Unit 48
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.
注（1）：本文選自Time; 08/09/99, p60, 3/5p, 2c
注（2）：本文習(xí)題命題模仿對象2002年真題text 4
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：
本文是一篇說明文，介紹了在癌癥研究方面的新突破。第一段概要介紹了以往的研究和遭遇的困難；第二段介紹了麻省理工學(xué)院科學(xué)家的研究突破；第三段介紹了過去科學(xué)家的研究對這次發(fā)現(xiàn)的影響；第四段介紹了這次研究的具體內(nèi)容；最后一段介紹了這一突破的重大意義。
詞匯注釋：
scramble: [5skrAmbl] v. 攪亂, 使混雜
nucleus: [5nju:kliEs] n. 細(xì)胞核
measured: [5meVEd] adj. 標(biāo)準(zhǔn)的, 整齊的, 有規(guī)則的
untangle: [5Qn5tAN^l] v. 理清（某個讓人迷惑或復(fù)雜難解的事物）；澄清或解決
cancerous: [`kAnsErEs] adj. 癌的
biomedical: [7baiEu5medikE] adj. 生物（學(xué)和）醫(yī)學(xué)的
malignant: [mE5li^nEnt] adj. 惡性的（腫瘤）
manipulation: [mE7nipju5leiFEn] n. 處理, 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（在染色體端位上的著色點）
chromosome: [5krEumEsEum] n. [生物]染色體
tissue: [5tisju:] n. 〈生〉組織
mutate: [mju:5teit] v. 變異
tumor: [5tju:mE] n. 腫塊，腫瘤
tease: [ti:z] v. 切取（組織）供檢用將（例如組織） 切成片狀供檢用
chemotherapy: [7kemEu5WerEpi] n. 化療，化學(xué)療法
難句突破：
1.That enzyme keeps caplike structures called telomeres on the ends of chromosomes from getting shorter with each round of cell division.
主體句式：that enzyme keeps caplike structures …from getting shorter…
結(jié)構(gòu)分析：這一句是個簡單句，但因為賓語的修飾語較長，容易引起理解方面的錯誤。賓語caplike structure帶了一個過去分詞called引導(dǎo)的定語，而介詞from之后的動名詞短語又帶有自己的狀語with each round of cell division.
句子譯文：這種生物酶使染色體末端的一種叫做端粒的冒狀結(jié)構(gòu)不會在每次細(xì)胞分裂時變短。
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.
主體句式：The finding could lead to drugs …
結(jié)構(gòu)分析：本句是一個簡單句，難點就是詞組tailor to的用法。tailor to 意為“適合，適應(yīng)”的意思，本句還包括一個由分詞lessening引起的結(jié)果狀語。
句子譯文：這一發(fā)現(xiàn)還能帶來專治特定類型癌癥的藥物，并因此減輕我們對于會破壞組織的化療和輻射的依賴。
題目分析：
1. 答案為B，屬事實細(xì)節(jié)題。文章第一段講到當(dāng)細(xì)胞癌變時，“細(xì)胞突然不再有規(guī)則地分裂，而開始大量復(fù)制自身。不同于普通細(xì)胞的是，這種復(fù)制活動永無休止?！笨梢姶鸢笐?yīng)為B.
2. 答案為C，屬事實細(xì)節(jié)題。這可以從第二段第四行“they appear to be a crucial step in understanding the disease”一句看出。
3. 答案為B，屬事實細(xì)節(jié)題。文章第三段提到科學(xué)家在老鼠細(xì)胞上的成功實驗無法在人類細(xì)胞上取得同樣的成功，接著說“since then scientists have known…”來說明導(dǎo)致上述實驗失敗的一個主要原因是老鼠細(xì)胞和人類細(xì)胞的端粒酶水平差異。
4. 答案為A，屬推理判斷題。理解tailored一詞的關(guān)鍵是看后文中“specific types of cancer”的意思，既然是特定類型的癌癥，可見這種藥是專門用于治療這些特定類型癌癥的，答案應(yīng)為A.
5. 答案為D，屬推理判斷題。文中最后一段第四行提到這項研究可能帶來一些專門用于特定類型癌癥的藥物，因此減少我們對“tissue-destroying”的化療和輻射的依賴，可見癌癥患者有可能在治療時不再如以前一樣痛苦。
參考譯文：
二十多年前科學(xué)家就已經(jīng)知道癌癥是一種基因病變。細(xì)胞核內(nèi)的DNA被某種物質(zhì)打亂，細(xì)胞突然不再有規(guī)則地分裂，而開始大量復(fù)制自身。不同于普通細(xì)胞的是，這種復(fù)制活動永無休止。不過，描述這個過程和理解它是兩回事。癌癥細(xì)胞和正常細(xì)胞差異極大，要理清造成這種差異的事件的先后順序幾乎是不可能的。所以很多年來研究人員一直在攻關(guān)這一難題，通過研究健康細(xì)胞，他們試圖確定是什么變化使得這些健康細(xì)胞變成了癌細(xì)胞——但卻總是以失敗告終。
現(xiàn)在情況出現(xiàn)了轉(zhuǎn)機。根據(jù)最近的一期《自然》雜志刊載的報道，麻省理工學(xué)院“白首生物醫(yī)學(xué)研究所”（Whitehead Institute for Biomedical Research）的一個科研小組終于成功將人類細(xì)胞轉(zhuǎn)變?yōu)閻盒约?xì)胞——他們采用了兩種不同的細(xì)胞類型，通過把三種經(jīng)過改變的基因嵌入這些細(xì)胞的DNA中而取得這一成績。雖然這些操作都只是在實驗室的器皿里完成的，不會立刻帶來任何治療方法，但它們顯然是理解這種疾病的關(guān)鍵一步。這是一篇“意義重大的論文”，巴黎巴斯德研究所的喬納森·魏茨曼和莫什·雅尼夫在隨同發(fā)表的一篇評論文章中寫道。
這一引人注目的新成果還要回溯到1983年的一次重大突破。當(dāng)時白首的羅伯特·溫伯格和同事們證明老鼠的細(xì)胞被注入兩種經(jīng)過改變的基因后就變成了癌細(xì)胞。但當(dāng)他們在人體細(xì)胞上嘗試這種改變時卻遭遇了失敗。從那以后，科學(xué)家們了解到老鼠細(xì)胞和人體細(xì)胞的一個重大區(qū)別就在于：它們的一種叫做端粒酶的生物酶水平較高。這種生物酶使染色體末端的一種叫做端粒的冒狀結(jié)構(gòu)不會在每次細(xì)胞分裂時變短。而這種變短正是細(xì)胞老化過程的一部分。由于癌細(xì)胞不斷分裂，白首研究小組推理認(rèn)為，如果使人體細(xì)胞變的像老鼠細(xì)胞，那就有可能使它們成為癌細(xì)胞。
這一策略果然奏效?？茖W(xué)家們用結(jié)締組織和腎細(xì)胞作實驗，并且注入了三種變異基因——一種可使細(xì)胞加速分裂；另外一種會使控制過度分裂的物質(zhì)無法正常工作；第三種有助于端粒酶的產(chǎn)生，而端粒酶會使細(xì)胞無限分裂。他們在一支試管里創(chuàng)造了一個腫瘤。“一些人認(rèn)為端粒酶并沒有那么重要，”這項研究的首席作者，白首的威廉·哈恩說?！艾F(xiàn)在我們可以肯定地說，端粒酶很重要?！?BR> 了解實驗室里的癌細(xì)胞當(dāng)然不等于了解它們在活人體內(nèi)的行為方式。不過，通過組織切片找出正常細(xì)胞和惡性細(xì)胞之間的關(guān)鍵差異，醫(yī)生們也許就能夠在今后設(shè)計出一些能夠發(fā)現(xiàn)癌癥苗頭的檢驗方式。這一發(fā)現(xiàn)還能帶來專治特定類型癌癥的藥物，并因此減輕我們對于會破壞組織的化療和輻射的依賴。此外，白首的研究表明這種復(fù)雜頑癥也許病源很簡單，辨認(rèn)出那種病源也許會帶來最重大的發(fā)現(xiàn)。
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.
注（1）：本文選自Time; 08/09/99, p60, 3/5p, 2c
注（2）：本文習(xí)題命題模仿對象2002年真題text 4
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：
本文是一篇說明文，介紹了在癌癥研究方面的新突破。第一段概要介紹了以往的研究和遭遇的困難；第二段介紹了麻省理工學(xué)院科學(xué)家的研究突破；第三段介紹了過去科學(xué)家的研究對這次發(fā)現(xiàn)的影響；第四段介紹了這次研究的具體內(nèi)容；最后一段介紹了這一突破的重大意義。
詞匯注釋：
scramble: [5skrAmbl] v. 攪亂, 使混雜
nucleus: [5nju:kliEs] n. 細(xì)胞核
measured: [5meVEd] adj. 標(biāo)準(zhǔn)的, 整齊的, 有規(guī)則的
untangle: [5Qn5tAN^l] v. 理清（某個讓人迷惑或復(fù)雜難解的事物）；澄清或解決
cancerous: [`kAnsErEs] adj. 癌的
biomedical: [7baiEu5medikE] adj. 生物（學(xué)和）醫(yī)學(xué)的
malignant: [mE5li^nEnt] adj. 惡性的（腫瘤）
manipulation: [mE7nipju5leiFEn] n. 處理, 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（在染色體端位上的著色點）
chromosome: [5krEumEsEum] n. [生物]染色體
tissue: [5tisju:] n. 〈生〉組織
mutate: [mju:5teit] v. 變異
tumor: [5tju:mE] n. 腫塊，腫瘤
tease: [ti:z] v. 切取（組織）供檢用將（例如組織） 切成片狀供檢用
chemotherapy: [7kemEu5WerEpi] n. 化療，化學(xué)療法
難句突破：
1.That enzyme keeps caplike structures called telomeres on the ends of chromosomes from getting shorter with each round of cell division.
主體句式：that enzyme keeps caplike structures …from getting shorter…
結(jié)構(gòu)分析：這一句是個簡單句，但因為賓語的修飾語較長，容易引起理解方面的錯誤。賓語caplike structure帶了一個過去分詞called引導(dǎo)的定語，而介詞from之后的動名詞短語又帶有自己的狀語with each round of cell division.
句子譯文：這種生物酶使染色體末端的一種叫做端粒的冒狀結(jié)構(gòu)不會在每次細(xì)胞分裂時變短。
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.
主體句式：The finding could lead to drugs …
結(jié)構(gòu)分析：本句是一個簡單句，難點就是詞組tailor to的用法。tailor to 意為“適合，適應(yīng)”的意思，本句還包括一個由分詞lessening引起的結(jié)果狀語。
句子譯文：這一發(fā)現(xiàn)還能帶來專治特定類型癌癥的藥物，并因此減輕我們對于會破壞組織的化療和輻射的依賴。
題目分析：
1. 答案為B，屬事實細(xì)節(jié)題。文章第一段講到當(dāng)細(xì)胞癌變時，“細(xì)胞突然不再有規(guī)則地分裂，而開始大量復(fù)制自身。不同于普通細(xì)胞的是，這種復(fù)制活動永無休止?！笨梢姶鸢笐?yīng)為B.
2. 答案為C，屬事實細(xì)節(jié)題。這可以從第二段第四行“they appear to be a crucial step in understanding the disease”一句看出。
3. 答案為B，屬事實細(xì)節(jié)題。文章第三段提到科學(xué)家在老鼠細(xì)胞上的成功實驗無法在人類細(xì)胞上取得同樣的成功，接著說“since then scientists have known…”來說明導(dǎo)致上述實驗失敗的一個主要原因是老鼠細(xì)胞和人類細(xì)胞的端粒酶水平差異。
4. 答案為A，屬推理判斷題。理解tailored一詞的關(guān)鍵是看后文中“specific types of cancer”的意思，既然是特定類型的癌癥，可見這種藥是專門用于治療這些特定類型癌癥的，答案應(yīng)為A.
5. 答案為D，屬推理判斷題。文中最后一段第四行提到這項研究可能帶來一些專門用于特定類型癌癥的藥物，因此減少我們對“tissue-destroying”的化療和輻射的依賴，可見癌癥患者有可能在治療時不再如以前一樣痛苦。
參考譯文：
二十多年前科學(xué)家就已經(jīng)知道癌癥是一種基因病變。細(xì)胞核內(nèi)的DNA被某種物質(zhì)打亂，細(xì)胞突然不再有規(guī)則地分裂，而開始大量復(fù)制自身。不同于普通細(xì)胞的是，這種復(fù)制活動永無休止。不過，描述這個過程和理解它是兩回事。癌癥細(xì)胞和正常細(xì)胞差異極大，要理清造成這種差異的事件的先后順序幾乎是不可能的。所以很多年來研究人員一直在攻關(guān)這一難題，通過研究健康細(xì)胞，他們試圖確定是什么變化使得這些健康細(xì)胞變成了癌細(xì)胞——但卻總是以失敗告終。
現(xiàn)在情況出現(xiàn)了轉(zhuǎn)機。根據(jù)最近的一期《自然》雜志刊載的報道，麻省理工學(xué)院“白首生物醫(yī)學(xué)研究所”（Whitehead Institute for Biomedical Research）的一個科研小組終于成功將人類細(xì)胞轉(zhuǎn)變?yōu)閻盒约?xì)胞——他們采用了兩種不同的細(xì)胞類型，通過把三種經(jīng)過改變的基因嵌入這些細(xì)胞的DNA中而取得這一成績。雖然這些操作都只是在實驗室的器皿里完成的，不會立刻帶來任何治療方法，但它們顯然是理解這種疾病的關(guān)鍵一步。這是一篇“意義重大的論文”，巴黎巴斯德研究所的喬納森·魏茨曼和莫什·雅尼夫在隨同發(fā)表的一篇評論文章中寫道。
這一引人注目的新成果還要回溯到1983年的一次重大突破。當(dāng)時白首的羅伯特·溫伯格和同事們證明老鼠的細(xì)胞被注入兩種經(jīng)過改變的基因后就變成了癌細(xì)胞。但當(dāng)他們在人體細(xì)胞上嘗試這種改變時卻遭遇了失敗。從那以后，科學(xué)家們了解到老鼠細(xì)胞和人體細(xì)胞的一個重大區(qū)別就在于：它們的一種叫做端粒酶的生物酶水平較高。這種生物酶使染色體末端的一種叫做端粒的冒狀結(jié)構(gòu)不會在每次細(xì)胞分裂時變短。而這種變短正是細(xì)胞老化過程的一部分。由于癌細(xì)胞不斷分裂，白首研究小組推理認(rèn)為，如果使人體細(xì)胞變的像老鼠細(xì)胞，那就有可能使它們成為癌細(xì)胞。
這一策略果然奏效?？茖W(xué)家們用結(jié)締組織和腎細(xì)胞作實驗，并且注入了三種變異基因——一種可使細(xì)胞加速分裂；另外一種會使控制過度分裂的物質(zhì)無法正常工作；第三種有助于端粒酶的產(chǎn)生，而端粒酶會使細(xì)胞無限分裂。他們在一支試管里創(chuàng)造了一個腫瘤。“一些人認(rèn)為端粒酶并沒有那么重要，”這項研究的首席作者，白首的威廉·哈恩說?！艾F(xiàn)在我們可以肯定地說，端粒酶很重要?！?BR> 了解實驗室里的癌細(xì)胞當(dāng)然不等于了解它們在活人體內(nèi)的行為方式。不過，通過組織切片找出正常細(xì)胞和惡性細(xì)胞之間的關(guān)鍵差異，醫(yī)生們也許就能夠在今后設(shè)計出一些能夠發(fā)現(xiàn)癌癥苗頭的檢驗方式。這一發(fā)現(xiàn)還能帶來專治特定類型癌癥的藥物，并因此減輕我們對于會破壞組織的化療和輻射的依賴。此外，白首的研究表明這種復(fù)雜頑癥也許病源很簡單，辨認(rèn)出那種病源也許會帶來最重大的發(fā)現(xiàn)。