlining the role of epigenetics in the development of cancer progenitor cells and metastasis. Overall, breast cancer subtypes may have a similar epigenetic signal that promotes cancer development, and treatment may be most effective if both epigenetic and genetic differences are targeted.

Do epigenetic drug treatments hold the key to killing cancer progenitor cells?

Shannon Byler​‌ & Sibaji Sarkar​‌

The current paradigm states that cancer develops from environmental and genetic changes to cancer progenitor cells. These changes are the result of mutations, exposure to toxic substances or hormonal imbalances. Cancer progression is extremely complex, however. It also is well known that new mutations and the activation of more cancer causing genes occur throughout the development and progression of cancer. "If we believe that everything in nature occurs in an organized fashion, then it is logical to assume that cancer development cannot be as disorganized as it may seem," said Sibaji Sarkar, PhD, instructor of medicine at BUSM and the articles corresponding author. "There should be a general mechanism that initiates cancer progression from predisposed progenitor cells, which likely involves epigenetic changes."

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