Lexicographer review — Page 14 of 37 S2

“ 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 .

He believed colon cancer might also arise from multiple “ hits “ on cancer suppressor genes , because it often seems to develop in stages .

It often is preceded by the development of polyps in the bowel , which in some cases become increasingly malignant in identifiable stages -- progressing from less severe to deadly -- as though a cascade of genetic damage might be occurring .

Dr. Vogelstein and a doctoral student , Eric Fearon , began months of tedious and often frustrating probing of the chromosomes searching for signs of genetic damage .

They began uncovering a confusing variety of genetic deletions , some existing only in benign polyps , others in malignant cells and many in both polyps and malignant cells .

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

He believed colon cancer might also arise from multiple “ hits “ on cancer suppressor genes , because it often seems to develop in stages .

It often is preceded by the development of polyps in the bowel , which in some cases become increasingly malignant in identifiable stages -- progressing from less severe to deadly -- as though a cascade of genetic damage might be occurring .

Dr. Vogelstein and a doctoral student , Eric Fearon , began months of tedious and often frustrating probing of the chromosomes searching for signs of genetic damage .

They began uncovering a confusing variety of genetic deletions , some existing only in benign polyps , others in malignant cells and many in both polyps and malignant cells .

They focused on chromosome 17 .

For months the Johns Hopkins researchers , using gene probes , experimentally crawled down the length of chromosome 17 , looking for the smallest common bit of genetic material lost in all tumor cells .

Such a piece of DNA would probably constitute a gene .

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 .

For months the Johns Hopkins researchers , using gene probes , experimentally crawled down the length of chromosome 17 , looking for the smallest common bit of genetic material lost in all tumor cells .

Such a piece of DNA would probably constitute a gene .

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 .

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 .

The p53 gene has just been implicated in lung cancer .

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 .

The p53 gene has just been implicated in lung cancer .

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 .

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 .

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 .