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Cell:重磅!科学家成功绘制出人类癌细胞的全局基因互作网络!

2017-02-04 生物谷 生物谷

癌症是一种异质性疾病(heterogeneous disease),而且不同的癌症亚型之间也有着不同的遗传根源,因此多种类型的癌症往往会依赖于多种途径得以发展,而且其对抗癌制剂的反应也并不相同,目前对于研究人员最大的挑战就是如何精确地定义癌症利用的多种途径,以及寻找癌症易感性来帮助开发新

图片来源:www.sciencedaily.com

癌症是一种异质性疾病(heterogeneous disease),而且不同的癌症亚型之间也有着不同的遗传根源,因此多种类型的癌症往往会依赖于多种途径得以发展,而且其对抗癌制剂的反应也并不相同,目前对于研究人员最大的挑战就是如何精确地定义癌症利用的多种途径,以及寻找癌症易感性来帮助开发新型抗癌疗法。

近日,刊登在国际著名杂志Cell上的一篇研究报告中,来自怀海德研究所和博德研究所的研究人员就取得了巨大突破,他们成功鉴别出了对14种人类急性髓性白血病癌细胞增殖和生存必须的一系列关键基因,此前研究人员并未利用基因组测序手段对这些癌细胞的特性进行研究;这项研究中研究人员将基因本质图谱同当前的遗传信息相结合进行研究阐明了多种癌症的特性。

文章中,研究者重点对和Ras癌基因相关联的基因和蛋白通路进行了研究,Ras基因是很多人类癌症中经常发生突变的癌基因,而且其在急性髓性白血病的发病过程中扮演着重要角色,研究者Tim Wang说道,从很大程度上来讲,突变的Ras蛋白自身往往被认为是无法用药物进行靶向作用的,但在本文研究中我们找到了另外一种方法,并且基于这种方法发现了Ras突变的癌症所依赖的一些基因,而且我们希望这些基因是利用药物可以进行控制的,但很不幸的是诸如这些Ras合成致死性基因往往很难进行鉴别。

利用基于CRISPR的基因编辑技术,研究人员测定了敲除掉人类基因组中18000个蛋白编码基因中每一个基因后的影响,这或许能够帮助研究者快速鉴别出仅在Ras突变细胞中需要的候选基因;同时研究者们还认为利用一般的方法也能够帮助寻找很多类型癌症的脆弱点。除了定义Ras特异性的基因网络外,本文研究数据还能够帮助研究人员解析此前未进行研究的基因的分子功能。

首先研究人员开始关注那些对于某些细胞必需但对于某些细胞可有可无的基因来进行研究,对于每一个基因而言,研究者都会进行数据筛选来寻找能够进行匹配的基因;但本文研究让研究者比较兴奋的一点就是他们能够广泛利用特殊技术来阐明大量人类基因基因功能组织的相关信息以及这些基因在人类疾病中所扮演的角色。

原始出处:

Tim Wang, Haiyan Yu, Nicholas W. Hughes, Bingxu Liu, Arek Kendirli, Klara Klein, Walter W. Chen, Eric S. Lander Eric S. Lander, David M. Sabatini8.Gene Essentiality Profiling Reveals Gene Networks and Synthetic Lethal Interactions with Oncogenic Ras.doi:10.1016/j.cell.2017.01.013


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    2017-02-19 维他命
  3. 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    2017-02-05 yxch36
  4. 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    2017-02-05 ylz8405
  5. 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    2017-02-05 xxxx1054
  6. 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    2017-02-05 wmu姿

    太厉害了

    0

  7. 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    2017-02-05 wmu姿

    太厉害了

    0

  8. 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    2017-02-05 ann y

    科学家成功绘制出人类癌细胞的全局基因互作网络

    0

  9. 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    2017-02-05 ann y

    科学家成功绘制出人类癌细胞的全局基因互作网络

    0

  10. 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    2017-02-05 ann y

    科学家成功绘制出人类癌细胞的全局基因互作网络

    0

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图片来源:www.sciencedaily.com 很多人都知道,利用放疗能够治疗很多类型的癌症,然而有些人却并不会意识到有些癌细胞或许对放疗并没有反应,口腔鳞状细胞癌(OSCC)就是其中一种癌症,近日,来自日本熊本大学的研究人员就通过研究寻找能够抵御癌细胞对放疗产生耐受性的方法,相比直接作用癌细胞而言,他们试图去寻找一种方法来控制细胞的生物学机制从而帮助抵御癌细胞对放疗产生耐受性,

Gene Dev:揭示癌细胞在体内扩散机制

每天,在美国有1600多人死于癌症,在英国有450人死于癌症,主要是因为癌症已发生转移,产生治疗抵抗性。尽管人们已开展几十年的研究,但是理解癌细胞如何变成浸润性的仍然是个谜。 在一项新的研究中,来自英国牛津大学路德维格癌症研究所的Colin Goding博士及其团队鉴定出一种在进化过程中保守的古老细胞反应促进侵袭性皮肤癌(即黑色素瘤)扩散。这项研究揭示了黑色素瘤内的有害条件在让一小部分肿

Oncogene:抗p53缺陷癌细胞的新靶点!

双功能酶6-磷酸果糖-2-激酶/果糖-2,6-二磷酸酶-4(PFKFB4)通过糖酵解的变构调节控制代谢通量。近期,一篇发表在Ocogene杂志上的文章展示了p53调节PFKFB4的表达和p53缺陷癌细胞高度依赖这种酶的功能。研究表明p53可以通过绑定到其启动子下调PFKFB4的表达,并且通过组蛋白脱乙酰酶介导转录抑制作用。 PFKFB4从p53缺陷癌细胞的耗竭增加了变构调节剂果糖-2,6-二磷酸的

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