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New Hope For Cancer
This little pill targets cancer cells with uncanny precision. Is it the breakthrough we've been waiting for? (article from TIME MAGAZINE)
Sunday, May. 20, 2001
By February of last year, Victoria Reiter, 63, figured she had only a few months to live. A writer and translator living in Manhattan, she was suffering from chronic myeloid leukemia, an especially deadly form of blood cancer. The only treatment available was interferon, an immune-system booster that wasn't really working and that made her violently ill. Reiter had spent most of 1999 in bed, too sick to read, to walk, to do much of anything — although she had managed to put together lists dividing her possessions between her two daughters.Then she went on an experimental drug called Gleevec, and within weeks everything changed. "All my energy started coming back," she says. "Suddenly I could read. I could take a walk." By August, tests showed her bone marrow was clear of leukemia cells; in December, she took up the Argentine tango. She still has the lists of what her daughters will get, but, she exults, "They're not going to get it yet!"
For Bob Ferber, a Los Angeles prosecutor specializing in animal-abuse cases, the Gleevec experience was very much the same. Less than two years ago, he was lying in a hospital room considering suicide to escape the pain radiating from his bones. "From crawling across the floor on my knees to go to the bathroom, I'm now back at work," says Ferber, 48. "I go to the gym. I'm volunteering for an animal-rescue group. I have a girlfriend. It's the dream of any cancer patient in the world to be able to take a pill that works like this. It's truly a miracle."
That's a tempting way to look at it, anyhow. Gleevec is effective enough that the U.S. Food and Drug Administration approved it in record time two weeks ago — even as researchers announced that it also works against a rare form of stomach cancer. The drug doesn't help everyone, and it can have side effects, including nausea, muscle cramps and skin rash. Moreover, nobody is claiming that it actually cures cancer. Patients may have to continue taking the drug, probably for the rest of their lives, and unless Gleevec is used in combination with some other drugs, it is likely their cancer will come back.
Despite all these caveats, Gleevec is still a breakthrough — not only for what it does but, more important, for the revolutionary strategy it represents. A full 30 years have passed since President Richard Nixon declared war on cancer and called for a national commitment comparable to the effort to land on the moon or split the atom. But over those three decades, researchers have come up with one potential miracle cure after another — only to suffer one disappointment after another. Aside from surgery, which almost invariably leaves behind some malignant cells, the standard treatment for most cancers continues to be radiation and chemotherapy — relatively crude disease-fighting weapons that have limited effectiveness and leave patients weak and nauseated.
Along the way, though, scientists have amassed a wealth of information about how cancer works at the molecular level, from its first awakening in the aberrant dna of a single cell's nucleus to its rapacious, all-out assault on the body. Armed with that information, they have been developing a broad array of weapons to attack the disease every step along the way. Many of these therapies are just beginning to reach clinical trials and won't be available to save lives for years to come. If you have cancer today, these treatments are likely to come too late to help you. But, says Dr. Larry Norton, a medical director at Memorial Sloan-Kettering Cancer Center in New York City: "I think there is no question that the war on cancer is winnable."
That sentiment was pounded home last week at the annual meeting of the American Society of Clinical Oncology in San Francisco, where a record 26,000 cancer specialists from around the world briefed each other on the good news starting to pour out of their laboratories. Unlike chemo and radiation, which use carpet-bombing tactics that destroy cancer cells and healthy cells alike, these new medicines are like a troop of snipers, firing on cancer cells alone and targeting their weakest links.
Some of these therapies prevent a class of chemicals called growth factors from reaching a tumor, blocking signals that would otherwise instruct the cell to grow out of control. Others tip the delicate balance that every cell maintains between life and death, driving cancerous cells to self-destruct. Still others block enzymes that cancer cells use to chew openings in normal tissues and give themselves room to expand. And, most famously, the class of compounds known as angiogenesis inhibitors keep tumors from building new blood vessels to supply themselves with food and oxygen. Three years ago, Nobel laureate James Watson, co-discoverer of the structure of dna, was quoted as saying Dr. Judah Folkman, the Harvard researcher, would use these inhibitors to "cure cancer within two years."
He later claimed that he had been misquoted — and no wonder. Scientists who know anything about cancer are exceedingly cautious about using the C word. That's partly because it too easily raises false hopes and partly because doctors are increasingly convinced that a cure is not the only way to beat cancer. Instead, experts believe, by throwing a series of monkey wrenches into the cancer cell's machinery, the new therapies could transform cancer from an intractable, frequently lethal illness to a chronic but manageable one akin to diabetes and high blood pressure. Says Dr. Leonard Saltz, a colon-cancer specialist at Memorial Sloan-Kettering: "I don't think we're going to hit home runs, but if we can get a series of line-drive singles going and put enough singles back to back, we can score runs."
Four years ago, for example, researchers at IDEC Pharmaceuticals in San Diego, Calif., hit just such a line-drive single with Rituxan, the first drug that successfully targeted proteins on cancer cells. Scientists had learned over the years that cancer cells are studded with an unusually large number of receptacles that compounds essential for survival, including growth factors, can plug into and fuel the cells' growth. Rituxan is a monoclonal antibody, a molecule specifically engineered to fit into the receptacles on non-Hodgkin's lymphoma cells and, in this case, single out the cancer cell for destruction by the immune system. Back in the early 1980s, monoclonal antibodies were hyped in the media as "magic bullets" that would wipe out cancer.
That proved far too strong a claim, but monoclonal antibodies have finally begun to live up to more modest expectations. Rituxan was the first, but just a year later, the same approach led to Herceptin, a drug that keeps growth factors from feeding certain kinds of breast-cancer cells. Such targeted treatments are effective only when the appropriate target exists. Herceptin, for example, latches onto a receptor known as her2, which is abnormally abundant in only about 30% of breast-cancer tumors. A biopsy can tell doctors whether a patient is likely to respond to Herceptin, but they'd hoped to find a molecule that would plug into a growth-factor receptor more prevalent in cancer cells.
Sure enough, they found one. Dr. John Mendelsohn, then at the University of California, San Diego, and now president of the M.D. Anderson Cancer Center in Houston, had been focusing since 1981 on a receptor called egfr, which is host to a protein called epidermal growth factor (EGF). It's a close cousin to her2, and Mendelsohn and his team know that it is present in a huge variety of tumors; two-thirds of all cancer types, in fact, are blanketed with EGF receptors. In 1984 Mendelsohn and his team showed in mice that blocking the EGF receptor with a growth-factor decoy prevented a cell from growing and dividing.
Making a drug out of that decoy would prove tricky, since the receptor, like her2, also shows up on noncancerous cells. Researchers are now learning, however, that normal cells are more adept than cancer cells at finding other growth factors on which to rely when EGFR is blocked. But when Mendelsohn applied for his first grant from the National Cancer Institute in 1983, he was rejected. "Nobody thought it would work," he says. The following year he turned to philanthropic sources for research dollars. Last year he wowed colleagues with a compound called imc-c225, which proved effective in treating colon tumors in a small number of patients.
Then just this year researchers at Sloan-Kettering showed that the drug could dramatically boost the effectiveness of standard colorectal-cancer chemotherapy, shrinking tumors in more than a fifth of otherwise hopeless cases. Says Sloan-Kettering's Saltz: "The fact that we got a 20% response rate is staggering." What is happening, he surmises, is that the growth-factor inhibitor weakens the tumor enough for chemotherapy to finish it off.
Buoyed by those results, Saltz will begin testing imc-c225 in less advanced patients this summer. And because combination therapy seemed to work so well, he is combining the EGFR inhibitor with not one but two chemotherapy agents to pack a triple punch.
Those are only two drugs that keep EGF from doing its job. Gleevec, which reversed Reiter's and Ferber's leukemia so dramatically, is another; so is Tarceva, a drug from OSI Pharmaceuticals in Uniondale, N.Y., which is showing promise against some lung tumors as well as head and neck cancers. Neither of these compounds keeps EGF from docking with cells; instead, each worms its way inside the cells, where it intercepts growth messages percolating in from the surface. Astra Zeneca, headquartered in London, is testing a similar compound, Iressa, against some lung, stomach and prostate cancers.
And that's just the start. Gleevec, Tarceva and Iressa all break one of the most common signaling pathways by blocking an enzyme known as a tyrosine kinase. But the message that encourages a cancer cell to grow involves hundreds of biochemical signals that can travel by hundreds of different pathways. Each of those pathways represents a target, a link that could be interrupted with the properly designed drug.
Another reason cancers grow inexorably is that unlike normal cells, which die a natural death after a fixed number of divisions, cancer cells live forever. Scientists have been looking for compounds that will rewire tumor cells so they will know when it's time to go. The research is still in its early stages, but scientists in several labs have started looking at a group of enzymes called caspaces; inhibiting these enzymes disrupts the process of DNA repair that occurs each time a cell divides.
In Cambridge, Mass., Millennium Pharmaceuticals is focusing on proteins called proteasomes, which evidently play a role in giving cancer cells unnaturally long lives. The company is in Phase II trials with LDP341, a proteasome-inhibiting substance that is showing promise against multiple myeloma and chronic lymphocytic leukemia. Phase I studies on the top five solid tumors (breast, pancreatic, prostate, lung and colon) are under way, and at this point the inhibitor seems to be working — at least in mice.
By far the most celebrated of the new cancer fighters are the antiangiogenesis drugs. Like monoclonal antibodies before them, these compounds, which keep tumors from growing their own blood supplies, were briefly touted as magic one-shot cancer cures — although Folkman, who pioneered the field in the 1970s, was always circumspect about making premature claims. "I think the antiangiogenesis field got some unfair negative publicity," says Saltz. "Our expectations were too high, but there is a lot of brilliant science behind it."
Indeed, while the execution has proved difficult, the idea is very simple. Tumors, like any other cells, need oxygen and nutrients to survive. At first they eat their way through healthy tissue, looking for blood vessels to tap for these essentials. Eventually, though, they start to grow their own capillaries and vessels, like oil companies eager to guarantee a steady flow of crude.
Folkman's insight was to look for substances that prevent tumors from building those pipelines. This approach worked beautifully in mice. Now more than 50 angiogenesis inhibitors are being studied in humans with a wide range of cancers; a dozen are in the final stages of testing. Thus far, only a tiny number of human patients treated with these compounds have seen their tumors shrink or disappear. Clinicians are nonetheless encouraged; while angiogenesis inhibitors don't make cancer go away, they do appear to slow tumor growth. And that means they may work best in conjunction with some of the other new treatments to batter cancer from several directions at once.
"We've seen results in very few patients yet," says Folkman. "But we have seem some patients with stable disease. We have seen some patients whose tumors have stopped growing. And we have seen some patients whose tumors slowly regressed. I think the approach is promising, but we are still learning."
While many scientists focus their attention on potential weaknesses in the cancer cell, others are concentrating on the flip side — recruiting the body's immune system to seek and destroy the renegade tissues. So far, this approach has proved less successful, largely because no matter how badly they are misbehaving, tumor cells are purely homegrown and thus presumed innocent by the immune system. When it finally catches on that something is wrong, it's usually too late.
That problem may not be insurmountable, as scientists at last week's clinical-oncology meeting made clear. The trick, it turns out, may be to put aside 99% of the immune system and focus on dendritic cells, a tiny but especially sensitive population of white blood cells that act as sentries to warn against invaders of all kinds. Scientists at California-based Cell Genesys, for example, have taken tumor cells from a number of cancers, genetically engineered them to pump out a hormone that stimulates production of a host of immune cells, and vaccinated late-stage lung-cancer patients with the mixture to boost chances that dendritic cells would sound the alarm against the tumors. In the latest study, three of 22 patients saw their tumors disappear completely, and four saw them stop growing.
Researchers at Stanford University have harvested dendritic cells from advanced-cancer patients, exposed the cells to potent growth factors, added tumor-specific proteins to sensitize them and reintroduced the mixture into patients as a vaccine. Of 12 patients with advanced colorectal and lung cancer, two watched their tumors shrivel away, and another is still tumor free a year after receiving the vaccine.
Whether you're talking about conventional therapy or one of these promising new approaches, experts agree the earlier you catch a cancer, the better your chances of controlling it. And thanks to a growing understanding of the cancer cell's natural life cycle, doctors are learning how to detect the disease at its very earliest stages. One well-known example is the prostate-specific antigen (PSA) test, which identifies a protein secreted by abnormally growing prostate cells before any symptoms appear. (The test is not perfect, however, since PSA is also secreted, albeit in smaller amounts, by benignly growing prostate cells.)
Researchers such as Dr. David Sidransky, an oncologist at Johns Hopkins University, are searching for diagnostics that will pick up other cancers in their preliminary stages. Others are focusing on an even earlier stage, trying to lower the risk of developing cancer to begin with. Here the most exciting work centers on the cycooxygenase inhibitor called COX-2. This pain reliever was originally developed to clamp down on inflammation as aspirin does but without aspirin's tendency to eat through the lining of the stomach.
It turns out that COX-2 inhibitor drugs also have anticancer effects, reducing the number of precancerous polyps in patients with a hereditary form of colon cancer, perhaps through antiangiogenesis. Scientists are currently studying its effect on noninherited colon cancers. And because the receptor for COX-2 is overexpressed on a range of human cancer types, the hope is that COX-2 inhibitors may be useful in preventing a wider range of cancers, including head and neck, bladder, non–small cell lung and breast cancers.
As promising as these therapies are, there remain many questions for researchers to answer. Among the most important: Which treatments should be given to which patients? Says Sidransky: "Within five years, it might be almost impossible to bring a drug forward without having a test to help doctors decide whom the drug is for."
Eventually, the goal is to detect precisely which molecular processes have gone wrong in an individual patient's cancer. Rather than being identified as lung cancer or breast cancer or kidney cancer, tumors will be tagged as EGFR positive, for example, or COX-2 positive. "The dream," says M.D. Anderson's Mendelsohn, "is that if Mrs. Smith gets a breast biopsy, we'll be able to say, 'Here are the four genes that are abnormal in her tumor,' pull open a drawer, pick out the antibodies or small molecules designed against the abnormal products of those genes, and give her a cocktail targeting the genes that caused her cancer."
That dream comes at a price. Staying on Gleevec, for example, may end up costing patients like Victoria Reiter as much as $2,400 every month — nearly $30,000 a year — for the rest of her newly prolonged life. While the National Cancer Institute funds basic research into cancer biology, the bulk of drug development is done by for-profit pharmaceutical firms. These companies claim that it costs them between $500 million and $1 billion to bring a single new medicine to market — partly because it can take 15 years for the exhaustive testing in animals and humans required by U.S. law and partly because for every medicine finally approved by the FDA, 5,000 others fail somewhere along the way. The drug companies count on that one success to pay for the 5,000 failures. Meanwhile, pharmaceutical firms are under attack both for allegedly conspiring to keep cut-rate competitors out of the market and for profiting handsomely from basic research that was originally funded by the taxpayers.
Now that Gleevec has been taken off the experimental list, insurance companies will probably pick up the tab. Cancer most often strikes the elderly, however, and Medicare's role in paying for prescription drugs is still undecided. President Bush's drug plan would add $153 billion for Medicare drug benefits through 2011. Democrats call the amount "inadequate," and even congressional Republicans agree it is not enough. The final numbers will be hammered out later this year.
At least the drug companies and politicians have something to argue about. Given the painfully slow development of effective cancer treatments over the past three decades, the flood of positive results reported at last week's oncology conference was especially gratifying. "Cancer treatment has always been a satisfying profession," says Dr. Michael Gordon, a cancer specialist at the University of Arizona. "But now it's truly exciting. I've been wondering to myself about where I will be in 20 to 25 years, and I'm thinking that I might just be out of a job. And that will be great."
MORE FROM TIME : Cancer Drugs: Find out what's available now and about drugs in the pipeWith reporting by Dan Cray/Los Angeles and Christine Gorman/New York
Monoclonal Antibodies
Lili Duda, VMD, Section Editor of the OncoLink Veterinary Oncology Menu
Monoclonal antibody treatment (CL/MAb 231, Sybiotics Corporation) is licensed for the treatment of canine lymphoma has been used for about 10 years. The success rate is comparable to conventional chemotherapy protocols. Although there are several theoretical advantages to the use of MAb, it has not become a standard therapeutic option in canine lymphoma for a variety of reasons. However, it is a reasonable treatment option if it is available through your veterinarian or veterinary oncologist.
The typical protocol used starts with two "cycles" of standard chemotherapy. If the dog is in complete remission following chemotherapy (no detectable evidence of lymphoma), the dog is given a three week rest to allow the immune system to recover. If the dog continues to remain in remission, monoclonal antibodies are administered over one week. The dog then receives no further treatment until relapse of the lymphoma occurs.
At that time, the above protocol can be repeated if the dog goes into remission after another two "cycles" of standard chemotherapy. However, if the dog does not go into a complete second remission, monoclonal antibodies are not administered a second time, and other "rescue" chemotherapy protocols are used.
VACCINE FOR THE TREATMENT OF MELANOMA IN ANIMALS
April 4, 2001
PORTLAND, Ore. and NEW YORK, April 4, 2001 /PRNewswire/ -- Bioject Medical Technologies Inc. (Nasdaq: BJCT), the leading manufacturer of jet injection devices for needle-free drug delivery and the Animal Medical Center today announced the introduction of a DNA-based vaccine treatment for melanoma in animals.
Previous clinical studies in mice have indicated that the vaccine, when delivered with the Biojector(R) 2000 jet injector, elicits a statistically significant higher immune response than the vaccine delivered with needle and syringe. The DNA-based melanoma vaccine was developed by researchers at Memorial Sloan-Kettering Cancer Center under direction of Dr. Alan Houghton and Dr. Jedd Wolchok.
The treatment will be available exclusively at the Animal Medical Center, a leading companion animal veterinary hospital located in New York City.
"Melanoma is a very serious form of cancer in both humans and companion animals," said Dr. Phil Bergman, Chief of Oncology at the Animal Medical Center. "Currently available treatment methods are not effective for all types of the disease. DNA-based therapeutic vaccines are among the most promising new treatments becoming available to combat cancer."
"Through our research collaborations, Bioject has been focused on the delivery of DNA vaccines for some time," said Jim O'Shea, Bioject's chairman, president and CEO. "By improving the efficacy of DNA-based vaccines, our needle-free technology can add value to the efforts of researchers developing ways to combat deadly diseases like cancer."
The Animal Medical Center is a non-profit veterinary hospital with a staff of 80 veterinarians specializing in more than 20 areas of surgery and medicine. Since 1910, when AMC was founded by the New York Women's League for Animals, AMC has provided the highest quality medical services to companion animals. The AMC is dedicated to treating each one of over 60,000 patients seen each year with the personal care and attention a member of your family deserves.
Bioject Medical Technologies, Inc., located in Portland, Oregon, is an innovative developer and manufacturer of drug delivery systems. The Company's advanced delivery system, the Biojector(R) 2000, injects medication without a needle. The Biojector(R) employs compressed gas as a power source to force medication at high speeds through a tiny orifice, penetrating the skin and delivering medication without use of a needle. Using needle-free technology to administer injections virtually eliminates the risk of contaminated needlestick injury and resulting blood-borne pathogen transmission, a major concern throughout the healthcare industry. The Biojector 2000 has received
the Seal of Acceptance from the Alliance of Children's Hospitals, Inc.This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995, including statements concerning the ability of the company's products to enhance delivery of DNA-based vaccines. Such forward looking-statements involve known and unknown risks, uncertainties and other factors which may cause the actual results, performance or achievements of the company, or industry results, to be materially different from any future results, performance, or achievements expressed or implied by such forward-looking statements. Such risks,
uncertainties and other factors include, without limitation, the risk that research and development results will not show that the company's products enhance delivery of DNA-based vaccines and uncertainties related to i.) the time required to complete research and development, ii.) obtaining necessary clinical data, and iii.) the Memorial Sloan-Kettering Cancer Center's continuing commitment to the project. Readers of this press release are referred to the company's filings with the Securities and Exchange Commission, including the company's Annual Report on Form 10-K for the year ended
March 31, 1999 for further discussion of factors which could affect future results.Forward-looking statements are based on the estimates and opinions of management on the date the statements are made, and the Company assumes no obligation to update forward-looking statements if conditions or management's estimates or opinions should change.
CONTACT: Jim O'Shea, Chairman, President, & CEO, or Sam Nickerson, Investor Relations, both of Bioject Medical Technologies Inc., 503-639-7221, ext. 565; or Philip J. Bergman, BDM, MS, Ph.D, of Animal Medical Center, 212-838-8100, or philip.bergman@amcny.org; or Kristen Hammer of Noonan/Russo Communications, Inc., 212-696-4455, ext. 249, or news@noonanrusso.com, for Bioject Medical Technologies, Inc./Company News On-Call: http://www.prnewswire.com/comp/101750.html or fax, 800-758-5804, ext. 101750/Web site: http://www.bioject.com (see Dog cured article on NEWS STORIES PAGE)
Tall-104
Please read the below information on Tall-104. Initial trials have been
extremely promising for an actual CURE for several cancers and good
remissions for others. However, a drug manufacturer is needed to produce
these cells so that they will be avilable for cancer trials and treatment
for both animals and people and so far none have stepped up to the plate.
Time is passing and the cancer is continuing to grow and kill its victims.
Your e-mail indicating your desire to get this treatment for cancer victims
will be a BIG help in having a drug manufacturer spend their time and money
to produce this protocol.
Please help by forwarding an e-mail saying you want Tall-104 on the market.
Send to Dr. Santoli at: santoli@wistar.upenn.edu or FAX: (215)573-7919
The San Diego Union-Tribune
Wed, Jan 14 1998
Beginning three years ago, researchers from the Wistar Institute in
Philadelphia gave an experimental therapy to 19 dogs dying of cancer.
The pets were considered too sick to derive much benefit, but their
reactions would show whether the therapy, called TALL-104, had toxic side
effects. If it was safe, the next step would be proving it worked. To the
researchers' astonishment, six of the 19 dogs temporarily went into
remission - and one was completely cured. There were no serious side
effects. And the therapy not only attacked cancerous cells, but stimulated
some of the dogs' immune systems to take over the attack. "We really did not
expect much, so having seven responses was a remarkable thing," said Wistar
immunologist Daniela Santoli, research team leader. TALL-104 has proven to
be so effective in treating cancer in dogs and cats that Santoli and her
colleague plan to seek federal marketing approval of the therapy for
veterinary use. It also has begun human testing. A trial at Children's
Hospital of Philadelphia is enrolling children with advanced leukemia,
lymphoma, and bone, brain or kidney cancer; another trial at the Hospital of
the University of Pennsylvania is enrolling women with advanced, spreading
breast cancer.
The new approach relies on T-cells, human immune system cells that are
programmed by the body to destroy foreign invaders and cancerous cells. Ten
years ago, Santoli was studying T-cells taken from a child with acute
lymphoblastic leukemia, a blood cancer in which immature T-cells multiply
uncontrollably. Under the microscope, Santoli saw that the child's T-cells
were filled with toxic proteins.
She wondered whether these malignant immune cells could be harnessed to kill
other malignant cells. She began growing batches of the child's cells,
dubbed TALL for T-cell acute lymphoblastic leukemia, and treating mice. TALL
cells were prevented from causing leukemia in the mice by bombarding the
cells with radiation. Surprisingly, the cells did not trigger significant
rejection, even when testing moved from mice to dogs and cats, animals with
immune systems similar to those of humans. TALL-104 had no serious side
effects in animals. It apparently attacks only cancer cells. Equally
important, TALL-104 somehow alerts the patient's immune system to attack
lingering cancer cells, thus preventing cancer from recurring.
TALL-104 is currently being tested on 45 dogs and 16 cats with less advanced
cancers. All are now in remission, and many are beyond the point when they
would be expected to suffer a recurrence of cancer, Santoli said. It will
take at least another year to obtain federal approval for TALL-104, and to
find a biotechnology company to mass produce the cells. Santoli said her lab
spends about $80 to
produce a single dose. TALL-104 therapy for humans is farther off -- if the
trials go well. Phased testing to evaluate the toxicity, dosing and
effectiveness in humans of a new drug normally takes at least five years.
But most drugs that are promising in animals don't pan out in humans.
So far, only four children and a few women have begun receiving TALL-104.
Their doses are lower than those found to be effective in animals, because
early testing is designed to evaluate toxicity and dosing regimens. "This is
very novel and it is met with tremendous skepticism" by scientists, said
pediatric oncologist Beverly L. Lange, who is leading the trial at
Children's Hospital of Philadelphia. "But it's a reasonable thing to try."
(Copyright 1998)
_______________________________________________________________________
FOR IMMEDIATE RELEASE: 10 MAY 1999
Contact: Diana Cutshall
dcutshall@wistar.upenn.edu
215-898-3716
Wistar Institute
Wistar Scientist Awarded American Cancer
Society Grant For Research On Tumor Killing
Cells
Philadelphia-- Daniela Santoli, Ph.D., a professor in The Wistar
Institute's Tumor Immunology Program, has been awarded a $300,000 two-year
grant from the American Cancer Society for a Phase I/II trial of TALL-104
cells in patients with metastatic melanoma.
TALL-104 is a "killer" cell line derived from the cells of a child
with a rare form of T-cell leukemia. Dr. Santoli has found that TALL-104
cells can recognize and selectively kill malignant cells. Her research team
has used TALL-104 cells to treat pet dogs and cats with various terminal
cancers that were unresponsive to conventional therapy. In many of these
companion animals, the TALL-104 cells caused complete, long-lasting
remissions.
Phase I clinical trials of TALL-104, which tested the safety of the
treatment on humans and established safe dosage ranges for further efficacy
trials, were conducted on children with advanced cancers and women with
metastatic breast cancer. In these trials, no toxicity was shown up to the
planned maximum dose. With the recently awarded American Cancer Society
funds, Dr. Santoli and her clinical
collaborator, Dr. Lynn Schuchter at the Cancer Center of the Hospital of the
University of Pennsylvania, will focus on the development of a TALL-104
regimen that will be effective and safe in melanoma patients with metastatic
disease. These trials are not expected to start until later this year.
The American Cancer Society is the nationwide, community-based
voluntary health organization dedicated to eliminating cancer as a major
health problem by preventing cancer, saving lives and diminishing suffering
from cancer through research, education, advocacy and service. Last year,
the American Cancer Society contributed $93.3 million to research facilities
throughout the country.
The Wistar Institute, established in 1892, was the first independent
medical research facility in the country. For more than 100 years, Wistar
scientists have been making history and improving world health through their
development of vaccines for diseases that include rabies, German measles,
infantile gastroenteritis (rotavirus), and cytomegalovirus; discovery of
molecules like interleukin-12, which are helping the immune system fight
bacteria, parasites, viruses and cancer; and location of genes that
contribute to the development of diseases like breast, lung and prostate
cancer. Wistar is a National Cancer Institute Cancer Center
Curing Man and His Best Friend
Vet and Doc Collaborate, Improve Bone Cancer Treatment
This article taken from ABC-TV's "20/20" (for FULL STORY click here)
Sept. 8 2000 — Ross Wilkins and Stephen Withrow are doctors working together in the fight against bone cancer.
But their collaboration does not happen in the same hospital or research center — they can’t meet on the job because they work on different species. Still, their unusual partnership has led them to become leaders not only in helping their patients survive bone cancer with chemotherapy, but in preserving limbs that almost certainly would have been amputated in the past.
Wilkins, an orthopedic surgeon, practices at a state-of-the-art human care facility, the Institute for Limb Preservation at St. Luke’s Presbyterian Hospital in Denver. Withrow, a veterinarian specializing in treating cancer in animals, practices 70 miles north of Denver in the world’s largest veterinary cancer center at Colorado State University. Wilkins began to tap into Withrow’s knowledge of animal treatment for a very good reason: bone cancer occurs in large dogs 10 times more frequently than it does in humans.Pioneering Techniques
Withrow helped pioneer a technique that makes bone grafts — a surgery in which a cadaver bone is transplanted into the affected area — more effective by using surgical cement to fill and strengthen the bone before it’s transplanted. Antibiotics are added as well to fight potential infections. Wilkins remembers when they discussed such a procedure over pizzas.
“If you think about a bone, it’s a hollow tube. We felt that if we could fill that tube with something that’s hard and strong, you could put antibiotics in. That would protect the graft from infection,” he says. “We sort of started doing this in animals, and we started doing it in humans.”
Withrow performed state-of-the-art surgery on Dakota, a black Labrador, to try to avoid amputation of his front leg. A day later, Dakota was out on the lawn, retrieving a ball. (ABCNEWS.com)
News
Fish oil helps dogs with lymphoma live longer
April 28, 2000NEW YORK (Reuters Health) - A diet supplemented with fish oil and the amino acid arginine appears to increase survival time in dogs with lymphoma, a cancer that affects white blood cells.
Dogs with this kind of cancer, similar to non-Hodgkin's lymphoma in humans, are easily treated, but as with humans, their cancer tends to return. A team of researchers led by Dr. Gregory Ogilvie of Colorado State University in Fort Kent, studied the effects of adding fish oil and arginine to the diets of 32 dogs being treated for lymphoma.
Half of the dogs received a special chow with the two supplements in it, and the other half ate chow with soybean oil added. The two chows were identical in nutritional value, and formulated to be equally tasty to the dogs. All the dogs were being treated with the anti-cancer drug doxorubicin every three weeks, and were living at home with their owners.
Previous research has shown that some polyunsaturated fatty acids, like those found in fish oil, may help prevent the growth and spread of cancer tumors, and may help prevent cachexia -- the devastating weight loss and muscle wasting seen in some cancer patients despite adequate nutrition. Likewise, arginine supplements have been reported to improve immune responses, and might help the body fight cancer.
The dogs were fed one of the chows twice a day during and after their cancer treatment. The researchers report that compared to the control dogs, those who ate the supplemented chow showed higher blood levels of two fatty acids called C20:5 and C22:6 that seem particularly effective in fighting cancer. Dogs with more of these fatty acids in their blood also tended to have more normal levels of lactic acid, which tends to accumulate in the blood when metabolism is disrupted in cancer patients.
In addition, report Ogilvie and colleagues, the dogs with higher levels of these two fatty acids survived longer than those with lower levels, and had longer remissions, periods of time before their disease came back.
Writing in the journal Cancer, the researchers suggest that the fatty acids may help both dogs and humans by slowing down the spread of cancer cells and by increasing the cells' susceptibility to anti-cancer drugs like the doxorubicin used in this study.
Ogilvie and colleagues also note that their findings fit in with previous research showing that the fatty acids they studied appear to help fight cancer and its effects in both humans and animals.
