Study: Cutting fat can't stop hormone-fueled cancer

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Study: Cutting fat can't stop hormone-fueled cancer

December 16, 2006

SAN ANTONIO, Texas (AP) -- The first experiment to show that low-fat diets could help prevent a return of breast cancer now reveals, with longer follow-up, that the benefit was almost exclusively to women whose tumor growth was not driven by hormones.

That could be huge -- the new results suggest but cannot prove that these women might be able to cut their risk of dying by up to 66 percent with such diets.

"That's as great or better than any treatment intervention that we've given" for this type of cancer, which is notoriously hard to treat, said Dr. C. Kent Osborne of Baylor College of Medicine in Houston, who had no role in the study.

However, for women whose cancers are fueled by hormones -- the vast majority of breast cancer patients -- the diet change seemed to make little difference in the risk of recurrence or survival. Questions remained about whether those who did benefit truly were helped by cutting fat or by the weight loss that resulted.

"Maybe it raises as many issues as it answers," said John Milner, chief of nutrition science research for the National Cancer Institute, which paid for the first phase of the study.

Initial findings from the study were reported at a cancer conference in 2005 and will appear in this week's Journal of the National Cancer Institute. Updated results with longer follow-up on many of the original participants were presented Saturday at the San Antonio Breast Cancer Symposium.

The mixed results were a surprise because doctors had expected all women to benefit, said Dr. Rowan Chlebowski of the University of California at Los Angeles, who led the work.

Hormones might play such a strong role in some cancers that dietary changes have only weak impact on future risk, experts said.

The study involved 2,437 women with early stage breast cancer, average age 58, at 39 sites around the country. All had surgery followed by chemotherapy and five years of tamoxifen if their tumors were hormone-fueled.

At the start of the study, 29 percent of their calories came from fat -- 10 percent to 12 percent lower than the typical American diet. Doctors told 1,462 of them to continue their normal diets. The other 975 had counseling with dietitians to cut fat to around 20 percent of daily calories.

The diet group averaged 33.3 grams of fat a day compared to 51.3 grams for the others, and lost five to six pounds during the study.

Five years later, cancer had returned in 9.8 percent of the diet group and 12.4 percent of those on standard diets, which translated to a modest 24 percent lower risk for the group as a whole.

But the result barely reached statistical significance, meaning that the difference almost could have occurred by chance alone. The new results, with longer follow-up, put the difference for the overall group at 21 percent and even weaker statistically.

Researchers' ability to study the women beyond the first five years was hampered by the federal grant running out. Two charities -- the Breast Cancer Research Foundation and the American Institute for Cancer Research -- gave money so they could resume.

Ten of the original 39 study sites have provided complete information on their participants for an additional two years, and information on deaths is available for all women in the study, Chlebowski said.

The new results: 14 percent of women on low-fat diets and 17 percent of the others have had a recurrence or second cancer. About 8 percent of dieters and 10 percent of the others have died.

However, there was a huge difference in the subgroup of women whose tumors were fueled by neither estrogen nor progesterone. Only 6 percent on low-fat diets died compared with 17 percent of the others. That translated to 66 percent lower risk of death for those who trimmed fat.

Was the benefit due to weight loss, eating more fruits and vegetables or something else? Researchers do not know.

"When you change the diet, you're probably changing thousands of circulating proteins that could interact with other targets," like insulin, that might impact cancer risk in different ways depending on hormones, Chlebowski said.

"Excess calories, be they fat or otherwise, are associated with cancer risk," Milner said.

Some earlier studies did not find low-fat diets to reduce breast cancer risk. The new one's conclusion that some may benefit from substantially cutting fat "suggests that getting below a certain threshold of fat intake may be important," said Dr. JoAnn Manson, a women's health expert at Harvard-affiliated Brigham and Women's Hospital.

Chlebowski will help lead a new study in the United States and Canada that will start next year and test weight loss and increased exercise in addition to low-fat diets to try to reduce cancer risk in women whose tumors are helped to grow by estrogen.

#2

I need to grab some research that will help me further understand why the hell they can't cure cancer, what it is, etc...We've all lost family and friends to cancer man, and I know we all got to go somehow someway, but I think Cancer has run its course...

#3

'Magic bullet' drug joins fight against cancer

A "MAGIC bullet" drug that opens a new frontier in cancer treatment was launched in Britain today.

Sutent is licensed to treat two highly deadly cancers affecting the kidneys and gut.

It works in a unique way, deploying two chemical "bullets" which attack specific molecular targets.

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Although its present use is limited, in future it could be used to treat a range of different diseases. Early trial results suggest Sutent may be effective against breast, lung and pancreatic cancers.

The drug, produced by the pharmaceutical company Pfizer, is a "Mark II" version of Glivec, the first "smart" cancer drug that caused a sensation when it was launched in 2001.

Both block an enzyme called tyrosine kinase that signals cells to multiply, and in some cancers is over-active. But unlike Glivec, Sutent also has another weapon.

A second compound targets a protein that promotes the growth of blood vessels connected to the tumour. Dr Paul Nathan, consultant medical oncologist at Mount Vernon Cancer Centre in Northwood, Middlesex, said: "We have a couple of hundred new kidney cancer patients each year. I'd expect to treat about 50 with Sutent.

"This drug and others like it, we think, are a very major advance in the treatment of this disease."

It remains to be seen how willing funding authorities will be to pay for Sutent.

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New Protein Target May Advance Design Of HIV And Cancer Drugs [/color]

Science Daily ¢¢¬¢‚¬ Using small molecules containing platinum, Virginia Commonwealth University Massey Cancer Center researchers have created a process to inhibit a class of proteins important in HIV and cancer.

NaNThe findings may help researchers develop new drugs to fight HIV or cancer by selectively targeting proteins known as zinc fingers.

In the May 30 issue of the journal Chemistry & Biology, researchers reported that a zinc finger protein, known as HIV NCp7, can be inhibited when it is exposed to a platinum complex. They observed that when the HIV NCp7 protein interacts with platinum, the zinc portion of the molecule is ejected from the protein chain. This causes the protein to lose its tertiary structure or overall shape. For these molecules, shape is an important property that enables the protein to carry out certain biological functions.

The process, active site displacement, involved design of a platinum drug with higher affinity for the protein peptide backbone, thus eliminating the zinc from its active site.

In the specific case discussed in the paper, the HIV NCp7 protein is responsible for the proliferation of the HIV virus. If researchers can inhibit the action of this zinc finger protein, they can stop the spread of the virus.

"When we target specific viruses with drugs, over time patients can become resistant to treatment and the drug becomes ineffective. Therefore, novel biological processes and proteins are attractive targets for antiviral drug development," said lead author Nicholas Farrell, Ph.D., professor and chair in the Department of Chemistry at VCU and a member scientist with the VCU Massey Cancer Center.

According to Farrell, these study findings may also one day be applied to the selective targeting of zinc fingers involved in the biological processes responsible for the spread of cancer. By applying the concept to development of anticancer drugs, the researchers hope to design more specific clinical agents with reduced side effects compared to the very useful, but toxic, cisplatin and congeners.

This work was supported by a grant from the National Science Foundation and the American Cancer Society.

Researchers in the VCU departments of chemistry and biochemistry, and the VCU Institute for Structural Biology and Drug Discovery collaborated on this research. Researchers included A. I. Anzellotti, Ph.D., Q. Liu, Ph.D., M.J. Bloemink, Ph.D., and J. N. Scarsdale, Ph.D., who is also affiliated with Massey Cancer Center.

About the VCU Massey Cancer Center: The VCU Massey Cancer Center, one of 61 National Cancer Institute-designated research institutions, is VCU's focal point for basic and clinical cancer research, education, prevention and cancer health care. Since 1975, Massey has served as an internationally recognized center of excellence. Its 175 doctors and researchers are dedicated to improving the quality of human life by developing effective means to prevent, control and ultimately to cure cancer. Visit Massey online at www.massey.vcu.edu.

Note: This story has been adapted from a news release issued by Virginia Commonwealth University.

#5

Experimental cancer drug attacks tumors in novel way

LONDON (Reuters) - Scientists said on Wednesday they were developing new experimental drugs that block the blood supply to tumors in a novel way which could be effective for treating difficult types of cancer.

Unlike other drugs that starve tumors of blood by preventing the growth of blood vessels, or angiogenesis, the new treatment takes a different approach.

It increases the formation of blood vessels but they do not work well so the tumor cannot grow and survive.

"You seem to end up with more blood vessels but they are less functional," Dr Gavin Thurston, of Regeneron Pharmaceuticals in Tarrytown, New York, said in an interview.

"This approach of blocking tumor vessels is still in its early stages. There are drugs out there that are already helping patients but there is still more to be learned in this particular area. This is another step along that path," he added.

Avastin, developed by San Francisco-based Genentech and sold by Roche is a leading anti-angiogenic drug. It targets a protein called vascular endothelia growth factor (VEGF) which tells cells to grow new blood vessels.

Several other anti-VEGF drugs have been developed but they are not effective against all tumors.

In two separate reports in the science journal Nature, Thurston and his team and scientists at Genentech, led by Minhong Yan, describe how the new approach targets a different molecule called Delta-like ligand 4 (Dll4).

"Contrary to conventional wisdom, the extra blood vessels formed through the blockade of Dll4 served to choke the tumors rather than feed them," Thurston explained.

He added that having both approaches, which may be mixed and combined, could be more powerful than just one.