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  3. The time-enduring metaphor of the war on cancer, as overused as it may be, is as evocative as ever to describe our efforts to be

The time-enduring metaphor of the war on cancer, as overused as it may be, is as evocative as ever to describe our efforts to be

admin2019-08-01  37
问题     The time-enduring metaphor of the war on cancer, as overused as it may be, is as evocative as ever to describe our efforts to beat the disease that will claim nearly 566,000 American lives this year alone. So let’s fall back on martial imagery to describe our current position: We now know the enemy far better than ever before. And that promises much more precise targets.
    【R1】______ But mounting discoveries about the astoundingly complex essence of cancer—that its causes lie in multitudes of genes gone awry—are also pointing the way toward treatments aimed in laser-like fashion at a patient’s unique set of genetic limitations. In mid-October, scientists reported in Nature that they’ve identified 26 key mutated genes linked to lung cancer, for example.
    【R2】______Yet until quite recently, the only tools available—the blunt-force mainstays of surgery, chemotherapy, and radiation—treated everyone much the same. Then, in the 1990s, powerful new computing technology allowed researchers to begin comparing the DNA of cancerous and healthy tissues and gain a look at the very blueprints of similar-looking but markedly different tumors.
    【R3】______It seems that many of the abnormal genes operate together to create trouble in a smaller number of distinct cellular pathways—the molecular processes that make a cancer cell so deadly. These common pathways are the likely drug targets. Think of it this way: Multiple cars are taking separate routes to the same garage, and instead of trying to stop each car on the road, you block the driveway. The pathways are shared by cancers in different organs; the new lung cancer study, for example, revealed mutations also fingered in cancer of the retina and colon, among others, suggesting that drugs can be used against a panoply of tumors.
    【R4】______Theoretically, that means drugs could be much better matched to patients. That kind of matching is only occasionally available now. Lung cancer drugs Tarceva and Iressa target the cell-growth receptor EGFR; for reasons not yet fully understood but most likely involving mutations in EGFR, they work better in some patients than in others.
    【R5】______For one thing, finding all the mutations linked to a certain cancer isn’t enough. How and why are genes turned on and off? And how do the signaling pathways affect and influence each other? Even when a target is identified as important and a drug made to block it, chances are the tumor has another way to reach the same end—or will find one as it continues to grow and mutate, which explains why people develop resistance to targeted therapies that work at first.
    What this all suggests, many say, is that just as HIV is now managed by a drug cocktail, cancer may one day be handled as a chronic disease controlled by a changing mix of several drugs at once in sequence or combination. The race is on to expand the arsenal. According to a recent Datamonitor report, 10 new targeted drugs have entered the marketplace since 2005, and researchers are studying existing therapies to see if they’re more effective together.
[A]It’s been clear for years, for example, that cancers vary widely even if they look the same under a microscope: Some are slow growing, others are aggressive; some patients respond to one drug, while others are not helped at all.
[B]Devising treatments to combat every single mutation would be a huge task—but that may not be necessary, experts say.
[C]Of course, as even Sun Tzu recognized, intel must be translated into effective action, and in this struggle, that effort has been all too plagued by failure.
[D]Within just a few years, the technology may be available to sequence an individual tumor’s genes and find out exactly what pathways need blocking, says Raymond DuBois, dean of M. D. Anderson Cancer Center in Houston and president of the American Association for Cancer Research.
[E]A new study has found that mutations in either of two genes are involved in the development of lung cancer.
[F]Studies have found that the epidermal growth factor receptor(EGFR)gene is mutated in many non-smallcell lung cancers and that these mutations are associated with increased sensitivity to gefitinib(Iressa)or erlotinib(Tarceva), tyrosine kinase(TK)inhibitors that target EGFR.
[G]Clearly, converting this mass of new genetic information into perfectly tailored therapies isn’t a quick and dirty exercise.
【R3】
选项
答案B
解析 由上文我们得知癌症变化的幅度很广，下文按照逻辑，设计研究者应该设计出对抗每一个变异的癌症的方法，根据常识，研究者肯定用的是相反的方法。[B]刚好指出设计出对抗每一个变异的癌症的方法将是一项巨大的工作——而专家也说，那也没有必要。故[B]为本题答案。
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