Scientists have known for more than two decades that cancer is a disease of the genes. Something scrambles the Dna inside a nucleus, and suddenly, instead of dividing in a measured fashion, a cell begins to copy itself furiously. Unlike an ordinary cell, it never stops. But describing the process isn't the same as figuring it out. Cancer cells are so radically different from normal ones that it's almost impossible to untangle the sequence of events that made them that way. So for years researchers have been attacking the problem by taking normal cells and trying to determine what changes will turn them cancerous--always without success.
Until now. According to a report in the current issue of Nature, a team of scientists based at M.I.T.'s Whitehead Institute for Biomedical Research has finally managed to make human cells malignant--a feat they accomplished with two different cell types by inserting just three altered genes into their DNA. While these manipulations were done only in lab dishes and won't lead to any immediate treatment, they appear to be a crucial step in understanding the disease. This is a "landmark paper," wrote Jonathan Weitzman and Moshe Yaniv of the Pasteur Institute in Paris, in an accompanying commentary.
The dramatic new result traces back to a breakthrough in 1983, when the Whitehead's Robert Weinberg and colleagues showed that mouse cells would become cancerous when spiked with two altered genes. But when they tried such alterations on human cells, they didn't work. Since then, scientists have learned that mouse cells differ from human cells in an important respect: they have higher levels of an enzyme called telomerase. That enzyme keeps caplike structures called telomeres on the ends of chromosomes from getting shorter with each round of cell division. Such shortening is part of a cell's aging process, and since cancer cells keep dividing forever, the Whitehead group reasoned that making human cells more mouselike might also make them cancerous.
The strategy worked. The scientists took connective-tissue and kidney cells and introduced three mutated genes--one that makes cells divide rapidly; another that disables two substances meant to rein in excessive division; and a third that promotes the production of telomerase, which made the cells essentially immortal. They'd created a tumor in a test tube. "Some people believed that telomerase wasn't that important," says the Whitehead's William Hahn, the study's lead author. "This allows us to say with some certainty that it is."
Understanding cancer cells in the lab isn't the same as understanding how it behaves in a living body, of course. But by teasing out the key differences between normal and malignant cells, doctors may someday be able to design tests to pick up cancer in its earliest stages. The finding could also lead to drugs tailored to attack specific types of cancer, thereby lessening our dependence on tissue-destroying chemotherapy and radiation. Beyond that, the Whitehead research suggests that this stubbornly complex disease may have a simple origin, and the identification of that origin may turn out to be the most important step of all.
1.From the first paragraph, we learn that ________________.
[A] scientists had understood what happened to normal cells that made them behave strangely
[B] when a cell begins to copy itself without stopping, it becomes cancerous
[C] normal cells do no copy themselves
[D] the DNA inside a nucleus divides regularly
2.Which of the following statements is true according to the text
[A] The scientists traced the source of cancers by figuring out their DNA order.
[B] A treatment to cancers will be available within a year or two.
[C] The finding paves way for tackling cancer.
[D] The scientists successfully turned cancerous cells into healthy cells.
3.According to the author, one of the problems in previous cancer research is ________.
[A] enzyme kept telomeres from getting shorter
[B] scientists didn’t know there existed different levels of telomerase between mouse cells and human cells
[C] scientists failed to understand the connection between a cell’s aging process and cell division.
[D] human cells are mouselike
4.Which of the following best defines the word “tailored” (Line 4, Paragraph 5)
[A] made specifically
[B] used mainly
[C] targeted
[D] aimed
5.The Whitehead research will probably result in ___________.
[A] a thorough understanding of the disease
[B] beating out cancers
[C] solving the cancer mystery
[D] drugs that leave patients less painful
答案:B C B A D
篇章剖析:
本文是一篇说明文,介绍了在癌症研究方面的新突破。第一段概要介绍了以往的研究和遭遇的困难;第二段介绍了麻省理工学院科学家的研究突破;第三段介绍了过去科学家的研究对这次发现的影响;第四段介绍了这次研究的具体内容;最后一段介绍了这一突破的重大意义。
词汇注释:
scramble: [5skrAmbl] v. 搅乱, 使混杂
nucleus: [5nju:kliEs] n. 细胞核
measured: [5meVEd] adj. 标准的, 整齐的, 有规则的
untangle: [5Qn5tAN^l] v. 理清(某个让人迷惑或复杂难解的事物);澄清或解决
cancerous: [`kAnsErEs] adj. 癌的
biomedical: [7baiEu5medikE] adj. 生物(学和)医学的
malignant: [mE5li^nEnt] adj. 恶性的(肿瘤)
manipulation: [mE7nipju5leiFEn] n. 处理, 操作
spike: [spaik] v. 穿刺
enzyme: [5enzaIm] n. [生化]酶
telomerase: [tE5lCmEreiz] n. 端粒酶
telomere: [5telEmiE] n. [生]端粒(在染色体端位上的着色点)
chromosome: [5krEumEsEum] n. [生物]染色体
tissue: [5tisju:] n. 〈生〉组织
mutate: [mju:5teit] v. 变异
tumor: [5tju:mE] n. 肿块,肿瘤
tease: [ti:z] v. 切取(组织)供检用将(例如组织) 切成片状供检用
chemotherapy: [7kemEu5WerEpi] n. 化疗,化学疗法
难句突破: 1.That enzyme keeps caplike structures called telomeres on the ends of chromosomes from getting shorter with each round of cell division.
主体句式:that enzyme keeps caplike structures …from getting shorter…
结构分析:这一句是个简单句,但因为宾语的修饰语较长,容易引起理解方面的错误。宾语caplike structure带了一个过去分词called引导的定语,而介词from之后的动名词短语又带有自己的状语with each round of cell division。
句子译文:这种生物酶使染色体末端的一种叫做端粒的冒状结构不会在每次细胞分裂时变短。 2.The finding could also lead to drugs tailored to attack specific types of cancer, thereby lessening our dependence on tissue-destroying chemotherapy and radiation.
主体句式:The finding could lead to drugs …
结构分析:本句是一个简单句,难点就是词组tailor to的用法。tailor to 意为“适合,适应”的意思,本句还包括一个由分词lessening引起的结果状语。
句子译文:这一发现还能带来专治特定类型癌症的药物,并因此减轻我们对于会破坏组织的化疗和辐射的依赖。
题目分析:
1. 答案为B,属事实细节题。文章第一段讲到当细胞癌变时,“细胞突然不再有规则地分裂,而开始大量复制自身。不同于普通细胞的是,这种复制活动永无休止。”可见答案应为B。
2. 答案为C,属事实细节题。这可以从第二段第四行“they appear to be a crucial step in understanding the disease”一句看出。
3. 答案为B,属事实细节题。文章第三段提到科学家在老鼠细胞上的成功实验无法在人类细胞上取得同样的成功,接着说“since then scientists have known…”来说明导致上述实验失败的一个主要原因是老鼠细胞和人类细胞的端粒酶水平差异。
4. 答案为A,属推理判断题。理解tailored一词的关键是看后文中“specific types of cancer”的意思,既然是特定类型的癌症,可见这种药是专门用于治疗这些特定类型癌症的,答案应为A。
5. 答案为D,属推理判断题。文中最后一段第四行提到这项研究可能带来一些专门用于特定类型癌症的药物,因此减少我们对“tissue-destroying”的化疗和辐射的依赖,可见癌症患者有可能在治疗时不再如以前一样痛苦。
参考译文:
二十多年前科学家就已经知道癌症是一种基因病变。细胞核内的DNA被某种物质打乱,细胞突然不再有规则地分裂,而开始大量复制自身。不同于普通细胞的是,这种复制活动永无休止。不过,描述这个过程和理解它是两回事。癌症细胞和正常细胞差异极大,要理清造成这种差异的事件的先后顺序几乎是不可能的。所以很多年来研究人员一直在攻关这一难题,通过研究健康细胞,他们试图确定是什么变化使得这些健康细胞变成了癌细胞---但却总是以失败告终。
现在情况出现了转机。根据最近的一期《自然》杂志刊载的报道,麻省理工学院“白首生物医学研究所”(Whitehead Institute for Biomedical Research)的一个科研小组终于成功将人类细胞转变为恶性细胞---他们采用了两种不同的细胞类型,通过把三种经过改变的基因嵌入这些细胞的DNA中而取得这一成绩。虽然这些操作都只是在实验室的器皿里完成的,不会立刻带来任何治疗方法,但它们显然是理解这种疾病的关键一步。这是一篇“意义重大的论文”,巴黎巴斯德研究所的乔纳森·魏茨曼和莫什·雅尼夫在随同发表的一篇评论文章中写道。
这一引人注目的新成果还要回溯到1983年的一次重大突破。当时白首的罗伯特·温伯格和同事们证明老鼠的细胞被注入两种经过改变的基因后就变成了癌细胞。但当他们在人体细胞上尝试这种改变时却遭遇了失败。从那以后,科学家们了解到老鼠细胞和人体细胞的一个重大区别就在于:它们的一种叫做端粒酶的生物酶水平较高。这种生物酶使染色体末端的一种叫做端粒的冒状结构不会在每次细胞分裂时变短。而这种变短正是细胞老化过程的一部分。由于癌细胞不断分裂,白首研究小组推理认为,如果使人体细胞变的像老鼠细胞,那就有可能使它们成为癌细胞。
这一策略果然奏效。科学家们用结缔组织和肾细胞作实验,并且注入了三种变异基因---一种可使细胞加速分裂;另外一种会使控制过度分裂的物质无法正常工作;第三种有助于端粒酶的产生,而端粒酶会使细胞无限分裂。他们在一支试管里创造了一个肿瘤。“一些人认为端粒酶并没有那么重要,”这项研究的首席作者,白首的威廉·哈恩说。“现在我们可以肯定地说,端粒酶很重要。”
了解实验室里的癌细胞当然不等于了解它们在活人体内的行为方式。不过,通过组织切片找出正常细胞和恶性细胞之间的关键差异,医生们也许就能够在今后设计出一些能够发现癌症苗头的检验方式。这一发现还能带来专治特定类型癌症的药物,并因此减轻我们对于会破坏组织的化疗和辐射的依赖。此外,白首的研究表明这种复杂顽症也许病源很简单,辨认出那种病源也许会带来最重大的发现。