NEW YORK — High rates of health care spending in the United States does not seem to correlate with improved survival for cancer patients, according to a new study in the American Journal of Public Health (AJPH).

Similar survival rates were found among people in certain parts of the U.S. and Ontario, Canada, for three types of cancer: colon, lung, and Hodgkin’s disease. Only survival rates for breast cancer patients in the U.S. were better, which may be related to this country’s greater use of screening mammography.

Researchers from the U.S. General Accounting Office (GAO) in Washington, D.C., note that the United States has the most expensive health care system in the world — both in terms of per capita spending and proportion of gross domestic product devoted to health.

“Many U.S. citizens assume that greater resources will lead to better care,” they state. “Yet the growing literature on comparative health care outcomes suggests that the high level of health care spending in the United States has not led to clearly superior results for U.S. patients.”

Using 1978-1986 government cancer data compiled for nine regions in the U.S. and the Canadian province of Ontario, survival rates for the four cancers were computed for patients aged 15 through 84 years.

During the follow-up period of up to 13 years, overall (cumulative) survival chances were about the same for American and Canadian patients. More Americans diagnosed with lung cancer were alive after one year, but the survival rate statistically favored the Canadians at 13 years.

For colon cancer, a similar picture emerged, and no significant difference was found during the follow-up period for Hodgkin’s disease.

“Breast cancer is the only one of the four diseases examined for which U.S. patients evidence superior survival over the 13-year period of study,” the researchers say.

The GAO researchers point to findings from Washington State and British Columbia suggesting “that the prevalence of screening for breast cancer in the United States and Canada may be quite different... that mammography was two to three times more common in the United States.”

They say this means that more women in the U.S. would be diagnosed earlier in the course of their disease, thereby promoting more effective treatment.

However, the researchers conclude, “The similarity in survival rates for the other three cancers indicates that one health system is not categorically better than the other with respect to cancer outcomes.”

Another study appearing in this issue of the AJPH suggests that lower cancer survival rates among lower socioeconomic groups in the U.S. may be linked to better health care access in Canada. Canadian researchers at the University of Windsor, compared people in low-income areas of Detroit, Michigan, to those in Toronto. They found an increased survival advantage for 13 out of 15 cancers at one- and five-year follow-ups.

“No such between-country differentials were observed in the middle- or high-income groups,” according to the researchers.

They say that if all segments of the U.S. population enjoyed equal access to preventive and therapeutic services, the apparent survival advantage noted in Canada would probably disappear.

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Study: Concentrated Anti-Cancer Agent in Broccoli Sprouts (970917)

WASHINGTON — Tender sprouts of broccoli just emerging from the seeds contain up to 50 times more anti-cancer chemical than the mature vegetable and don’t have the broccoli flavor that so many people find distasteful, researchers say.

In a study published today in the Proceedings of the National Academy of Sciences, researchers at Johns Hopkins University say they have found broccoli sprouts are loaded with a concentrated form of sulforaphane, a power cancer fighter.

Dr. Paul Talalay, head of a team at Hopkins that discovered sulforaphane five years ago, said he was surprised the sprouts contained such a high level of the anti-cancer compound.

“If these are developed commercially, this could be a really easy way for people to get the benefits of chemoprotection against cancer,” said Talalay.

Earlier studies showed that sulforaphane, found in broccoli, cauliflower and some other vegetables, prompts the body to make an enzyme that prevents tumors from forming. In laboratory animals exposed to carcinogens, a 1994 study found cancer development was reduced by 60 percent to 80 percent when the animals were fed sulforaphane extracted from broccoli.

Talalay said diet studies have shown that eating 2 pounds of broccoli a week — an unappetizing thought to many people — can provide enough sulforaphane to lower colon cancer risk by half.

But Talalay said his lab has found the sulforaphane levels of broccoli from a grocery store can vary by a factor of eight or 10 and there is no way to identify a vegetable loaded with the compound from one that is not.

“They look the same,” he said. “It is impossible to tell a highly protective broccoli from a poorly protective broccoli.”

Broccoli sprouts may solve this problem, said Talalay, because the baby plants have a uniformly high level of sulforaphane.

“Because of the high content (of sulforaphane), it is possible to consume far lower quantities of the sprouts and get the same protection,” he said.

Broccoli sprouts resemble the alfalfa sprouts now common in grocery stores, but they have more flavor, said Talalay. And the broccoli sprouts do not have the sharp tang of mature broccoli that many people, such as former President Bush, find unpleasant.

“They have a far more interesting taste than ordinary sprouts,” said Talalay. “You can use them in sandwiches or salads.”

Talalay said the broccoli sprouts take just three days to grow from seeds, in contrast to the 55 to 70 days it takes to grow a mature broccoli plant.

Broccoli sprouts are not now grown commercially, but Talalay said that if other researchers confirm the findings of his lab, it could encourage growers to start producing the baby broccoli as a new vegetable for health-conscious shoppers.

“This is an important finding,” said Michael Bennett, a professor at the University of Texas, Southwest Medical Center and an expert on diet and cancer. He said that diets rich in broccoli and other vegetables have a proven benefit to health but that “the important thing is getting people to eat them.”

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Sunbathing may be linked to rise in blood cancers (970917)

LONDON, Sept 17 — Sunbathing, pollution and an increase in the use of antibiotics could be contributing to an alarming rise in blood cancers in Britain, medical experts say.

A new study of leukaemia, lymphoma and other blood diseases, the largest of its kind in Britain, showed a 40 percent increase in non-Hodgkin’s lymphoma (NHL) over the past 10 years in the 30-79 age group.

It also found that more men than women, particularly over the age of 50, are likely to develop cancers of the blood.

If the current rise continues, researchers predict the disease will be the sixth most common form of cancer by the year 2000.

“The increase in NHL is extremely worrying and clearly requires much closer investigation because we don’t know what is causing it,” said Professor Ray Cartwright, director of the Leukaemia Research Fund Centre which conducted the study.

Doctors say part of the rise may be due to better diagnosis and to an ageing population but exposure to sunlight is becoming the top possibility.

“So far sunbathing is the strongest theory,” Cartwright said in an interview on Wednesday.

“The people who get skin cancer also get more lymphomas which is interesting and people with lymphoma get more skin cancers, so it goes both ways.”

Doctors believe the ultraviolet light from the sun attacks the white blood cells as they go through the capillaries in the skin. Sunscreens, which protect the skin from the sun’s harmful rays, provide no defence for the white blood cells.

Evidence in Scandinavian countries supports the theory.

“The number of NHL cases increase the further north you get. It seems to be associated with the fair skin and that means that the UV energy could penetrate deeper into their skins than it would in black populations,” Cartwright said.

The leukaemia study covered 27,000 cases of leukaemia, lymphoma, and other blood diseases diagnosed between 1984-1993 from a population base of more than 11 million people.

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Most Cancerous Chemical Possibly Found (971024)

LONDON — Japanese scientists suspect that a chemical found in the exhaust fumes of diesel engines may be the most carcinogenic ever found, and the cause of a rise in urban lung cancers, the New Scientist magazine said Thursday.

The compound, 3-nitrobenzanthrone, had the highest ever score on a standard test for cancer-causing potential of toxic chemicals. It also caused chromosomal aberrations in the blood cells of mice.

“I personally believe that the recent increase in the number of lung cancer patients in vehicle-congested areas is closely linked with respirable carcinogens such as 3-nitrobenzanthrone,” said Hitomi Suzuki, a chemist at Kyoto University, who conducted the study.

When Suzuki tested the compound on a strain of salmonella he found that if caused more mutations than 1.6 dinitropyrene, the previous most powerful known mutagen.

Although both compounds are found only in minute quantites, they are so dangerous that “it is easily understandable that they would contribute considerably to the total mutagenic activity of diesel exhaust particle extracts,” Suzuki added.

He called for stronger limits on the loads that diesel trucks can carry because there are more emissions from engines under heavier loads.

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Doctors Aim at Cancer With Magic Bullet (971030)

LONDON — Scientists are close to testing a genetically engineered “magic bullet” that could treat half of the most common cancers, New Scientist magazine said Wednesday.

Early laboratory tests have shown that the “bullets,” which destroy the tumors by injecting them with a deadly toxin, were effective in treating adenocarcinomas which are found in lung, ovary, prostate, colon and breast cancers.

Clinical trials with colon cancer sufferers could begin within the next 15 months.

A magic bullet is a treatment that targets the cancerous cells without harming any of the healthy cells around them — unlike chemotherapy which can harm healthy cells and result in serious side-effects.

“Medical Targeting Recognition (MTR) Technologies, the Jerusalem-based company that developed the bullets, say that they might work better than other such treatments because their toxins actually penetrate cancer cells,” the magazine said.

Earlier attempts at the approach failed because although the antibodies on the bullets found the cancerous cells they could not penetrate and destroy them without harming healthy cells as well.

MTR developed fusion proteins that isolate the dangerous cells and inject them with a bacterial toxin while leaving healthy cells alone.

One half of the re-engineered protein binds to the receptor on adenocarcinoma cells and the second half fires a fatal dose of the toxin that kills them by preventing them from making proteins.

“The Israelis modified the natural toxin so that immune cells previously exposed to the bacteria would not recognize and attack it,” the magazine explained.

Seragen, a Massachusetts-based company, is using a similar approach against a rare form of leukemia called cutaneous T cell lymphoma.

Its protein binds to a site on the cancer cells called interleukin-2 growth factor receptor to fire the toxin. It is already close to completing clinical trails and is applying to the U.S. Food and Drug Administration for approval of the drug.

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Companies Approach New Cancer Drugs (971107)

WASHINGTON — Advances in molecular biology have allowed drug companies to take dramatic new approaches to treating cancer, the journal Science reported Thursday.

Most cancer treatments today involve blunt-instrument approaches such as surgery or the use of poisonous chemicals or radiation that can kill healthy cells.

New understanding of the basic cellular processes involved in cancer have encouraged the development of drugs that block cancer at various stages of its development and that should be much gentler on the patient.

Scientists also understand that genetic mutations are a basic cause of nearly all cancers and are finding ways to counter their effects.

They are all still at experimental stages, but some of the new approaches being taken by drug companies include antibodies that block the effects of proteins that start the uncontrolled cell replication that marks cancer, molecules that block the chemical doorways, or receptors, used by enzymes and genetic approaches aimed at restoring normal gene activity.

— Cell Pathways Inc’s FGN-1 brings on apoptosis, the natural cell ‘suicide’ process that removes damaged and potentially cancerous cells.

— Tyrosine kinase inhibitors, which block tumor growth by stopping the development of blood vessels that feed them, are being developed by Sugen, Zeneca, Oncogene Science and Pfizer.

— Janssen, a unit of Johnson & Johnson, is working on a farnesyl transferase inhibitor it hopes will prevent activity by ras, believed to be the second-most-common gene involved in cancer. It tells cells whether to divide.

— Hoechst Marion Roussel, a subsidiary of Germany’s Hoechst, is pursuing CDK (cyclin-dependent kinase) inhibitors, which should block the out-of-control growth cycle of cancer cells.

— Genentech is developing an antibody that blocks the HER2 growth receptor, which is overexpressed in breast cancer patients, while rival ImClone Systems is working on one that blocks the EGF (epidermal growth factor) receptor.

There are also several genetic approaches.

— Seattle’s targeted Genetics is trying out gene therapy to replace faulty HER2 genes.

— Introgen Therapeutics, working with Rhone-Poulenc division RPR Gencell, and rival Schering-Plough subsidiary Canji Inc., have engineered cold viruses to carry the p53 tumor suppressor gene to cells that have lost it. The p53 gene is involved in up to half of all cancers.

— Onyx Pharmaceuticals is taking the opposite approach, with a modified virus that kills cells that lack p53.

— Antisense therapy, which blocks the effects of genes involved in cancer by interfering with protein production, is also showing promise. Biotech company Genta Inc. is developing BCL-2 antisense to restore apoptosis.

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New Clues to Cancer Cell Death Found (971114)

LONDON — Cancer researchers have discovered a vital clue about how malignant cells die which could hasten the development of more effective and less toxic drugs, they said Thursday.

Scientists at the Imperial Cancer Research Fund found that an on/off switch that tells a defective cell to kill itself is routed through the exterior of the cell.

The finding offers hope for millions of cancer sufferers because, unlike the cell’s interior which is protected by an impermeable membrane, the outside is much more accessible. It should be easier to manipulate with a new generation of drugs that could be developed over the next 20 years.

“This new discovery of how cell death is triggered is very important for understanding how cancer cells arise and form tumors,” Professor Gerard Evan, the head of the research team, told a news conference.

“It is an enabling piece of knowledge which in the future will suggest different ways of tackling cancer.”

The results of the research, reported in the journal Science, came as a surprise because scientists did not suspect that the “abort” program that destroys tumors would operate on the cell surface.

“It took some time even for me to believe the results because it was so unexpected,” said Dr. Anne‑Odile Hueber, the lead author of the study.

“We have now found that the suicide program activated by the growth promoting genes is routed out of the cell and then back through its surface,” Evan added.

Cancer tumors develop when the control signals in a normal cell go wrong causing an abnormal cell which replicates uncontrollably. Defective cells lose their ability to recognize signals that tell it to commit suicide in a process called apoptosis.

Scientists knew that cell growth and apoptosis, which prevents mutated cells from taking over the body, were triggered by the same process.

“However, in cancer, the suicide program becomes blocked in some way — for example — by signals from other cells that suppress cell death or through mutations that inactivate the mechanism that implements cell suicide,” Evan said.

The finding could have far‑reaching implications.

Scientists predict that one in three people will be affected by cancer at some stage in their lives. Although there are over 200 types of cancer, all of them start in the same way — when the control signals malfunctions.

Evan’s team showed that the oncogene (cancer causing gene) called c‑Myc works with the molecules CD95 and CD95L to cause apoptosis. It travels to the cell surface where it interacts with the molecules to generate the killing signal.

In cancer cells they believe something goes wrong with the wiring between the gene and the molecules that prevents apoptosis. The finding could help scientists to find ways of identifying the breakage and trying to repair it.

The molecules in apoptosis are also the same ones used by the immune system to kill cells infected by viruses.

Apart from surgery to remove the tumor, radiation and chemotherapy — using toxic chemicals to kill the cancerous cells — are the chief methods of fighting the disease.

Both treatments can harm healthy cells and result in uncomfortable or serious side effects. Secondary tumors can also build up a resistance to the drugs.

The discovery will allow drug companies to develop more advanced cancer treatments that could control the life and death of a tumor by manipulating the on/off switch on the cell surface.

Evan hopes it will help to make cancer a “controllable and confinable disease” and not a death sentence.

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Molecules Offer New Approach to Cancer (980216)

PHILADELPHIA — A chemistry professor who has “a vendetta against cancer” said Saturday he may have invented a new molecule to fight the disease.

Jonathan Sessler, a chemistry professor at the University of Texas at Austin, said his Texas-size molecules, or texaphryns, might offer a more effective approach to cancer therapy.

“It began 20 years ago when I myself was diagnosed with a cancer,” Sessler told a news conference at annual meeting of the American Association for the Advancement of Science.

He was diagnosed with Hodgkins disease, a cancer of the lymphatic system. Then a PhD student in chemistry at California’s Stanford University, he was being treated by a local oncologist, Dr Richard Miller.

“He said, ‘you’re a chemist — you should be able to find a better cancer agent,”‘ Sessler said. So he did.

“Obviously I have a vendetta against cancer. ... If and when I got my own chemistry set, that is what I was going to do.”

He worked with porphyrins, molecules that include the hemes (haems) that put the color into hemoglobin in blood. Normal porphyrins have four nitrogen atoms making up the molecule — his have five.

By nature such molecules attach easily to metal atoms. The iron in the heme porphyrin is what makes blood look red.

But they are limited in size, and cannot hook up with larger metal atoms that might work in medical therapy. Sessler thought his larger molecules might work better.

Sessler has dubbed his extra-large porphyrins texaphryns — short for Texas-size porphyrins. He and Miller have set up a company, Pharmacyclics Ltd, to exploit and develop any drugs that come from their work.

“I don’t know of any other story where a cancer patient and his doctor team up to fight cancer like this,” Sessler said.

They have combined their texaphryns with two different metals, gadolinium and lutetium. These metals are too big to fit into normal porphyrins, but can attach to the texaphryns.

Gadolinium captures X-rays and helps make magnetic resonance imaging (MRI) work better, while lutetium captures light.

The texaphryns also home in on rapidly reproducing cells such as tumor cells. “The texaphryns localize very effectively to cancer cells,” Sessler said.

His idea has been to use them for light-activated tumor therapy — an established approach that uses laser or red LED (light-emitting diode) light to activate a drug at a specific site, such as a tumor. He also hopes they can help radiotherapy work more effectively.

The idea is to kill tumor cells without causing the toxic side-effects of chemotherapy and X-ray therapy that affect the entire body — including hair loss, nausea and immune system suppression.

They have brought two of their texaphryns to clinical trials. So far, the 20 or so brain tumor patients they have worked on in live on average a year, as compared to the norm of four months.

Sessler showed scans of one brain tumor that disappeared entirely.

“This is moderate progress — anecdotal and interesting ... but not statistically significant,” Sessler said. The team is conducting Phase II clinical trials, which test for safety and efficacy.

The National Cancer Institute is also interested and is helping fund the work.

Sessler admits he does not know how the texaphryns work, if they do work. When activated by light or X-rays they might release charged molecules that destroy cells.

X-rays work in part by creating hydroxy radicals, or free radicals that damage cells. The same mechanism might be at work in the texaphryn technology.

American Cancer Society researchers said this week they expect 1.2 million Americans to be diagnosed with invasive cancer, and more than 500,000 to die of it.

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Childhood Nutrition Affects Cancer Risk (980213)

NEW YORK — A new study suggests that children who overeat have a higher risk of developing certain cancers in adulthood.

Dr. Stephen Frankel and colleagues at the University of Bristol, England, report in the British Medical Journal for February 14th that they have found “a positive association between energy intake during early life and later mortality from cancers other than those related to smoking.”

Frankel’s team followed up on 3,834 people who had been part of a nutrition study in 1937 to 1939, when they were age 16 or younger. In that earlier study, families took painstaking measures to record their typical dietary intake over the course of one week. They inventoried and weighed the food they had on hand at the beginning and end of the week, recorded all their food purchases, and recorded any meals they ate while away from home.

Using a national database of health information, the British researchers determined which of the children who participated in that study had developed cancer as adults. They found that “higher levels of energy intake in childhood increase the risk of the later development of cancer,” not including cancers related to smoking — these include cancer of the mouth, pharynx, esophagus, pancreas, respiratory tract, and urinary tract.

For each increase of 1 MJ (about 250 calories) in a child’s typical daily diet, there is a 20% increased risk of death from certain cancers, the researchers calculated.

Frankel and his colleagues conclude that their findings “confirm the importance of optimal nutrition in childhood and suggest that the unfavourable trends seen in the incidence of some cancers may have their origins in early life.”

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Fall in lung cancer rate poses smoking puzzle (980217)

Asthma group urges cigarette clampdown

CASES of lung cancer have fallen considerably faster than can be explained by the decrease in smoking, particularly among young men, according to new research.

Over a 30-year period the incidence of lung cancer fell annually by 2 to 3 per cent more than was expected from the fall in tobacco consumption, the research shows.

But a separate study yesterday brought bad news about smoking among adolescents: even if 12 to 17-year-olds have no intention of taking up smoking, tobacco advertising and promotional items may lead a third of them to try.

The research into British lung cancer, published today in the Journal of Epidemiology and Community Health, compared rates of lung cancer from 1955 to 1985 with smoking data from Cambridge University’s 1984-85 health and lifestyle study and a record of cancer inpatients in 60 hospitals.

In men, the lung cancer rate fell faster than predicted in those under 44. Among women, the rate was as expected in younger and older age groups but lower for those aged between 35 and 44.

The study took into account all aspects of cigarette smoking, such as age, tar content of cigarettes and daily consumption. It was compiled for the tobacco company Philip Morris by Peter Lee, who runs a statistics and computing firm at Sutton, South London. “We can see nothing in our analysis that explains this,” Mr Lee said.

The survey of adolescent smokers, conducted by the University of California in San Diego, began in 1993 with 1,752 boys and girls between 12 and 17 who had never smoked and said they would not start even if a friend offered them a cigarette.

Three years later, the 56 per cent who had had a favourite cigarette advertisement in 1993 were twice as likely to have started smoking or be willing to start as those who did not have a favourite cigarette advert. The 5 per cent who owned a promotional item supplied by a tobacco company were nearly three times as likely to have begun smoking than those unwilling to use such a promotional item.

“This study provides clear evidence that tobacco industry advertising and promotional activities can influence nonsusceptible ‘never-smokers’ to start the process of becoming addicted to cigarettes,” the researchers report in the Journal of the American Medical Association. “Our data established that the influence of tobacco promotional activities was present before adolescents showed any susceptibility to become smokers ... Exposure to other smokers does not appear to significantly influence which adolescents begin the smoking uptake process.”

Nearly half of the group had become susceptible to smoking - that is, were no longer adamant that they would not smoke - by 1996.

Three quarters of children between 11 and 15 think the legal age for buying cigarettes should be raised from 16 to 18, according to a poll by Respect, the anti-smoking campaign which is funded by the Health Department.

Asthma group urges cigarette clampdown

Asthma campaigners will today press the Government to outlaw smoking in public places, including parks and shopping centres, to prevent thousands of tobacco-related hospital admissions each year. The National Asthma Campaign says that nearly 50 children a day are admitted to hospital because of passive smoking, which had a unique effect on asthmatics: “It takes a long time for the effects of cigarette smoke to show up in people with conditions like lung cancer, but, for people with asthma, the effect is immediate,” a spokeswoman said.

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Doctors Aim at Cancer With Magic Bullet (971030)

LONDON — Scientists are close to testing a genetically engineered “magic bullet” that could treat half of the most common cancers, New Scientist magazine said Wednesday.

Clinical trials with colon cancer sufferers could begin within the next 15 months.

Earlier attempts at the approach failed because although the antibodies on the bullets found the cancerous cells they could not penetrate and destroy them without harming healthy cells as well.

MTR developed fusion proteins that isolate the dangerous cells and inject them with a bacterial toxin while leaving healthy cells alone.

One half of the re-engineered protein binds to the receptor on adenocarcinoma cells and the second half fires a fatal dose of the toxin that kills them by preventing them from making proteins.

“The Israelis modified the natural toxin so that immune cells previously exposed to the bacteria would not recognize and attack it,” the magazine explained.

Seragen, a Massachusetts-based company, is using a similar approach against a rare form of leukemia called cutaneous T cell lymphoma.

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Eat Your Carrots — Vitamin A May Kill Cancer Cells (980414)

WASHINGTON — A common derivative of vitamin A, retinoic acid, may block cancer in the body, researchers said on Monday.

The study, published in the American Association for Cancer Research’s journal Cancer Research, adds to a growing body of evidence that vitamin A can help kill off cancer cells.

“This is one more reason to listen to your mother and eat your vegetables,” Andrew Yen, a cancer biologist at New York’s Cornell University, said in a statement.

The body makes retinoic acid from vitamin A, which comes from the yellow or orange compounds known as carotenes found in vegetables ranging from carrots to squash.

Yen’s group, working on cells in test tubes and not in living animals, showed that retinoic acid could stop the out-of-control cell growth that marks cancer.

“Now we need a deeper understanding of how retinoic acid causes these changes,” he said.

“In the meantime, I think we’re adding evidence that an adequate supply of carotene in the diet is obviously beneficial for anyone who wishes to stay healthy and avoid cancer.”

Last June, researchers at the National Heart, Lung and Blood Institute at the National Institutes of Health said they found retinoic acid can reverse the effects of emphysema in laboratory rats.

Retinoic acid is currently used to treat acne but has shown promise against cancer before.

Last August a team at the University of Texas in Houston reported finding strong evidence that a synthetic version of vitamin A can fight cancer by making tumor cells self destruct.

They said a retinoid known as 4HPR could cause cancer cells to commit “suicide,” a natural process known as apoptosis.

Most cells usually die automatically when they are damaged or just too old. But in cancer this process, known as apoptosis, fails. The result is uncontrolled cell growth and a tumor.

Various studies have shown that retinoids can destroy cancer cells including leukoplakia, a type of tongue cancer, and cancers of the head, neck, lung and liver.

Retinoids have also been tried against cervical cancer in a combination with interferon, a natural immune system chemical.

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Childhood Nutrition Affects Cancer Risk (980213)

NEW YORK — A new study suggests that children who overeat have a higher risk of developing certain cancers in adulthood.

For each increase of 1 MJ (about 250 calories) in a child’s typical daily diet, there is a 20% increased risk of death from certain cancers, the researchers calculated.

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Scientists Excited About Cancer Drugs (980504)

NEW YORK — Government scientists are excited about progress with tests on two cancer drugs that are eradicating any type of cancer in mice, The New York Times reported Sunday.

The drugs, known as angiostatin and endostatin, have been made a top priority at the National Cancer Institute, the newspaper quoted the agency’s director, Dr. Richard Klausner, as saying.

“I am putting nothing on higher priority than getting this into clinical trials,” Klausner told the newspaper, adding that they were “the single most exciting thing on the horizon” for cancer treatment.

But Klausner and other experts stressed that the drugs had only been tested in mice — and in mice specially bred to develop cancer. Many drugs that work in such mice do not work in the same way in humans.

“If you have cancer and you are a mouse, we can take care of you,” Dr. Judah Folkman at Children’s Hospital in Boston, who discovered the drugs, told the newspaper.

Angiostatin stops the development of blood vessels that tumors need to grow. Endostatin comes from a piece of a protein and seems to be produced by tumors to stop other tumors from developing in the body. It explains why some people become literally ridden with cancer after a tumor is removed — once the big tumor is gone, there is nothing to stop other tumors from growing.

Together, the drugs seem to stop tumor growth completely.

Several companies are also working to develop the drugs, and both have been reported about extensively, but Klausner said most people did not know that clinical trials in humans were only about a year away.

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Cancer survivors’ quality of life varies (980512)

NEW YORK — How well a cancer survivor copes with the long-term aftermath of their ordeal often depends on their type of cancer, treatments received and personal attitude, researchers say.

“Quality of life reported by survivors varies a great deal,” say researchers reporting in the current issue of the Journal of the National Cancer Institute. They believe that “the amount of (survivor) dysfunction varies according to site of disease and treatment.”

Researchers Drs. Carolyn Cook Gotay and Miles Muraoka of the Cancer Research Center of Hawaii at the University of Hawaii in Honolulu conducted a broad review of 34 studies published between 1980-1998. Each of the studies focused on quality of life issues of long-term (5 years or more after diagnosis) cancer survivors.

They found that “considerable numbers of survivors continue to experience negative impacts of cancer and/or treatment on their daily lives.”

They say the level of psychological, physical, and sexual dysfunction experienced by survivors often depends on the physical aftermath of particular cancer treatments.

For example, they point out that “as arduous as bone marrow transplantation is at the time it is performed, the treatment does not pose visible everyday disabilities” over the long-term. In fact, one 1995 study found that 88% of bone marrow transplant recipients “reported that the benefits of their transplant outweighed negative side effects and... 80% rated their current quality of life and physical health status as good to excellent.”

However, the report authors say long-term quality of life can be severely compromised by treatments that leave survivors disabled or visibly maimed. For example, survivors of esophageal cancer often “must live daily with a modified pattern of eating,” the authors say, while “a breast cancer patient is confronted with a changed body as she dresses herself each day.”

Long-term survivors of Hodgkin’s disease (cancer of the lymph nodes), breast, testicular, and other cancers were especially concerned with post-therapy declines in either sexual performance or desire. A third of breast cancer survivors “reported a decrease in sexual desire and/or dissatisfaction with their sex lives,” the researchers report, while sexual dysfunction affected 40% of survivors of testicular cancer.

The report also found that psychological problems centered around fears of cancer recurrence, or general increases in depression or anxiety, affected long-term survivors of a variety of cancers.

Still, the authors were greatly impressed by the large numbers of men and women who felt their lives had actually been somehow enhanced by their cancer ordeal. For example, one study found that 93% of malignant melanoma survivors regarded the changes in their quality of life as positive, declaring “changes in self-awareness, with a re-ordering of priorities, and a sense of living for today.”

Gotay and Muraoka believe these testimonials remind us that “human beings have an amazing capacity to meet and adapt to challenges they face, and cancer survivorship exemplifies the strength of the body and spirit.”

SOURCE: Journal of the National Cancer Institute (1998;90:656-667)

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U.S. cancer meeting to highlight new advances (980515)

LOS ANGELES, May 14 — The world’s largest cancer conference starts this weekend with close to 20,000 doctors discussing breakthroughs they hope will lead to a cure for the killer disease.

Cancer treatments have made big news recently as a new drugs and vaccines have offered new hope doctors may be close to curing the disease second only to heart attacks as a cause of death in the United States.

The American Society of Clinical Oncology (ASCO) expects doctors from all over the world to attend its 34th annual meeting in Los Angeles where 2,000 presentations are planned over the four days starting from Saturday through Tuesday.

Topics expected to take center stage include potential new treatments for the prevention of breast and prostate cancer. About 180,000 cases of breast cancer are diagnosed annually, according to ASCO.

New approaches to treating cancer will be discussed including widely publicized anti-angiogenesis drugs, which kill tumors by depriving them of blood supply, as well as using monoclonal antibodies to enable the body’s immune system to attack cancer cells.

The Los Angeles meeting will also discuss doctors’ views on the controversial issue of physician-aided suicide.

Results from human trials of new cancer drugs seeking regulatory approval will be presented at the conference including data on lung cancer and colorectal cancer.

About half of those diagnosed with cancer do not survive. In 1998 about 1.2 million patients in the United States are expected to be diagnosed with cancer with about 565,000 people expected to die of the disease this year, ASCO said.

The most prevalent form of cancer in women is breast cancer with about 44,000 deaths per year in the United States. Results will be presented on the potential prevention of breast cancer through the use of the drugs raloxifene and tamoxifen.

Tamoxifen, marketed by Zeneca Group Plc as Nolvadex, is already widely used in early and late-stage breast cancer and is seeking approval to be used as a preventive drug.

Trials in the United States of tamoxifen as a drug to prevent breast cancer were called off early when successful results were reported.

Results of that trial will be discussed in detail at the meeting as will a two-year trial of raloxifene.

Raloxifene is marketed by Eli Lilly & Co. as Evista to treat osteoporosis. Data will be produced on the drugs’ potential for preventing breast cancer in post-menopausal women.

In recent weeks anti-angiogenesis drugs have been hailed in some quarters as a potential “miracle cure” for cancer.

The drugs, which kill cancer by starving tumors of their blood supply, have been a talking point since it was revealed that EntreMed Inc.’s drugs, angiostatin and endostatin, had cured cancer in mice.

Since then a number of other companies have announced similar drugs that have cured cancer in mice. Many experts have played down this potential cure by noting the drugs have been known for years and it is much more difficult to cure cancer in humans than mice.

In order to grow larger than a pinpoint, tumors need to form new blood vessels. At ASCO’s meeting presentations will be made showing encouraging early results on the safety of anti-angiogenesis drugs on human patients.

Data on new vaccines that fight cancer by stimulating the immune system will be publicized as well as new information on gene therapy, which tries to fix damaged DNA or add new DNA in an attempt to mend faulty genes.

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Scientists Excited About Cancer Drugs (980503)

NEW YORK — Government scientists are excited about progress with tests on two cancer drugs that are eradicating any type of cancer in mice, The New York Times reported Sunday.

The drugs, known as angiostatin and endostatin, have been made a top priority at the National Cancer Institute, the newspaper quoted the agency’s director, Dr. Richard Klausner, as saying.

“If you have cancer and you are a mouse, we can take care of you,” Dr. Judah Folkman at Children’s Hospital in Boston, who discovered the drugs, told the newspaper.

Together, the drugs seem to stop tumor growth completely.

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Hormone Tests Stumble Upon Gender Distinctions (980513)

WASHINGTON — A new finding about how the body reacts to “male” and “female” hormones may offer a better treatment for prostate cancer, researchers reported on Tuesday.

Researchers said they found hormone regulators that previously were thought to respond only to male hormones also responded to the “female” hormone estrogen.

They said their findings could open better ways to treat prostate cancer, and could explain some of the processes behind male development in the womb.

It also serves to further blur the gender distinctions between so‑called “male” hormones such as testosterone, and “female” hormones such as estrogen. In fact, all hormones are found in both sexes, only in differing amounts.

Researchers have known that the male hormone testosterone activates the androgen receptor, which controls the “expression’ or activation of a male hormone gene.

The androgen receptor is also important in the development of the male reproductive system.

Writing in the Proceedings of the National Academy of Sciences, Chawnshang Chang and colleagues at the University of Rochester said they found in tests that both natural estrogen and testosterone acted on this receptor.

They found the receptor reacted to estrogen when a certain co‑activator was also added. This co‑activator worked with natural estrogen but not with synthetic estrogen.

They said their findings may explain why synthetic estrogens work better to suppress prostate cancer, which has hormonal causes, than natural estrogens.

They also noted that there was some evidence that estrogen could in some way be responsible for the abnormal growth of prostate cells in prostate cancer.

The findings could open better ways to treat prostate cancer, the Rochester researchers said.

“Even after several decades, surgical or medical castration, combined with the administration of anti‑androgens, remains as the major treatment for disseminated prostate cancer,” they wrote.

But estrogens were sometimes used instead to suppress the effects of male hormones, and were cheaper. The finding that natural estrogen works differently from synthetic estrogen could be an important point.

“Further studies of this (estrogen to androgen receptor) pathway may therefore allow us to develop new hormonal therapies for the treatment of prostate cancer and other androgen‑related disorders,” they concluded.

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Doctors alarmed to find smoking may stop breast cancer (980521)

WASHINGTON, May 19 — Smoking, a major cause of lung cancer and heart disease, may help reduce the chance of breast cancer in women who have rare genes that put them at risk of the disease, researchers said on Tuesday.

The finding both surprised and dismayed the international team of scientists who did the study, but they said it may shed light on some of the mechanisms behind breast cancer.

“We would hate it if women started smoking because of this study,” Dr. Paul Kleiheus of the World Health Organization, which helped sponsor the study, said in a telephone interview.

The study found that smoking reduces by 50 percent the risk of developing breast cancer in women who have a genetic mutation that can lead to to the disease. The mutation, in the genes BRCA1 and BRCA2, affects on average one in 250 women.

Kleiheus, who directs WHO’s International Agency for Research on Cancer, and colleagues were checking for a variety of lifestyle factors that could affect women with the mutation. It is known that just having a “bad” gene does not guarantee disease — outside factors count, too.

So they were looking for which factors these might be, and surveyed more than 300 women in the United States and Canada who had BRCA1 or BRCA2 mutations. Half, 186 of them, had developed cancer and half had not.

They asked them about various factors, such as when they had children, what they ate — and whether they smoked.

The first thing that jumped out at the researchers was the clear link to smoking. “It was a surprise that smoking was the most striking result,” Kleiheus said.

“We are a little bit embarrassed,” said Gilbert Lenoir, a biologist at the IARC who also worked on the study, which was published in the Journal of the National Cancer Institute. “We are embarrassed because we feel that the tobacco industry may propagate this without being responsible.”

The researchers point out that many more women in industrialized countries such as the United States die from lung cancer than die from breast cancer.

The American Cancer Society predicts 80,000 women will develop lung cancer this year and 67,000 women will die from it, as compared to 43,500 deaths from breast cancer. And more women die of heart disease than of any kind of cancer.

“I think it wouldn’t be a good idea to take up the habit,” Kleiheus said. “But on the other hand it is important for us, for the scientific community, and for the families that we have some hope for new research to try to come to some preventative measure.”

The researchers think there is probably a clear mechanism for explaining why smoking has this effect, and they hope that drugs can emulate the effect.

“The best scenario would be that this study would lead to the development of drugs that do the same thing without all the bad side-effects of smoking,” said Dr. Michael Thun of the American Cancer Society.

Kleiheus believed something in tobacco smoke slows down the breakdown of the female hormone estrogen in the body. Breast cancer is known to be linked to estrogen.

He said perhaps drugs that interfere with estrogen could be developed to prevent breast cancer.

In fact, they have. Researchers this week said two drugs, the established cancer drug Tamoxifen and the osteoporosis drug raloxifene, sold as Evista, can prevent breast cancer in women. Both interfere with the way estrogen is used by the body.

Kleiheus and Thun said the drugs needed to be tested on women who carry the BRCA1 and BRCA2 genes to see if the protective effects extend to them.

“Women who have a very strong family history of breast cancer or who know that they carry one of these high-risk genes are in an extremely difficult position because they really don’t have any clear guidance on what they should do about it,” Thun said.

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A Wave of Cancer Advances Boosts Researchers (980521)

LOS ANGELES — With good reason, cancer docs are the greatest skeptics in the conservative art of healing. Yet even these cautious souls stretch for superlatives when describing the changes sweeping over them.

Their big annual meeting, which concluded Tuesday, is ordinarily a rather gloomy affair. Advances, when they happen at all, inch forward glacially. Much of what looks promising in test tubes and lab mice turns out to be a bust when tried on sick people.

“We see this stuff go by, year after year, and nothing works,” says Dr. Craig Henderson of the University of California, San Francisco. “If you are a practicing doctor, you have to be skeptical. All of a sudden, we are entering a new era.”

The new era is one of exquisitely targeted therapy. The blunderbuss approach of chemotherapy — poisons that kill good cells and bad ones alike, often with frightful side effects — will be augmented or even replaced by chemicals that zero in on malignant cells and leave healthy ones alone.

“This is the beginning of a large tidal wave,” says Dr. Laura Hutchins of the Arkansas Cancer Research Center in Little Rock, Ark.

Traditionally, scientists have tackled cancer by screening thousands of compounds in the lab, hoping to stumble over one that kills tumors more efficiently than it kills normal growth. Researchers often test medicines with little real understanding of how they do whatever they do.

The new approach comes from the opposite direction: Understand what’s wrong inside the cancerous cell, then design a medicine that corrects just that.

“Throwing bigger bombs at the disease wasn’t going to get us a lot further,” says Dr. Dennis Slamon of the University of California, Los Angeles. “If we show what’s broken and target it, we may be able to develop more effective and less toxic therapies.”

The fundamental difference between cancerous and normal cells lies in the genes. Genetic errors, accumulated over a lifetime, turn good cells into bad ones that escape the normal cycle of life and death.

At this week’s meeting of the American Society for Clinical Oncology, Slamon and scientists from the biotech firm Genentech showed how understanding these genetic miscues can pay off with a unique new therapy.

Slamon laid the foundation with basic research that showed how some particularly aggressive forms of breast cancer escape the body’s usual controls: The cancerous cells’ genetic mistake makes them overreact to growth-stimulating hormones. Knowing this, Genentech set about crafting a solution — and cloned an antibody, named Herceptin, that blocks the cancerous cell’s ability to receive the growth hormone.

Results released at the meeting show the approach works. While no magic bullet, it significantly increases the effects of traditional chemotherapy in terminally ill cancer patients and may be even more impressive when given earlier in the disease.

Yet perhaps more important even than developing a new cancer drug is what the process shows about science’s potential ability to control cancer by going to its genetic core.

“This is not like anything we have ever seen before,” says Dr. Larry Norton of Memorial Sloan-Kettering Cancer Center in New York City. “This opens up a whole new chapter in the development of anti-cancer therapy.”

Most other therapies designed to exploit cancer’s unique vulnerabilities are less far along than Herceptin, which Genentech hopes to have on the market in the fall.

Another idea is to use drugs to thwart the tumor’s ability to connect with the blood supply of surrounding healthy tissue. In theory, a cancer starved of blood will not grow and spread.

News reports two weeks ago about two possible drugs to do this, called angiostatin and endostatin, stirred an enthusiastic buzz about a cancer cure. But that’s highly unlikely, say many at the cancer conference, considering how complicated and resistant to attack human tumors are.

Among the 1,000 presentations at this week’s meeting were dozens aimed at precisely targeting malignancy. Among the examples:

—Doctors have hooked radioactive iodine onto antibodies designed to seek cancer cells in people with follicular lymphoma, an incurable form of blood cancer. Two-thirds of the 32 patients treated at the University of Michigan are free of all signs of the disease after six to 18 months. It’s too soon to know if the cancer will come back.

—At Baylor College of Medicine in Texas, researchers inserted a herpes gene into a cold virus, then injected the virus into men’s cancerous prostate glands. The virus infects the cancer cells and carries in the herpes gene. This allowed the tumor to be killed with a standard herpes drug. While this can be done safely, it’s too soon to know if it will wipe out the cancer completely

—Scientists at Memorial Sloan-Kettering are among many teams trying to create vaccines that stimulate the body to kill cancer by recognizing it as foreign. They are in early human testing of one that triggers a reaction against cells containing a protein necessary for the production of melanin, the skin pigment abundant in melanoma skin cancer.

“There is a coming together of focus,” says Dr. Derek Raghavan of the University of Southern California. “Science has actually made some real progress in the past 12 months.”

Some of the good news involves preventive measures rather than potential treatments for existing cancers. One study offers the first tentative evidence that checking blood with the PSA test, which stands for prostate specific antigen and is now a standard part of checkups for men over 50, saves lives by spotting prostate cancer early. Another suggests that the brittle-bone drug raloxifene may reduce the risk of breast cancer by two-thirds in older women.

Even the most optimistic projections, however, stop short of hinting at any across-the-board cure. It’s more likely, doctors say, that these approaches will make cancer a more manageable disease, like diabetes or high blood pressure.

“We won’t wake up one day with a cure for cancer,” Henderson says. “But if we can make you live 20 years with your disease, and you die of something else, what’s wrong with that?”

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Researchers report decline in prostate cancer deaths (980602)

SAN DIEGO (AP) — A blood test that detects prostate cancer early appears to be saving lives, according to studies released Monday.

The test looks for elevated levels of prostate-specific antigen, or PSA.

“Each year, we’re probably going to see the death rate fall” as the test becomes more widely accepted, said William Cantalona, a doctor at the Washington University School of Medicine.

One indicator of prostate cancer is an elevated PSA level. By the time other symptoms are evident, the cancer may already have spread, Cantalona said during a panel discussion at the American Urological Association’s annual meeting.

PSA, a protein, helps transform a gel-like substance in the prostate gland to a liquid that can transport sperm during ejaculation. In a diseased or enlarged prostate, a walnut-size gland located under the bladder, PSA seeps into the blood at higher levels, giving higher readings during testing.

A study by The Mayo Clinic reviewed 687 cases of known prostate cancer in Olmsted County, Minn., from 1983 to 1995. Researchers discovered the number of prostate cancer deaths consistently decreased from 1988 to 1995 when PSA screening was more widely used.

A University of Utah Medical Center study looked at more than 250,000 cases of prostate cancer from 1973 to 1994. On average, cancer was detected three years earlier in men and in less advanced stages when the test was administered. Researchers said future mortality rates must be looked at before concluding whether the test was responsible.

Some epidemiologists say the screening is expensive and not always accurate. They contend older men often die from other diseases before the slow-growing tumors kill them. Side-effects from radiation or surgery to remove the gland also can leave men impotent and unable to control their bladder.

Proponents of the test say the benefits far outweigh the risks.

PSA testing is likely to become routine over the next five years, Cantalona said, possibly reducing the death rate from prostate cancer by 30 percent to 40 percent.

Prostate cancer is the most commonly diagnosed cancer among U.S. men and the second deadliest, behind lung cancer. The American Cancer Society estimates that 184,500 U.S. men will be diagnosed with the disease this year; 39,200 will die.

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Basic discoveries into genetic roots of cancer begin to pay off (980627)

CAMBRIDGE, Mass. (AP) — Twenty years of research into the origins of malignancy jell into one profound insight: Cancer is a disease of genes gone bad.

Already, this idea has revolutionized the way scientists look at cancer, and it seems certain to change the way doctors treat it, too. Indeed, many believe medicine is on the brink of an entirely new approach to controlling this most feared of diseases, one that targets the genetic flubs at the heart of cancer and reverses them.

In hindsight, the biggest cancer news of modern times is so very simple. All tumors spring from typos in the assembly plans for proteins that tell cells when to grow and when to die.

Like many big ideas, the discovery of cancer’s roots dawned gradually. One experiment at a time, seemingly irrelevant bits of scientific fact mass into a new way of thinking.

Among these was an almost-forgotten experiment at Massachusetts Institute of Technology in 1981. A team led by molecular biologist Robert Weinberg explored whether some genetic element inside tumor cells could transform normal ones into cancer.

One day the scientists pulled the DNA out of a kind of rat cancer called a neuroblastoma and put the genes into mouse cells. Soon healthy cells became cancerous.

The seed turned out to be a flawed bit of genetic code, one of the first discoveries in a new class known as oncogenes. The scientists called it “neu” and moved on. They had no idea what they found would ever be relevant in treating breast cancer, a disease that kills 43,500 women yearly.

Yet in the completely unpredictable way basic discoveries morph into truly useful information, Weinberg’s rat gene became key. It is at the heart of the first effective human cancer treatment based on exploiting the genetic differences between cancer cells and healthy ones.

Herceptin, the medicine that grew out of that MIT experiment, is moving toward U.S. Food and Drug Administration approval for breast cancer and could be on the market this fall.

“The translation of this basic research into the clinic is just beginning,” says Weinberg, now a researcher at the Whitehead Institute for Biomedical Research in Cambridge. “We are seeing the harbinger of what is going to happen in the next decade of the new century.”

If treatments work as well as many believe they can, they will destroy malignant cells but leave healthy ones alone, sparing patients the frightful side effects of standard cancer therapy.

“Everyone in the field is excited because this black box called cancer is not such a mystery anymore,” says Dr. Bert Vogelstein of Johns Hopkins University, another of the field’s early explorers. “Once you understand something, medical history shows it’s only a matter of time before you can exploit that and do something about it.”

That matter of time, though, can be considerable. Several years passed after Weinberg’s discovery before other scientists found a human counterpart of neu, a gene they called HER-2/neu. The gene produces a protein on the surface of cells that serves as a receiving point for growth-stimulating hormones.

Dr. Dennis Slamon’s team at the University of California, Los Angeles, found that about 30 percent of women with breast cancer have many extra copies of this gene. The result: Their breast cells reproduce out of control and spread through their bodies.

Scientists reasoned that they might reduce HER-2/neu’s impact by somehow blocking the extra hormone docking points created by the gene. At Genentech Inc., they cloned antibodies designed to do this. One turned out to be Herceptin, which eventually proved able to shrink and sometimes even eliminate widely spread breast cancer.

The National Cancer Institute estimates that at least 10 to 20 drugs now in human testing are designed, like Herceptin, to stop cancer by fixing in bad genes.

What’s broken in cancer are the genes that rule the cell’s life cycle. Each gene contains the building plan for a protein, including ones that trigger the cell to divide and eventually to die in an orderly way.

When one of these normal genes develops a disastrous glitch, it’s called an oncogene. An oncogene may stay turned on, constantly pouring out growth-promoting protein that ordinarily occurs only in brief bursts. Or it may produce a protein that is overly powerful.

When all goes well, another class of genes, called tumor suppressor genes, detects these mistakes and orders the cell to either fix the foul-up or die. When the suppressor gene itself is broken, however, cancer moves another step closer.

Generally it takes several different genetic flaws, accumulated over a lifetime, to finally tip a cell into uncontrolled growth. Even when that happens, however, another decade or two may pass before it grows into a tumor large enough to be noticed.

Dr. Stephen Friend of Fred Hutchinson Cancer Research Center in Seattle, a co-discoverer of tumor suppressor genes, notes that only this year have researchers begun to feel confident about the potential of genetic approaches to cancer.

“You can bet we will have a significant effect on curing cancer,” he predicts. “It’s now no longer a question. It’s just which approach will prove out.”

Many experts doubt that any of the drugs now in human testing will be a slam-dunk cure for cancer — or for any of the 100-plus individual diseases that are called cancer. Like Herceptin, which adds three months to the lives of terminally ill breast cancer patients, these medicines may help some people some times, but they are likely to be used mostly in combination with standard chemotherapy, radiation and surgery.

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Molecule Seeks Out and Destroys Cancer Cells, Scientists Say (Foxnews, 011002)

WASHINGTON — Scientists have developed a molecule that appears to make cancer its own worst enemy.

In laboratory tests on mice, the molecule — called icon — killed tumors by destroying the blood vessels that feed them. It also caused the cancers to produce copies of icon, which spread through the body and attacked other cancers.

The process eliminated human melanoma and prostate cancers in the tested mice. The first trials in people are planned for next year.

Drugs that inhibit the growth of the blood vessels that feed cancer developed by researchers Alan Garen and Zhiwei Hu at Yale University, takes a different approach, attacking the cells lining the blood vessels in tumors rather than trying to prevent the growth of new blood vessels.

Their findings are reported in Tuesday’s issue of Proceedings of the National Academy of Sciences.

“We’re excited about it,” Garen said. But he cautioned, “From mice to men, that is a big jump. Until the trial is done with patients you can’t be sure.”

Dr. Albert Deisseroth of the Sidney Kimmel Cancer Center in San Diego is arranging clinical trials, which he hopes to launch next spring once approval is obtained from the Food and Drug Administration.

He also cautioned against jumping to conclusions about possible new cancer therapy. “There are differences between animals and human beings.”

But, Deisseroth added, “when studies in animals are so reproducible and encouraging ... then you feel justified to invite individuals who are not responding to other forms of therapy to participate” in trials.

The first trial will focus on people with melanoma — a type of skin cancer — that has spread throughout the body, he said.

While the animal tests have worked on prostate cancer and melanoma, in theory the therapy should work on any solid cancer, Deisseroth said.

Garen said that cells lining the blood vessels in tumors have a receptor on their surface called TF (tissue factor), which is not present on the cells lining blood vessels in other parts of the body.

His team found that a molecule circulating in the blood called fVII bonds strongly to TF.

The researchers created their new molecule by attaching an fVII molecule to a portion of a human antibody called Fc. Fc causes the breakdown of cells it binds to and activates the body’s immune system to attack those cells.

The new icon molecule was inserted in a harmless virus that was injected directly into a tumor. Once infected, the tumor cells produce more icon and secrete it into the blood, where it circulates. When it encounters a tumor, it binds to the TF in its blood vessels, destroying them.

In mice with human melanoma or prostate cancer that received the molecule, both the injected tumor and others that were not directly injected disappeared.

“The mice appeared to be free of the disease and in good health at the end of the experiments, which lasted up to 194 days,” the researchers reported.

Control mice with similar cancers that did not receive the molecule died within 63 days.

Derrick Grant, a blood-vessel expert at Thomas Jefferson University in Philadelphia, called the findings “very exciting.”

The paper “puts a new and important spin on Judah Folkmans hypotheses that destroying the tumor vasculature can stop tumor growth,” he said. Folkman, of Boston Children’s Hospital, is a pioneer in efforts to battle cancer by attacking its blood supply.

Transferring the molecule into a tumor in a virus that forces the tumor to make more of the anti-cancer molecule “is brilliant and deserves praise,” Grant said.

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