Individual

Go to List of Family Names Go to List of People    < Previous Next >

Birth:          8 Feb 1928 Philadelphia, Pa.
Death:          26 Dec 2016 Newtown Square, Pa.
Cause of Death: Alzheimers

Notes
!PUBL
1981 book:
Peter earned a B.A. in 1948 from Wesleyan University and graduated first in his class 
from the University of Pennsylvania Medical School.  He served in the army and was 
discharged in 1956.  Peter took a position on the faculty at the University of 
Pennsylvania. Peter is a pathologist at the Hospital of the University of Pennsylvania.  
With a colleague in 1960, he discovered an abnormal "Philadelphia chromosome", 
now useful in cancer studies.
In 1983, Peter and his family lived at 345 Mt. Alverno Rd., Media, Pa. 19063.
Source: Peter Nowell (him); Penna. Gazette, June 1985, p. 43
1930 in Upper Providence, Delaware Co., Pa. age 2y
www.genealogy.com/genealogy/users/k/r/a/Mark-E-Kraus/index.html
familytreemaker.genealogy.com/users/w/o/r/Robert-P-Worst/PDFODT4.pdf?
Welcome=1074569528
From: 	James Maule
To:	imm_fam (incl C&S)
Date: 	9/11/01 4:47PM
Subject: 	Peter Nowell article

For those of you who didn't see it, here's the article, plus one that Michael found in 
today's paper: Also two pictures (in color, no less) to let you decide if there is a 
resemblance.

Decades later, a discovery bears fruit
 Found by chance in 1958, the "Philadelphia Chromosome" led to a new 
understanding of cancer - and, this year, a new drug to fight it.
By Faye Flam 
INQUIRER STAFF WRITER 
The year was 1958 and scientists had no idea what caused cancer. DNA's double 
helix was a relatively recent discovery.
The number of chromosomes in a human cell had just been determined.
In his lab at the University of Pennsylvania, biologist Peter Nowell, 30, was using test 
tubes, slides and microscopes to try to find out what made leukemia cells grow.
He had a stroke of luck when he happened to use tap water, rather than the usual 
special solution, to wash his slides. When he next peered under the microscope, he 
spotted chromosomes - normally tangled and hard to make out - that were swollen with 
water and easy to see.
That serendipitous observation soon produced the first clear evidence that 
chromosome damage was associated with cancer - a key underpinning for our modern 
understanding of the disease.
One of the chromosomes on Nowell's slide eventually became known as the 
"Philadelphia Chromosome." And this past spring, more than four decades later, 
research on its abnormalities led to federal approval of one of the most promising new 
cancer drugs in years.
 Gleevec, made by Novartis Pharmaceuticals Corp. of East Hanover, N.J., fights only 
two relatively rare cancers: a type of gastrointestinal tumor and chronic myeloid 
leukemia, the type Nowell was studying. But people with those diseases have made 
remarkable recoveries, with virtually none of the side effects of conventional 
chemotherapy.
The drug represents a radical new approach to cancer therapy, one that some experts 
predict could spawn a new class of cancer drugs.
Most chemotherapy drugs are toxic - they work by attacking a broad range of cancer 
cells, destroying many normal cells in the process. Gleevec, on the other hand, targets 
only specific cancer cells by zeroing in on their genetic abnormalities.
"It's very gratifying to have spent 40 years and see something like this come to 
fruition," said Nowell, now 72 and still active at Penn researching leukemia.
Forty years ago, he had no way of knowing where his chance sighting of the 
chromosomes on the microscope slide would lead.
"I didn't know anything about chromosomes," he said, "but it seemed a shame to 
throw this away."
Nowell went looking for someone who knew more about chromosomes. At Fox Chase 
Cancer Center across town, he found David A. Hungerford, a graduate student who 
was studying chromosomes for his doctoral thesis.
Hungerford, who died in 1993, had become fascinated with these variously-sized 
clumps of DNA, which normally are spread out and overlap one another like strands in 
a plate of spaghetti. Only when cells are in the process of dividing do the 
chromosomes contract into separate, visible structures.
When Hungerford looked at the slide containing Nowell's leukemia cells, he noticed a 
chromosome that was abnormally stunted, as if a piece had been knocked off.
Nowell and Hungerford began looking at more blood samples from patients with 
chronic myeloid leukemia and found that the malignant ones all showed this same 
stunted chromosome. 
At the time, little was known about the chromosomes in cancer cells, and many 
researchers believed cancer was caused by a virus.
The two scientists continued to build up evidence linking their abnormal chromosome 
to chronic myeloid leukemia. They published a paper about their findings in 1960, 
proposing that this broken chromosome caused the disease. (The name "Philadelphia 
Chromosome" was coined by other researchers.)
Figuring out how this abnormality actually caused cancer would require a few more 
steps by researchers around the country.
In the mid-1970s, Janet Rawley, a molecular biologist at the University of Chicago, 
found that the chromosome in question (by then labeled Chromosome 22) appeared 
stunted because it had lost a piece of its DNA, which then had changed places with a 
chunk of Chromosome 9.
The point where a small piece of number 9 attached to number 22 was the site of the 
trouble.
By 1984, scientists had learned to zero in on individual genes within chromosomes. 
Looking at cancerous blood cells, they found that the joining of  Chromosome 22 with 
a piece of Chromosome 9 disrupted the code carried by a gene located right at the 
break point.
A normal gene, labeled Abl, was getting squashed into another normal gene, called 
Bcr. The combination produced an abnormal - and very dangerous - hybrid gene called 
Abl-Bcr. 
Normally, the Abl gene orders the production of a protein that orchestrates the division 
of white blood cells. The defective Abl-Bcr hybrid, however, leads to a protein that 
causes the blood cells to divide uncontrollably.
Technically, this is a genetic abnormality but not one that people are born with. It 
happens through some bit of bad luck when a cell divides and copies itself wrong.
In people with chronic myeloid leukemia, the number of white blood cells rises so high 
that the blood can become too viscous, blocking the supply of oxygen to vital organs. 
Chemotherapy can keep the disease at bay for some months, but eventually the 
cancer overwhelms the body.
Recoveries are rare and most patients die within three years. The disease kills 2,300 
Americans a year.
As the link between genetics and cancer became clear, scientists in Philadelphia and 
elsewhere began discovering whole new classes of genes that seemed to play a role. 
During the 1970s and '80s, they identified a group called oncogenes.
Just slight damage to an oncogene, such as Abl, could trigger a single normal cell to 
start growing into a cancer.
It's "like having the accelerator stuck in the 'on' position," said Brian Druker, an 
oncologist at the Oregon Health Sciences Center in Portland.
About 10 years ago, Druker decided to make it his goal to get the accelerator 
unstuck. Around the same time, researchers at what would later become the Swiss-
based drugmaking giant Novartis AG were seeking new approaches to cancer, 
including chronic myeloid leukemia. In targeting that disease, they started making 
hundreds of different molecules and testing them to see which ones reacted with the 
abnormal protein that made the white blood cells grow out of control.
Eventually Druker found one that seemed to work the way he wanted - attaching itself 
to the abnormal protein and disabling it in a way that stopped the division of the 
cancer cells while having no effect on the normal cells.
Druker moved on to animal testing and found it stopped the leukemia in mice. Human 
testing of the new drug began in 1998. 
"These were pretty ill patients," said Druker. "They may have had six months to live."
Early tests showed no major side effects. As doctors increased the dose, the patients 
began to improve, sometimes dramatically.
Druker and his colleagues at Novartis approached the U.S. Food and Drug 
Administration and urged them to approve speedy additional studies with larger 
numbers of patients.
Good results from subsequent trials led the FDA to approve Gleevec on May 10, one 
of the fastest actions on a new drug in the agency's history.
Meanwhile, the Philadelphia Chromosome and the drug it spawned were making history 
again. Margaret von Mehren, an oncologist at Fox Chase Cancer Center, realized that 
a gastrointestinal cancer known as GIST (gastrointestinal stromal tumor) created an 
abnormal protein in the tumor cells that was similar to the protein that causes chronic 
myeloid leukemia.
Like the leukemia, GIST is rare - about 5,000 Americans are diagnosed annually - and 
often fatal.
Von Mehren approached Raymond MacDonald, a GIST patient from Whiting, N.J., who 
had been told he was out of options after painful chemotherapy treatments failed to 
help his growing stomach tumors. Last year, she told the 78-year-old retiree that if he 
could hold on a few more months, she'd get him into a trial for an experimental drug.
MacDonald held on, and when he got the drug a year ago his tumors started to shrink. 
He returned to his hobby of carving decoys, left his wheelchair, and started planning 
to live. 
Three days after the FDA approved Gleevec for treatment of chronic myeloid 
leukemia, von Mehren told a meeting of the American Society for Clinical Oncology 
that the same drug helped 60 percent of the 89 patients in her study - some of them 
going from the brink of death to an active life with virtually no side effects.
Still, it's far too early to call the new drug a "cure." There's no telling whether patients 
will relapse later.
And it is unlikely to work on more common cancers: Lung, breast, prostate and colon 
cancers carry multiple combinations of genetic defects, creating a daunting task to 
figure out what to fix.
And yet Druker, the Oregon oncologist who led the first clinical trials on Gleevec, is 
optimistic about this new approach of targeting the specific mechanism by which a cell 
becomes malignant.
Gleevec may only work on two rare diseases, he says, but the idea of zeroing in on 
whatever protein causes a specific cancer is likely to be applied more broadly.
SECOND ARTICLE
Worth the wait 
Cancer drug tied to city yields encouraging results. 
Sciencetakes time. For some reason, folks think otherwise. 
They think, problem-solving is what science is for, isn't it? That's the scientist's job. 
Get to it.
But such folks forget: The more worthwhile the problem - splitting the atom, wrestling 
with the virus, reading the human genome - the harder it is. And the
harder it is, the longer it takes to solve - if a solution exists at all.
Take cancer. The word cancer is a blanket term for a group of diverse diseases. Yet 
people still speak of a "cure for cancer," as if disease and treatment were single 
entities. Not so. It's going to take hundreds of different approaches to address the 
many cancers in the human universe; each one is an uphill, thorny path.
No better illustration is there than the story of "the Philadelphia Chromosome." The 
tale began in 1958 and is only now bearing fruit for people with certain forms of 
cancer. 
By one of those lucky breaks often associated with scientific discovery, Peter Nowell 
of the University of Pennsylvania and David A. Hungerford of Fox Chase Cancer 
Center noticed a defect in chromosomes taken from the cells of certain leukemia 
patients. That discovery was the first indicator that some cancers are associated with 
genetic abnormalities. In this case, the defect causes the body's cells to create an 
abnormal protein, which in turn promotes cancerous cell growth.
In 1993, scientists began to study ST-571, an agent that blocked the action of the 
abnormal protein. Human tests were heartening. The resulting drug, now known as 
Gleevec and developed by Novartis Pharmaceuticals of East Hanover, N.J., was 
approved this year under FDA rules permitting accelerated development in special 
cases. Gleevec currently is indicated for chronic myeloid leukemia; tests in other 
cancers are under way. So far, results have been encouraging.
Where many cancer treatments attack all sorts of tissues, with the aim of arresting or 
killing cancerous ones in the process, Gleevec apparently is "protein-specific." That 
is, it lasers in on one wayward protein, thus killing or preventing the spread of one 
kind of cell - the cancerous kind. Such elegance, and such a step forward! 
From Philadelphia Chromosome to Gleevec took 43 years - two generations of human 
time, but a brief moment in the progress of human knowledge. So let no one talk glibly 
about cures for cancer just around the corner. Say only that Gleevec so far is helping 
people, enough to inspire awe and gratitude. 
Meanwhile, scientists and physicians all around us are taking on the most complicated 
challenges that ever faced our species. That's time well spent. 
In 1987 received the Cotlove Award from the Academy of Clinical Laboratory 
Physicians and Scientists (Penna Gazette Dec 1987 p 46)
In 1991 elected to membership in the Institute of Medicine, one of four organizations 
that make up the National Academy of Sciences. Phila Inquirer 1 Jul 1991
co-discoverer of chromosome 3 gene implicated in lung cancer (Phila Inquirer 2 June 
1991)
http://www.philly.com/inquirer/obituaries/20170101_Peter_Nowell__researcher_and_f
inder_of_chromosome.html
Dr. Peter C. Nowell, 88, formerly of Middletown Township, an acclaimed researcher 
and codiscoverer of the Philadelphia chromosome, which pointed for the first time to a 
genetic basis for cancer, died Dec. 26 of complications from Alzheimer's disease at 
White Horse Village, Newtown Square.
In 1960, while working in their laboratory, Dr. Nowell and colleague David A. 
Hungerford were "diddling around with leukemic cells in culture, and rinsing them with 
tap water." Dr. Nowell noticed that the cells were dividing, so he stained them with a 
special dye to make their chromosomes more visible, according to an account by the 
Lasker Foundation, an advocate for biomedical research.
The two men then made the startling observation that the number 22 chromosome in 
the tumor cells of individuals suffering from chronic myelogenous leukemia (CML) was 
abnormally small.
The discovery came at a time when genetics as a basis for cancer was not generally 
accepted, according to the foundation. The research broke new ground because it 
was the first consistent chromosome abnormality found in any kind of malignancy.
"The tiny Philadelphia chromosome became a clear and consistent marker of CML, a 
cancer of the myeloid or bone marrow cells, with broad implications for diagnosis and 
prognosis of disease," the foundation observed when, years later, it honored Dr. 
Nowell for his contribution to science.
At the time of the discovery, he was employed by the University of Pennsylvania 
School of Medicine, and Hungerford by Fox Chase Cancer Center's Institute for 
Cancer Research.
"It would take doctors and researchers around the world more than three decades to 
unravel the implications of this landmark discovery," wrote Jessica Wapner in her 
book The Philadelphia Chromosome: A Genetic Mystery, a Lethal Cancer, and the 
Improbable Invention of a Lifesaving Treatment.
"He lived long enough to see it developed into treatment to allow individuals to lead 
longer lives," said his son, Michael. Hungerford, of Jenkintown, died of lung cancer in 
1993 at age 66.
Born in Philadelphia to Foster Nowell and Margaret Moore Matlack Nowell, Dr. Nowell 
grew up in Rose Tree, Delaware County.
He attended the progressive School in Rose Valley and graduated in 1945 from 
Swarthmore High School before earning a fast-tracked bachelor of science in 
biochemistry from Wesleyan University in Middletown, Conn.
Dr. Nowell told his family that after reading the 1926 book Microbe Hunters by Paul 
Henry de Kruif, he chose the field of science. Later, he narrowed his focus to 
medicine, his son said.
He earned his medical degree from the University of Pennsylvania School of Medicine 
in 1952, did a rotating internship at Philadelphia General Hospital, and trained in 
pathology at Presbyterian Hospital.
He spent two years at the U.S. Naval Radiological Defense Laboratory in San 
Francisco, studying radiation and bone marrow transplantation, before returning to the 
University of Pennsylvania School of Medicine as an instructor, and later as a 
professor in the Department of Pathology. He served as chairman of the department 
from 1967 to 1973 and was the first director of the University of Pennsylvania Cancer 
Center, now known as the Abramson Cancer Center.

He received the Lindback Distinguished Teaching Award, the 1998 Albert Lasker 
Clinical Medical Research Award, and the Benjamin Franklin Medal in Life Science. In 
2015, the endowed Peter C. Nowell, M.D. Professorship was established in his honor 
at the University of Pennsylvania School of Medicine.

Despite the accolades, Dr. Nowell was short on hubris and long on self-effacing 
humor, his family said.

He liked to remind listeners that he was always a third stringer on any athletic bench; 
that his ineptitude with hand tools was legendary; and that his medical students had to 
suffer through his frequent puns.

"The teasing, humorous patter that became his signature, be it on the tennis court or 
in the boardroom, was with him to the end," his family said.

He was married in 1950 to Helen Walker Worst Nowell, a high school classmate. They 
moved to Middletown Township, Delaware County, in 1957 and reared five children. 
His wife died in 2004, and their daughter, Sharon, died in 2000.
  
Besides his son, he is survived by another son, Timothy; daughters Karen King and 
Kristin; a brother; and seven grandchildren. A sister and brother also died earlier.

Plans for a memorial service were pending. Interment will be private.

Contributions may be made to the School in Rose Valley, 20 School Lane, Rose 
Valley, Pa. 19063; or to Elwyn, 111 Elwyn Rd., Media, Pa. 19063

Parents
NOWELL Foster (26 Aug 1895 - Jun 1978)
MATLACK Margaret Moore (13 Oct 1897 - 11 Jan 1990)

Siblings
NOWELL Nancy Knight (1922 - 1925)
NOWELL Foster J. ("Jerry") ()
NOWELL Peter Carey (8 Feb 1928 - 26 Dec 2016)
NOWELL Samuel Matlack (15 Sep 1929 - 10 Sep 2000)

Marriage To WORST Helen Walker (31 Oct 1927 - 24 Nov 2004)
    m. 9 Sep 1950 Swarthmore, Pa.

Notes

Parents
WORST Clarence Walker ()
PEW Helen Glenn ()

Children by WORST Helen Walker 31 Oct 1927 - 24 Nov 2004
NOWELL Sharon Lee (6 Apr 1954 - 3 Apr 2000)
NOWELL Timothy Todd ()
NOWELL Karen Dale ()
NOWELL Kristin Lynne ()
NOWELL Michael Lane ()

Produced by Fzip 1.7 2/10/2021