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