Lexicographer review — Page 3 of 37 S1

No one speaks , and the snaking of the ropes seems to make as much sound as the bells themselves , muffled by the ceiling .

Totally absorbed , the ringers stare straight ahead , using peripheral vision ( they call it “ rope-sight “ ) to watch the other ropes and thus time their pulls .

Far above in the belfry , the huge bronze bells , mounted on wheels , swing madly through a full 360 degrees , starting and ending , surprisingly , in the inverted , or mouth-up position .

Skilled ringers use their wrists to advance or retard the next swing , so that one bell can swap places with another in the following change .

In a well-known detective-story involving church bells , English novelist Dorothy L. Sayers described ringing as a “ passion that finds its satisfaction in mathematical completeness and mechanical perfection . “

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 .

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 .

It hopes to speak to students at theological colleges about the joys of bell ringing and will shortly publish a booklet for every vicar in the country entitled , “ The Bells in Your Care . “

Says Mr. Baldwin , “ We recognize that we may no longer have as high a priority in church life and experience . “

Mr. Baldwin is also attacking the greater problem : lack of ringers .

One survey says that of the 100,000 trained bellringers in England today , only 40,000 of them still ring .

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

When functioning normally , they make proteins that hold a cell 's growth in check .

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 .

“ 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 .

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 .

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 .

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

Back then , scientists had no way of ferreting out specific genes , but under a microscope they could see the 23 pairs of chromosomes in the cells that contain the genes .

Occasionally , gross chromosome damage was visible .

Dr. Knudson found that some children with the eye cancer had inherited a damaged copy of chromosome No. 13 from a parent who had had the disease .

Under a microscope he could actually see that a bit of chromosome 13 was missing .

“ 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 .

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 .

The scientists say that since breast cancer often strikes multiple members of certain families , the gene , when inherited in a damaged form , may predispose women to the cancer .

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 .