Lexicographer review — Page 13 of 37 S2

The vicar , W.D. Jones , refuses to talk about it , saying it would “ reopen the wound . “

But C.J.B. Marshall , vicar of a nearby church , feels the fault is in the stairs from the bell tower that are located next to the altar .

“ So crunch , crunch , crunch , bang , bang , bang -- here come the ringers from above , making a very obvious exit while the congregation is at prayer , “ he says .

Vicar Marshall admits to mixed feelings about this issue , since he is both a vicar and an active bell-ringer himself .

“ The sound of bells is a net to draw people into the church , “ he says .

“ So crunch , crunch , crunch , bang , bang , bang -- here come the ringers from above , making a very obvious exit while the congregation is at prayer , “ he says .

Vicar Marshall admits to mixed feelings about this issue , since he is both a vicar and an active bell-ringer himself .

“ The sound of bells is a net to draw people into the church , “ he says .

“ I live in hopes that the ringers themselves will be drawn into that fuller life . “

The Central Council of Church Bell Ringers , a sort of parliament of ringing groups , aims to improve relations with vicars , says John C. Baldwin , president .

That is for the future .

Already , scientists are developing tests based on the newly identified genes that , for the first time , can predict whether an otherwise healthy individual is likely to get cancer .

“ It 's a super-exciting set of discoveries , “ says Bert Vogelstein , a Johns Hopkins University researcher who has just found a gene pivotal to the triggering of colon cancer .

“ Only a decade ago cancer was a black box about which we knew nothing at the molecular level .

Today , we know that the accumulation of several of these altered genes can initiate a cancer and , then , propel it into a deadly state . “

Already , scientists are developing tests based on the newly identified genes that , for the first time , can predict whether an otherwise healthy individual is likely to get cancer .

“ It 's a super-exciting set of discoveries , “ says Bert Vogelstein , a Johns Hopkins University researcher who has just found a gene pivotal to the triggering of colon cancer .

“ Only a decade ago cancer was a black box about which we knew nothing at the molecular level .

Today , we know that the accumulation of several of these altered genes can initiate a cancer and , then , propel it into a deadly state . “

Scientists call the new class of genes tumor-suppressors , or simply anti-cancer genes .

But if the genes are damaged -- perhaps by radiation , a chemical or through a chance accident in cell division -- their growth-suppressing proteins no longer work , and cells normally under control turn malignant .

The newly identified genes differ from a family of genes discovered in the early 1980s called oncogenes .

Oncogenes must be present for a cell to become malignant , but researchers have found them in normal as well as in cancerous cells , suggesting that oncogenes do n't cause cancer by themselves .

In recent months , researchers have come to believe the two types of cancer genes work in concert : An oncogene may turn proliferating cells malignant only after the tumor-suppressor gene has been damaged .

Like all genes , tumor-suppressor genes are inherited in two copies , one from each parent .

Like all genes , tumor-suppressor genes are inherited in two copies , one from each parent .

Either copy can make the proteins needed to control cell growth , so for cancer to arise , both copies must be impaired .

A person who is born with one defective copy of a suppressor gene , or in whom one copy is damaged early in life , is especially prone to cancer because he need only lose the other copy for a cancer to develop .

Emerging genetic tests will be able to spot such cancer-susceptible individuals , ushering in what some scientists believe is a new age of predictive cancer diagnosis .

Bill and Bonnie Quinlan are among the first beneficiaries of the new findings .

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 .

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

Dr. Dryja made his retinoblastoma discovery in 1986 .

Then last spring , researchers reported finding a gene called p53 which , if impaired , turns healthy colon cells cancerous .

Soon after that report , two other research teams uncovered evidence that the same damaged p53 gene is present in tissue from lung and breast cancers .

Colon , lung and breast cancers are the most common and lethal forms of the disease , collectively killing almost 200,000 Americans a year .

There is evidence that if people inherit defective versions of these genes , they are especially prone to cancer , perhaps explaining , finally , why some cancers seem to haunt certain families .

The story of tumor-suppressor genes goes back to the 1970s , when a pediatrician named Alfred G. Knudson Jr. proposed that retinoblastoma stemmed from two separate genetic defects .

He theorized that in the eye cancer , an infant inherited a damaged copy of a gene from one parent and a normal copy from the other .

The tumor , he suggested , developed when the second , normal copy also was damaged .

But there was no way to prove Dr. Knudson 's “ two-hit “ theory .

Then , a scientific team led by molecular geneticist Webster Cavenee , then at the University of Utah , found the answer .

The team used a battery of the newly developed “ gene probes , “ snippets of genetic material that can track a gene 's presence in a cell .

By analyzing cells extracted from eye tumors , they found defects in the second copy of chromosome 13 in the exact area as in the first copy of the chromosome .

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 .