Lexicographer review — Page 28 of 37 S4

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

He assumed the missing piece contained a gene or genes whose loss had a critical role in setting off the cancer .

But he did not know which gene or genes had disappeared .

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 .

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 .

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 .

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 .

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 .

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 .

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 .

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 .

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 .

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 .

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 .