Lexicographer review — Page 22 of 37 S3

say Verb

Instance: senseval2.d001.s026.t011 Dataset: Senseval-2

Because of the isolation of the retinoblastoma tumor-suppressor gene , it became possible last January to find out what threat the Quinlan baby faced .

A test using new “ genetic probes “ showed that little Will Quinlan had not inherited a damaged retinoblastoma supressor gene and , therefore , faced no more risk than other children of developing the rare cancer .

“ It made our New Year , “ says Mr. Quinlan .

This test was the first to predict reliably whether an individual could expect to develop cancer .

Equally important , the initial discovery of the gene that controls retinal cell growth , made by a Boston doctor named Thaddeus Dryja , has opened a field of cancer study , which in recent months has exploded .

“ It turns out that studying a tragic but uncommon tumor made possible some fundamental insights about the most basic workings of cancer , “ says Samuel Broder , director of the National Cancer Institute .

“ All this may not be obvious to the public , which is concerned about advances in treatment , but I am convinced this basic research will begin showing results there soon . “

To date , scientists have fingered two of these cancer-suppressors .

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believe Verb

Instance: senseval2.d001.s055.t003 Dataset: Senseval-2

The finding riveted medicine .

It was the first time anyone had showed that the loss of both copies of the same gene could lead to the eruption of a cancer .

“ It was extraordinarily satisfying , “ says Dr. Knudson , now at Fox Chase Cancer Research Center in Philadelphia .

“ I was convinced that what was true of retinoblastoma would be true for all cancers . “

It was an audacious claim .

But in Baltimore , Dr. Vogelstein , a young molecular biologist at Johns Hopkins Medical School , believed Dr. Knudson was right , and set out to repeat the Cavenee experiment in cells from other cancers .

His was one of two research teams in 1984 to report dual chromosome losses for a rare childhood cancer of the kidney called Wilm 's tumor .

Dr. Vogelstein next turned his attention colon cancer , the second biggest cancer killer in the U.S. after lung cancer .

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need Verb

Instance: senseval2.d001.s067.t002 Dataset: Senseval-2

Gradually , a coherent picture of cancer development emerged .

If both copies of a certain gene were knocked out , benign polyps would develop .

If both copies of a second gene were then deleted , the polyps would progress to malignancy .

It was clear that more than one gene had to be damaged for colon cancer to develop .

Their report galvanized other molecular biologists .

“ It was the confirming evidence we all needed that gene losses were critical to the development of a common tumor , “ says Ray White at Howard Hughes Medical Institute in Salt Lake City .

But Dr. Vogelstein had yet to nail the identity of the gene that , if damaged , flipped a colon cell into full-blown malignancy .

They focused on chromosome 17 .

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loss Noun

Instance: senseval2.d001.s067.t004 Dataset: Senseval-2

Gradually , a coherent picture of cancer development emerged .

If both copies of a certain gene were knocked out , benign polyps would develop .

If both copies of a second gene were then deleted , the polyps would progress to malignancy .

It was clear that more than one gene had to be damaged for colon cancer to develop .

Their report galvanized other molecular biologists .

“ It was the confirming evidence we all needed that gene losses were critical to the development of a common tumor , “ says Ray White at Howard Hughes Medical Institute in Salt Lake City .

But Dr. Vogelstein had yet to nail the identity of the gene that , if damaged , flipped a colon cell into full-blown malignancy .

They focused on chromosome 17 .

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say Verb

Instance: senseval2.d001.s067.t009 Dataset: Senseval-2

Gradually , a coherent picture of cancer development emerged .

If both copies of a certain gene were knocked out , benign polyps would develop .

If both copies of a second gene were then deleted , the polyps would progress to malignancy .

It was clear that more than one gene had to be damaged for colon cancer to develop .

Their report galvanized other molecular biologists .

“ It was the confirming evidence we all needed that gene losses were critical to the development of a common tumor , “ says Ray White at Howard Hughes Medical Institute in Salt Lake City .

But Dr. Vogelstein had yet to nail the identity of the gene that , if damaged , flipped a colon cell into full-blown malignancy .

They focused on chromosome 17 .

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say Verb

Instance: senseval2.d001.s077.t008 Dataset: Senseval-2

When they found it last winter , Dr. Vogelstein was dubious that the search was over .

His doubts stemmed from the fact that several years earlier a Princeton University researcher , Arnold Levine , had found in experiments with mice that a gene called p53 could transform normal cells into cancerous ones .

The deletion Dr. Vogelstein found was in exactly the same spot as p53 .

But Mr. Levine had said the p53 gene caused cancer by promoting growth , whereas the Johns Hopkins scientists were looking for a gene that suppressed growth .

Despite that , when the Johns Hopkins scientists compared the gene they had found in the human cancer cells with the Mr. Levine 's p53 gene they found the two were identical ; it turned out that in Mr. Levine 's cancer studies , he had unknowingly been observing a damaged form of p53 -- a cancer-suppressing gene .

The discovery “ suddenly puts an obscure gene right in the cockpit of cancer formation , “ says Robert Weinberg , a leader in cancer-gene research at Whitehead Institute in Cambridge , Mass .

Evidence now is emerging that the p53 suppressor gene is involved in other cancers , too .

Researchers in Edinburgh , Scotland , have found that in 23 of 38 breast tumors , one copy of chromosome 17 was mutated at the spot where gene p53 lies .

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believe Verb

Instance: senseval2.d001.s087.t000 Dataset: Senseval-2

In a report out last week , John Minna and colleagues at the National Cancer Institute say that about half the cells taken from lung cancer tissue they tested are missing this gene .

There also are reports from several labs , as yet unpublished , of missing p53 genes in tissue taken from kidney , brain and skin cancers .

At the same time , the Johns Hopkins team and others are rushing to pinpoint other tumor-suppressor genes .

Dr. Vogelstein hopes soon to isolate one on chromosome 18 , also involved in colon cancer .

Ray White in Utah and Walter Bodmer , a researcher in Great Britain , are close to finding another gene involved with some types of colon cancer , thought to be on chromosome 5 .

Dr. Minna believes people who inherit a defective gene somewhere on one of their two copies of chromosome 3 are especially prone to lung cancer .

Recently , he and others reported that the retinoblastoma suppressor gene may also be involved in some lung cancers , as well as several other more common cancers , too .

Where these discoveries will lead , scientists can only speculate .

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discovery Noun

Instance: senseval2.d001.s090.t010 Dataset: Senseval-2

Dr. Vogelstein hopes soon to isolate one on chromosome 18 , also involved in colon cancer .

Ray White in Utah and Walter Bodmer , a researcher in Great Britain , are close to finding another gene involved with some types of colon cancer , thought to be on chromosome 5 .

Dr. Minna believes people who inherit a defective gene somewhere on one of their two copies of chromosome 3 are especially prone to lung cancer .

Recently , he and others reported that the retinoblastoma suppressor gene may also be involved in some lung cancers , as well as several other more common cancers , too .

Where these discoveries will lead , scientists can only speculate .

Already two major pharmaceutical companies , the Squibb unit of Bristol-Myers Squibb Co. and Hoffmann-La Roche Inc. , are collaborating with gene hunters to turn the anticipated cascade of discoveries into predictive tests and , maybe , new therapies .

Some researchers say new cancer drugs to slow or reverse tumor growth may be based on the suppressor proteins normally produced by the genes .

The idea would be to administer to patients the growth-controlling proteins made by healthy versions of the damaged genes .

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say Verb

Instance: senseval2.d001.s094.t001 Dataset: Senseval-2

Where these discoveries will lead , scientists can only speculate .

Already two major pharmaceutical companies , the Squibb unit of Bristol-Myers Squibb Co. and Hoffmann-La Roche Inc. , are collaborating with gene hunters to turn the anticipated cascade of discoveries into predictive tests and , maybe , new therapies .

Some researchers say new cancer drugs to slow or reverse tumor growth may be based on the suppressor proteins normally produced by the genes .

The idea would be to administer to patients the growth-controlling proteins made by healthy versions of the damaged genes .

It may even be possible to replace defective genes with healthy versions , though no one has come close to doing that so far .

In any case , says Dr. Minna of the National Cancer Institute , “ We 're witnessing the discovery of one of the most important steps in the genesis of cancer .

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interest Noun

Instance: senseval2.d002.s003.t018 Dataset: Senseval-2

Why ca not we teach our children to read , write and reckon ?

It 's not that we do not know how to , because we do .

It 's that we do not want to .

And the reason we do not want to is that effective education would require us to relinquish some cherished metaphysical beliefs about human nature in general and the human nature of young people in particular , well as to violate some cherished vested interests .

These beliefs so dominate our educational establishment , our media , our politicians , and even our parents that it seems almost blasphemous to challenge them .

Here is an example .

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