***CANCER NEWS THREAD***May 2009

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http://www.dailymail.co.uk/health/article-1189113/.html

Major tumour-busting 'breakthrough' in fight against breast and ovarian cancer


Last updated at 9:16 AM on 28th May 2009


Major breakthrough: New insight into a breast cancer gene could save up to 150,000 lives. The woman pictured is being screened for the killer disease

A 'major breakthrough' in the fight against breast and ovarian cancers has been made by British researchers who have unlocked the secrets of a crucial tumour-busting gene.

The critical insight into the working of the BRCA1 gene - described as breast cancer's 'Achilles heel' - has thrown open paths to new treatments.

It could save the lives of more than 150,000 women in the UK.

Defects in BRCA1 have long been known to put women at much higher risk of developing aggressive cancers.

The mutation, which is hereditary, leaves the body unable to repair broken DNA and can lead to cancer-forming cells.

But exactly how the BRCA1 functions, and why a faulty version causes cancer, has remained a mystery - until now.

Scientists at the Medical Research Council found it has a 'working' relationship with a protein called CtlP.

A defective BRCA1 gene is unable to interact with CtlP, making it unable to repair damaged DNA and ward off tumours.

Lead author Dr Kevin Hiom called the findings a 'major breakthrough'.

He said: 'If you can understand how these things work better you can find their Achilles' heel. It gives us a better chance of finding the right treatment or prevention.

'Up to now, it was unclear how this accurate mechanism for repairing DNA breaks is turned on so we are very pleased with the result.

'Now we know what's wrong we can try and find ways to put it right.'

The BRCA1 'cancer susceptibility gene' is carried by one in 800 women and increases the risk of breast and ovarian cancers by up to 85 per cent.

The three-year study at the Laboratory of Molecular Biology in Cambridge, could lead to effective treatments, potentially saving the more than 150,000 women in the UK who develop breast cancer due to the BRCA1 mutation.


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The results, published in the last issue of Nature journal, are based on a study of DNA damage and repair in chicken cells.

The researchers found that strands of DNA were regularly broken by the 'wear and tear' of natural cell division.

If the BRCA1 gene is working correctly, it works with the protein CtlP to recreate an identical 'copy' of the broken DNA strand.

But if the BRAC1 is damaged, it cannot create new DNA strands, or accurately repair them with CtlP.

Dr Hiom, who has been working on the project since 2006, said: 'If you are lacking BRAC1 you cannot repair DNA accurately.

'Our findings help us to understand how breaks in DNA strands can be repaired in a way that preserves our genetic code so that harmful mutations, which may lead to cancer, are kept to a minimum.

'By promoting the interaction of BRCA1 with CtIP it might be possible to promote the accuracy of DNA repair - even in people with a faulty gene.'

Around 11 per cent of women will get breast cancer in their lifetime. Roughly a third of these are triggered by a defective BRCA1 gene.

Ed Yong, information manager at Cancer Research UK, explained the importance of CtIP in cell repair.

He said: 'Our cells have two major ways of repairing broken DNA and this study shows that the CtIP protein is a switch that flicks between them.

'In doing so, the protein helps our cells to mend damaged DNA and fix the sorts of faults that could eventually lead to cancer.

'It's one of a number of molecular guardians that keep watch over the integrity of our genes.'

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http://www.theday.com/re.aspx?re=903ddb ... acab3cfe07

The Total Colon Cancer Diet
The highs and lows of doing it right

The Topic of Cancer- The Diet Plan

Eating for success. Let me state unequivocally that I am a very successful eater in terms of consumption, calories and weight (gain). I tried out for the Olympic eating team but was declared a professional and not allowed to compete.

Nathan’s Fourth of July Hot Dog Eating Contest in New York City…you guessed it: the little Japanese guy who always wins sends me a check each year in late June just to make sure that I’m, er, busy on the Fourth.

Both chemotherapy and radiation can affect your appetite. Before my treatments started, I received another useful pamphlet from the National Cancer Institute called: Eating Hints- for Cancer Patients Before During and After Treatment. If you remember from previous blogs, dietary side-effects may include nausea, vomiting, diarrhea, constipation, changed sense of taste and smell, weight loss or gain and loss of appetite. Generally speaking, any of the aforementioned would go a long way toward making you lose your appetite.

Having colon cancer exacerbates the normal cancer diet plan prescribed during chemo. I had to make sure I didn’t eat anything fibrous. I like veggies okay, but I’ve never been a big roughage guy. I don’t eat salad because it is roughage, I eat salad because I like salad.

I needed an expert to help me map my diet menu for success during my treatments. That’s when I met Mary Ann Nash, Nutritionist at the Community Cancer Center at Lawrence and Memorial Hospital.

Mary Ann gave me the basics: rice, noodles, pasta and cereal with less than 1 gram of fiber is okay. Stay away from whole grain breads, bran, oatmeal and seeds. Sounds good so far.

Bananas are alright, but stay away from fruit with seeds. I believe seeds would include most fruits except, well, bananas (BTW- in my Eating Hints pamphlet, on page 32, there was a recipe that sounded good: Apple Prune Sauce. With all the diarrhea and constipation threatened in the chemo pamphlet, I thought I’d pass on this treat).

Potatoes and green beans are okay but stay away from the fibrous choices. So you’re saying pretty much all veggies except potatoes ands green beans.

Then, it kind of started to improve. Lean tender cuts of meat, fish, eggs, and poultry without skin. No nuts, tough meats, legumes or fried meats. My biggest problem with the meat choices was that it was apparent I couldn’t have fried chicken … Holy Colonel Sanders, Batman!

Two questions: 1) Why is kernel spelled colonel? 2) Why would KFC sell grilled chicken? I’m sure the honorable Colonel Sanders is probably very disappointed.

You probably never thought of this, but it’s hard to avoid roughage. On the old TV show All in the Family, Archie Bunker was sick and the doctor put him on a special diet. When Edith presented Archie with a plate of salad for dinner he asked, "What is this?"

Edith answered that, per doctor’s orders, it was a healthy dinner of salad because it has plenty of roughage. Archie was very disappointed and wanted to know when he was going to get some “soft-age.” Archie, I don’t know what your ailment was, but all you needed was colon cancer and then you, too, could enjoy a delectable diet of soft-age.

Eventually, Mary Ann and I established a routine whereby I would pass her in the hallway of the Community Cancer Center while I was on my way to get my radiation treatment. Our exchanges went something like this: "Hey Mary Ann, how’s about pancakes?"

"Pancakes are great -- just be sure to use plenty of butter and maple syrup for the extra calories."

"Mary Ann - how’s about milkshakes?"

"Milkshakes are fine -- and you should try McDonald’s shakes as they are actually made with a malt base and tend to be higher in protein."

This lady knows her milkshakes!

"Mary Ann - how’s about glazed donuts?"

"Yep, those are fine; they'll help keep your weight up."

It was at that moment that I realized that Mary Ann was one of the most beautiful women I had ever seen.

You see, this soft-age diet required that I eat no fiber AND that I keep my weight up! Hell, "up" is the only place my weight has ever been!

There were really only two tough parts to this diet, and they both had to do with liquids.

First, I was not to drink cold or hot drinks; all drinks were to be room temperature.

Nothing is better than big ole glass of lukewarm milk or tea, or soda, or water. Sorry, Mary Ann, I’ll be a star patient for the other rules, but I can’t do my liquids at body temperature. I promise I won’t tell you, so you’ll never know.

Second, no alcohol. I do appreciate a good martini before and, well, what the hell, after dinner, too. I assumed this was one of those things doctors and nutritionist tell you out of an abundance of caution. They want you not to drink because it’s just better for you than drinking -- especially when you have cancer. What would it hurt if I slipped a cocktail or two in a couple a times a week?

Then I got the answer. First of all, the chemo will make you too sick to drink. Secondly, the chemo is processed through the liver and any alcohol will interfere with the effectiveness of the chemo.

Back to earth, funny guy. Suddenly, I remembered that the diet is intended to help me fight my cancer and I should take it seriously.

Well, I guess I won’t drink to that.

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http://www.sciencedaily.com/releases/20 ... 120647.htm

The Vulnerable Cancer Cell: New Studies Reveal Broad, Hidden Network That Lets Tumors Thrive

This illustration highlights the key steps in the barcoding technique that HHMI researchers Stephen Elledge, Greg Hannon and their colleagues used to discover a number of new drug targets for cancer therapy. (Credit: Ji Luo, Elledge Laboratory, HHMI at Harvard Medical School)

ScienceDaily (May 28, 2009) — Howard Hughes Medical Institute researchers have identified many potential new drug targets for cancers long deemed “untouchable” due to the type of genetic mutation they contain. These studies are beginning to reveal new ways of attacking cancer by targeting a largely hidden network of normal genes that cancer cells rely on for survival.

Independent research teams led by Howard Hughes Medical Institute (HHMI) investigators D. Gary Gilliland of Brigham and Women’s Hospital (now senior vice president at Merck Research Laboratories) and Stephen J. Elledge at Harvard Medical School, used RNA interference (RNAi) technology to identify a host of genes that cancer cells depend on for survival. The researchers studied cells with mutations in KRAS, the most commonly mutated gene in human cancers.

KRAS, which was discovered nearly 30 years ago, is mutated in 30 percent of human tumors, including 90 percent of pancreatic cancers, 50 percent of colon cancers, and 30 percent of non-small cell lung cancers.

“Efforts to develop drugs that inhibit oncogenic RAS proteins have been largely unsuccessful, despite the fact that RAS gene family members are mutated in about 30 percent of human tumors,” said Gilliland, who directs the oncology program at Merck.

More than 18 months ago, Elledge and Gilliland decided to see if they could use the powerful RNAi technology to seek out genes that KRAS-mutant cancer cells need for survival. Their efforts, culminating in two reports in the May 29, 2009 issue of the journal Cell, have led to the identification of potentially promising drug targets: serine/threonine kinase 33 (STK33) and polo-like kinase 1 (PLK-1), as well as a host of other proteins.

“These targets represent a potential Achilles heel for tumors,” said Gilliland. “In the case of STK33, it is absolutely required for survival of cancer cells. Normal cells don’t require it.”

“The translational implications of both reports are important and immediate,” wrote Charles L. Sawyers, an HHMI investigator at Memorial Sloan-Kettering Cancer Center. Sawyers discussed the implications of the research in a preview article published in the same issue of Cell.

Sawyers points to the identification of the two kinases as validation of the approaches taken by Elledge and Gilliland. With the dramatic clinical success of cancer drugs, such as Gleevec and dasatinib, which target rogue kinases, Sawyers says any screen that turns up new kinases is worthy of further investigation.

“The new mantra, quite simply, is that cancers bearing oncogenic mutations in a kinase are dependent on that kinase for growth and survival,” writes Sawyers in Cell. “With rare exception, patients with such tumors have derived significant benefit (that is, their tumors shrink) when treated with an inhibitor of that mutant kinase. The probability of success in such patients is so high that drug discovery programs can (and should) be launched when a new kinase mutation is discovered in a subset of human cancers.”

“Hopefully drugs that target non-mutant, but synthetic lethal kinases will be similarly effective,” Sawyers added.

The concept of synthetic lethality – which is part of the intellectual framework of these two studies -- has its roots in yeast genetics. Synthetic lethality is defined as a genetic interaction where the combination of mutations in two or more genes leads to cell death. For example, two different strains of yeast may each harbor a mutation that is not lethal on its own. But when both mutations are combined in a single strain of yeast, death occurs – hence the name, synthetic lethality. “Synthetic lethality is actually co-lethality,” said Elledge.

During the last few years cancer researchers have become increasingly interested in developing synthetic lethality screens as a tool for uncovering genetic dependencies in cancer cells. The rationale behind the strategy is as follows: A mutated cancer-causing gene, or oncogene, causes a cell to grow abnormally. That abnormal growth can lead to the development of a tumor. But oncogenes do not cause cancer by themselves – they depend on the activity of other genes. These genes are considered “dependents,” in the sense that the cancer cell’s survival also depends on the activity of the oncogenes and its dependent genes. Many of these so-called dependent genes are not mutated in cancer cells, but they contribute to abnormal cell growth and cancer. By using RNAi to knock down the expression of individual genes in cells bearing mutations in an oncogene, such as KRAS, researchers can see which gene knock-downs affect cancer cells’ viability. Gene dependencies are uncovered in cancer cells that fail to thrive.

Until recently, however, researchers simply did not have the tools to undertake a large-scale, systematic analysis to uncover genetic dependencies in mammalian cells. The discovery of RNAi a little more than a decade ago is making it possible to do genetics in mammalian cells. The cellular machinery involved in RNAi first identifies short segments of suspicious-looking RNA, and then destroys all identical copies of that RNA. The result: None of the protein that the RNA encodes for gets made.

While the natural function of RNAi is to prevent viruses from replicating inside cells and to control endogenous gene expression, scientists discovered they could exploit the process to squelch individual gene products. To do so, they introduce a short segment of RNA that looks like one of the cell's normal genes. The RNA interference machinery grinds into action and shuts down production of the protein made from that gene.

Gilliland’s team, which included first authors, Claudia Scholl and Stefan Fröhling, as well as HHMI investigator Tyler Jacks at MIT, began their studies about two years ago. The team’s interest in leukemias informed their decision to focus on using short hairpin RNAs (shRNAs) -- single strands of RNA that fold back on themselves -- to selectively knock down the activity of serine/threonine kinases and tyrosine kinases. In recent years, kinase inhibitors have emerged as highly successful therapy for a subset of leukemias.

“We were looking at genes that we thought we could target easily with drugs,” Gilliland said. “We looked for genes that when knocked down would confer lethality to cells that were KRAS-mutant, but not KRAS-wild-type.” This approach is a particularly attractive concept in cancer research because normal cells don’t have the same dependencies on these genes. “If you find a vulnerability conferred by another gene, you should, in theory, have a great therapeutic window because you’re not going to affect normal cells,” he said.

Gilliland’s group began a collaboration with William C. Hahn at the RNAi Consortium at the Broad Institute to use the Broad’s automated RNAi screening technology to assess about 5,000 shRNAs targeting about 1,000 human genes in a panel of eight human cancer cell lines. The shRNAs were carried in lentiviral vectors, which the researchers used to infect four cell lines carrying KRAS mutations and four lines carrying KRAS-wild-type genes.

At the top of the “hits” identified in the screen was the serine/threonine kinase, STK33, which Gilliland describes as a “totally new gene” in cancer research circles. “There are a couple of older papers describing STK33’s genetic localization and exon structure, but otherwise nothing else is known about it.”

That’s about to change as Gilliland and his team begin to explore why STK33 represents a liability for KRAS-mutant cancer cells. Evidence presented in Cell shows that STK33 is not a part of the RAS signaling pathway, nor is it mutated in human cancer cell lines that were tested. Gilliland said his group’s experiments indicate that STK33 is involved in induction of the cell death pathway in cancer cells. “We don’t have all the answers yet, but STK33 is selectively required for the survival and proliferation of mutant KRAS-dependent cancer cells,” Gilliland said.

In the experiments reported in Cell, Elledge and his colleagues used an RNAi technique developed by Elledge and HHMI investigator Greg Hannon at Cold Spring Harbor Laboratory. “Overall, we were asking very simple questions: What do RAS cells need to survive? And is it different from what normal cells need to survive?” said Elledge.

Elledge’s team generated about 75,000 bits of short hairpin RNAs that can be inserted into retroviruses. When the altered retroviruses infected either normal cells or cells that differed by only a single mutation in KRAS, the shRNA bound to corresponding stretches of RNA in the cells, and prevented their translation into proteins.

If the shRNA knocked down production of a protein essential to keeping the cells alive, then the abundance of that particular shRNA quickly diminished as cells died. The researchers could track the identity of the shRNA – and its corresponding gene – by using a “barcoding” method to track the diverse pool of short hairpin RNAs in parallel. In the barcoding method, every short hairpin RNA that is made carries a unique genetic tag. This tag lets the researchers track the effect of thousands of the RNAs in a single pool of cells in a single lab dish. “These are experiments a single researcher can perform in their own lab without the need for complex robotic platforms,” said Elledge.

By tracking the abundance of each shRNA from the total pool and comparing cancer cells to cells from normal tissues, Elledge and his colleague Ji Luo identified many genes that KRAS is dependent on. In this manner, they were able to do a genome-wide survey, uncovering many new potential drug targets, including PLK-1, STK33, and a number of proteins involved in mitosis. “It will take some time to figure this out, but RAS is clearly having some effect on an important part of mitosis,” said Elledge. “Regardless of that mechanism, it provides a vulnerability that we can attack. And fortunately there are a lot of drugs already available that have anti-mitotic properties – and we showed that some of those drugs are more toxic to the RAS cells.”

Furthermore, Elledge’s group found that the expression levels of some of the genes on their “hit” list correlated with patient survival. “This argues that they really do have an important role in the clinical outcomes observed in cancer patients,” said Elledge.

Sawyers thinks these two studies are an important proof-of-concept, but much more work will be needed to identify all the underlying vulnerabilities of cancer cells. “The ultimate validation of the synthetic lethal screening strategies will be evidence that patients KRAS-mutant tumors benefit from treatment with STK33 or PLK1 inhibitors,” Sawyers said. “Unfortunately, we won’t have that answer for many years.”

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http://www.forbes.com/feeds/ap/2009/05/ ... 75585.html

Poniard reports positive cancer study data
Associated Press, 05.28.09, 10:49 AM EDT
pic

Poniard Pharmaceuticals Inc. said Thursday its colon and prostate cancer drug candidate met key treatment and safety goals in midstage studies.

The South San Francisco-based company said updated study results for a Phase II study of picoplatin showed the drug had similar antitumor activity in colon cancer patients when compared with standard chemotherapy treatment. The picoplatin regimen, though, was significantly less toxic.


The study specifically focused on patients with colon cancer that had metastasized, or spread. It involves 101 patients who have not received prior treatment for colon cancer.

A separate midstage study showed picoplatin is active as a treatment for prostate cancer that has spread.

Shares of Poniard rose 4 cents to $4.52 in morning trading.

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http://www.gympietimes.com.au/story/200 ... rous-weed/

Wonder weed 'beating cancer'

Jannette Parke | 29th May 2009

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Craig Warhurst

A GYMPIE couple using a “natural anti-cancer” lotion they are making from a weed called “Devil's Apples”, believe it is helping with Jack Kellerher's sun spots and prostate cancer.

Jack's partner Mavis Sommer says she's not trying to sell anything - just let people know about the plant so they have the opportunity to try the alternative treatment for themselves.

Devil's Apple (Solanum linnaeanum) is a nightshade species native to South Africa and is considered an invasive weed in Australia and New Zealand.

The plant is not uncommon in the Gympie region and Mavis and Jack have several specimens growing in their garden. Mavis says she puts the poisonous tomato-like fruit into a blender to mash them and then mixes that with olive oil - the resultant lotion is used topically.

Jack was diagnosed with prostate cancer in 1988 and he happily slathers the mixture on his skin.

“I rub it all over and I believe it is suppressing the cancer,” he says.

Jack is convinced it has helped him survive the disease - mates have not been as lucky he says.

“Friends who were diagnosed with cancer at the same time as me have passed on,” Jack said.

The former dairy farmer says it was well known that cows grazing on the plant never had uterus or skin cancer.

Australian biotech company Solbec Pharmaceuticals have been working with Solanum linnaeanum and developed Coramsine, a 1:1 mixture of the alkaloids solamargine and solasonine extracted from the plant's fruit.

A protocol for phase II trials against advanced solid tumours was presented in 2005 and research is continuing on the plant's compounds.

Studies have shown activity against ovarian cancer, renal cancer, melanoma, mesothelioma, colorectal and colon cancer, gastric cancer, bladder cancer, various skin cancers and prostate cancer.

The applications of devil's apple in combating cancer was tested and patented in the early 1980s by Bill Cham, who was then a medical researcher at the University of Queensland.

Cham, who developed a cream made from the devil's apple flower, followed up anecdotal evidence from livestock owners that the growth of skin cancers and lesions had slowed down or cleared up in horses and cattle that ate the weed.

Farmers were also known to rub the sap of the fruit to repair sunspots.

At nearly 80, Jack is fitter than some men half his age and he is adamant Mavis' homemade concoction is an alternative therapy that is working for him.

“We've got a lot of people using it,” he says. “Mavis just gives it away.”

And what does his doctor say?

“My doctor says if it's helping then why not?” Jack said.

“It's nice if we can help people - they should give it a go.”

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http://news.xinhuanet.com/english/2009- ... 453330.htm

Cancer relies on proteins to stay alive
www.chinaview.cn 2009-05-29 15:52:05

BEIJING, May 29 (Xinhuanet) -- U.S. researchers say they have identified new ways of attacking cancer by targeting a largely hidden network of normal genes that cancer cells rely on for survival.

Researchers at the Harvard Medical School and Brigham and Women's Hospital said they reduced the production of thousands of normal proteins to determine which were required for cancer cells to survive.

They found cancer cells growing in a dish rely heavily on many normal proteins and when some of those protein levels drop, cancer cells die.

The researchers studied cells with mutations in KRAS, the most commonly mutated gene in human cancers. KRAS, which was discovered nearly 30 years ago, is mutated in 30 percent of human tumors, including 90 percent of pancreatic cancers, 50 percent of colon cancers, and 30 percent of non-small cell lung cancers.

“Efforts to develop drugs that inhibit oncogenic RAS proteins have been largely unsuccessful, despite the fact that RAS gene family members are mutated in about 30 percent of human tumors,” said scientists.

More than 18 months ago, the resesrchers decided to see if they could use the powerful RNAi technology to seek out genes that KRAS-mutant cancer cells need for survival. Their efforts, culminating in two reports in the May 29, 2009 issue of the journal Cell, have led to the identification of potentially promising drug targets: serine/threonine kinase 33 (STK33) and polo-like kinase 1 (PLK-1), as well as a host of other proteins.

“These targets represent a potential Achilles heel for tumors,” said D. Gary Gilliland of Brigham and Women’s Hospital (now senior vice president at Merck Research Laboratories). “In the case of STK33, it is absolutely required for survival of cancer cells. Normal cells don’t require it.”

"The beauty of the strategy is that it would take only 50 to 70 percent knockdown of STK33 to kill a cancer cell," Gilliland said.

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http://www.winnipegfreepress.com/local/ ... 53162.html

Cranberry extract may cut risk of colon cancer

Studies show that nonsteroidal anti-inflammatory drugs (NSAIDs) are associated with a decreased risk of colon cancer. Now, researchers report that cranberry extracts may have the same effect. In the study, colon cancer cells were exposed to cranberry extract, and like NSAIDs, cranberry extract also triggered an anti-inflammatory response. Further research is needed to see if cranberry extract will help to decrease the number of people dying of large bowel malignancies. For more information see www.fruitessentials.com or call 1-877-328-3784.

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http://www.google.com/hostednews/ap/art ... wD98FJ0N00

Minn. boy who resisted chemo undergoes treatment

By PATRICK CONDON – 13 hours ago

MINNEAPOLIS (AP) — A 13-year-old boy cancer patient who fled the state with his mother rather than face chemotherapy underwent a round of the treatment he feared Thursday, a family spokesman said.

Jim Navarro said Daniel Hauser attended his second chemotherapy session at Children's Hospitals and Clinics but he had no immediate update on the teen's condition. The hospital wouldn't release information about the procedure, citing patient confidentiality.

The boy's parents, who initially resisted chemotherapy out of a preference for alternative treatments, faced legal consequences if they skipped the appointment. Daniel also attended an appointment a day earlier.

The family had said an earlier round of chemotherapy made Daniel, who suffers from Hodgkin's lymphoma, feel sick and hardened their resolve against further treatment. A Brown County judge ordered the treatment anyway, prompting Daniel and Colleen Hauser to leave their home in Sleepy Eye and spend a week on the lam.

The family prefers natural healing practices suggested by a religious group called the Nemenhah Band, which says it follows American Indian beliefs.

Earlier this week, the family agreed to accept chemotherapy when doctors vowed to integrate some natural treatments favored by the Hausers.

Although integrative medicine doctors said such therapy were not meant as an alternative to traditional cancer treatment, it can help patients deal with the effects of chemotherapy.

"A lot of people want to avoid chemotherapy because they're afraid of it, and what they're actually afraid of is the symptoms," said Dr. Lucille Marchand, clinical director of integrative oncology services at the University of Wisconsin Paul C. Carbone Cancer Center. "And symptoms can be treated."

Several integrative medicine specialists said acupuncture or acupressure has proven to be an effective way to treat the nausea that's an almost universal symptom of chemotherapy. Doctors said a young patient like Daniel also could respond to relaxation techniques like yoga or tai chi, as well as simple aerobic exercise.

But detractors such as R. Barker Bausell, a researcher at the University of Maryland School of Nursing who formerly worked at the school's complementary medicine program, said most integrative medical practices amount to little more than a placebo effect.

"You can't say it doesn't help, because you can't say placebos don't help," Bausell said. "People want to believe in it, and they're willing to pay for it. It's adding another layer of cost to our extremely expensive medical system."

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http://www.nytimes.com/2009/05/29/arts/ ... S_BRF.html

Depeche Mode Singer Has Cancer Surgery


Article Tools Sponsored By
Compiled by DAVE ITZKOFF
Published: May 28, 2009

The band Depeche Mode has canceled additional concerts after announcing that its lead singer, Dave Gahan, below, had surgery to remove a malignant tumor from his bladder, Agence France-Presse reported. Earlier this month the group canceled a concert in Athens hours before showtime as Mr. Gahan was taken to a hospital. The singer was initially given a diagnosis of severe gastroenteritis and the band postponed further appearances in Europe while he recovered. But in a statement on Thursday, the band said that while Mr. Gahan was hospitalized, “further medical tests revealed a low-grade malignant tumor in Dave’s bladder, which has since been successfully removed.” Depeche Mode has rescheduled or canceled performances in Britain, Germany and the Netherlands, and plans to resume its tour in Leipzig, Germany, on June 8.

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http://timesofindia.indiatimes.com/Heal ... 592967.cms

Cottonseed-based drug treats cancer
29 May 2009, 1322 hrs IST, ANI

WASHINGTON: Researchers at the University of Alabama at Birmingham (UAB) say that an experimental drug derived from cottonseeds appears to be efficacious in treating the recurrence of glioblastoma multiforme, which is considered to be the most lethal brain cancer.

The researchers came to this conclusion following the results of a Phase II clinical trial of AT-101, a pill manufactured from a potent compound in cottonseeds that overcomes the abnormal growth patterns of tumour cells.

Glioblastomas are more common in adults, and are considered fast-growing brain tumours that are very difficult to treat.

Research leader Dr John Fiveash, an associate professor in the UAB Department of Radiation Oncology, said that the cottonseed-based agent was found to halt the cancer's progression in many of the 56 patients.

He revealed that despite undergoing other treatments, including surgery, chemotherapy and radiation, the trial patients' brain cancer had begun to grow again prior to starting AT-101 treatments.

The trial-monitored patients took only AT-101 daily for three out of four weeks.

"After getting this drug some of these patients went many months without any new growth in their tumours. We are able to do that with a well-tolerated oral medication, and that is a major benefit," Fiveash said.

He believes that the drug would likely work best in combination with radiation and chemotherapy to boost the cancer-fighting properties of those treatments.

Fiveash and his colleagues are also trying to determine which patients are most likely to benefit from AT-101.

The initial results of the drug trial would be presented on May 30, during the poster discussion of central nervous system tumours at the American Society for Clinical Oncology annual meeting in Orlando, Florida.

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http://www.sciencedaily.com/releases/20 ... 112534.htm

Chemotherapy Combination Outcomes Differ For Aged, Younger Colon Cancer Patients

ScienceDaily (May 29, 2009) — The combination of chemotherapies 5FU and oxaliplatin compared to 5FU alone after surgery for colon cancer decreases colon cancer recurrence and promotes longer survival for patients under 70 -- but not for those who are older, according to Mayo Clinic and Dana-Farber Cancer Institute scientists who will present their findings at the American Society of Clinical Oncology's (ASCO) annual meeting in Orlando, Fla.

"By combining information about many patients from a collection of studies, our analysis determined that the more aggressive combination chemotherapy does not benefit older colon cancer patients as it does for those who are younger," said Nadine Jackson McCleary, MD, PhD, Dana-Farber gastrointestinal oncologist and the lead author on the study. Jackson-McCleary is the recipient of a 2008-2009 ASCO Young Investigator's Award.

The data will be presented on Saturday, May 30.

Adding oxaliplatin to chemotherapy treatment with 5FU reduces the risk of recurrence among patients less than 70 years of age who have had their primary cancer removed, the study determined, a finding that was expected based on the results of previous individual trials. Patients under 70 who were treated with 5FU and oxaliplatin had improved disease-free survival, with the addition of oxaliplatin relatively reducing the risk of recurrence or death by approximately 15 percent. Those patients aged 70 and older who were treated with the combined drug therapy, however, did not have improved outcomes compared to patients who received 5FU alone.

"We found that adding chemotherapy agents to the standard 5FU regimen in older patients after surgery did not provide the benefits that younger patients see," Dan Sargent, PhD, Mayo Clinic, a collaborator on the study, agreed. "For the older patient, this means that it is appropriate to choose the better tolerated treatment strategy of 5FU alone."

The benefit of post-surgical treatment for both young and older colon cancer patients with 5FU was documented in a 2001 New England Journal of Medicine study by Sargent and colleagues. By 2003, however, oxaliplatin was approved for use in combination with 5FU because the combination boosted the impact of 5FU on extending disease-free survival after colon cancer surgery. While the combined treatment carried additional risk of side effects, physicians prescribed the treatment strategy to patients of all ages. Initially, studies that examined age-related impact of the aggressive chemotherapy combination did not indicate a difference in survival or recurrence related to patient age.

The current study presented at the ASCO annual meeting includes a large enough patient base to powerfully discern differences related to age that are due to treatment regimen.

"The younger patients do get an additional boost from both drugs used together," Jackson McCleary noted. "Older patients don't benefit from that combination of treatment."

The findings arise from analysis of combined data collected within an expanded database by the Adjuvant Colon Cancer End Points (ACCENT) Group, a consortium of scientists. The ACCENT database includes data from more than 33,500 patients from the United States, Canada, Australia, and Europe. ACCENT is supported by the North Central Cancer Treatment Group (NCCTG); Sargent is chair of ACCENT.

"At this point we can only speculate as to why older patients do not benefit from combined chemotherapies," Jeffrey Meyerhardt, MD, MPH, of Dana-Farber and co-investigator on the trial said. "We do know that a higher number of older patients have to stop the drug before completing the full six month prescribed course of treatment."

"These studies add to the knowledge base that defines how to choose treatment strategies for every individual patient," Sargent said. "Age may become as important a consideration as tumor-specific factors when defining individual medical options for colorectal cancer patients."

Approximately half of all colon cancer patients are older than 70. While about half of the colon cancer patients over 70 will live for five years, those with recurrence typically develop additional tumors within three years. The disease is diagnosed in a million people worldwide every year. In the United States, colorectal cancer accounts for 10 percent of new cancer cases, as well as 10 percent of cancer-related deaths every year.

Jackson McCleary, Meyerhardt, and Sargent conducted the analysis on the expanded database in concert with an international team of scientists participating in ACCENT, including Erin Green, MD, Mayo Clinic; Greg Yothers, PhD, University of Pittsburgh; Aimery de Gramont, MD, Hopital Saint-Antoine, Paris; Eric Van Cutsem, MD, PhD, University of Leuven, Belgium; Michael O'Connell, MD, Mayo Clinic; Chris Twelves, MD, St James University Hospital, Leeds, England; and Leonard Saltz, MD, Memorial Sloan-Kettering Cancer Center, New York.

[garbovatwin]

http://www.alternativehealthjournal.com ... drome/3387

Remedies For Irritable Bowel Syndrome
By Dan Sevigny, Community Contributor -- Published: May 29, 2009

Usually people with IBS are doomed to a life of comfortable situations, what they do not realize is that there are many natural ways to treat IBS First and foremost, IBS stands for Irritable Bowel Syndrome and in essence, IBS is a chronic medical condition that is defined as a disorder of the gastrointestinal system, also labeled as ‘spastic colon syndrome’. While there may be countless medicines that will help relieve IBS, the natural ways to treat IBS are usually safer and have no side effects.

The first step in treating IBS is figuring out if you have this disorder, a simple test done by your doctor can confirm for you. After the test confirms that you have IBS, you then want to make sure that you are drinking enough water. Adding in at least eight glasses of water to your diet will help regulate your bowel movements and will flush out all the toxins in your body. This will calm your spasming colon down quite a bit.

Next, be sure that you are adding in some fiber into your diet. This is especially important for people with IBS as this too will help regulate your bowel movements and calm your IBS down. Now-a-day, fiber is popping up everywhere, from your everyday cereal all the way to the yogurt that you are probably already eating, so this should not be much of a change for you.

Now fiber and water are not the only natural ways to treat IBS, there are many foods that you can add into your diet that will assist with relieving some of your IBS symptoms. For instance, cabbage, guavas, figs, red apples and oranges are just a few of the foods that you should add into your diet to not only assist in regulating your bowel movements, but that will also help relieve your IBS discomfort. The cabbage has a lot of good fiber content, and you should be eating at least a bowlful a day – this will ensure proper functioning bowels.

The figs will need to be boiled in some water and if you drink the liquid before bed you will not only sleep better, but the liquid will work through your system throughout the night, so when you wake up in the morning your bowels should be in better shape. Peppermint oil is another great and natural way to treat IBS, put a little bit in your tea and you should be feeling better instantly.

Fruits and vegetables, legumes, whole grains, peanuts and beans are all other natural ways to treat IBS and if you add these into your regular diet, your IBS should be kept in check for days. Although, if you are the type of person that does not want to change their entire diet just so they can have some relieve of IBS, there is an herbal remedy called Bowtrol Colon Cleanser, this is another natural way to treat IBS.

There you have it! Just a few simple changes in your diet and lifestyle and you should see the difference in your IBS and your bowel movements in general. Keep eating a healthy and fiber-filled diet and your IBS will stay in check for a long while.

[garbovatwin]

http://health.msn.com/nutrition/article ... =100239205

Putting Red Meat in Perspective
When it comes to health, is meat an all-or-nothing proposition?
By Karen Collins, M.S., R.D., C.D.N., American Institute for Cancer Research
Karen Collins (c) AICR.org

The latest news reports about a major study looking at the health effects of red meat may have made many a meat lover take note. Before this latest study, the American Institute for Cancer Research’s recent report found that limiting red meat to no more than 18 ounces per week lowers our risk of colon cancer. Now, several studies are adding further insight regarding the recommendations to limit red meat. And as the studies show, it’s not all or nothing.

The latest study on red meat and health has linked eating relatively large amounts of red and processed meat to increased overall deaths, as well as deaths specifically related to cancer and heart disease. The study followed more than half a million people aged 50 to 71 for 10 years. Those who ate the most red meat were 31 (men) to 36 (women) percent more likely to die than those who ate the least. Red meat included all types of beef and pork. Those who ate the most processed meat—which included hot dogs, sausage and lunch meats made from beef, pork and poultry—were 16 (men) to 25 (women) percent more likely to die during the study than those who ate the least.

Keep red meat to modest amounts.

People who ate the most red meat consumed on average 4 to 5 ounces a day; people who ate the least ate about that same amount in an entire week. Those who were in the middle, consuming approximately 18 ounces of red meat per week, showed a slightly increased mortality rate compared to those who ate the least, but substantially below that seen among the highest red-meat consumers.

However, the increased risk linked to red meat was not tied to all animal meat consumption: People in the study who ate the most poultry showed lower overall and cancer-related mortality than those who ate the least. The group consuming the most white meat averaged just over four ounces a day.

Another large recent study supports this distinction between white and red meat. This study of middle-aged adults in Germany found that white meat consumption was unrelated to colon cancer risk. However, those who ate the most red meat showed greater tendency to form benign colon growths, which have the potential to become cancerous.

In a U.K. study of more than 64,000 adults, researchers found no difference in mortality rates between vegetarians and non-vegetarians. This study included a large number of relatively health-conscious people; mortality of the whole study group was about half that seen throughout England and Wales. The meat-eaters ate on average about two ounces a day; highest consumption was about 3 to 4 ounces daily.

These studies continue to support a relatively consistent message: keep red meat to modest amounts. Whether you prefer to achieve this as a vegetarian, with occasional meatless meals, or with moderate portions of poultry and seafood on a mostly plant-based plate seems to matter much less.

Find more from Karen Collins.

Karen Collins, D.C.N., M.S., R.D., serves as the nutrition advisor to the American Institute for Cancer Research (AICR). Karen writes two syndicated weekly columns, "Nutrition Notes" and "Nutrition-Wise," distributed by AICR. Karen was an expert reviewer for AICR's landmark international report, "Diet, Nutrition, Physical Activity and the Prevention of Cancer: A Global Perspective," which provides recommendations based on an examination of more than 7,000 research studies by a panel of internationally renowned scientists. (Read her full bio.)

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http://www.reuters.com/article/rbssHeal ... 2020090530

Hormone therapy lifts lung cancer death risk-study

ORLANDO, Fla., May 30 (Reuters) - The use of hormone-replacement therapy by menopausal women increases their risk of death from lung cancer by 60 percent after five years, U.S. researchers reported on Saturday.

Doctors once thought that hormone therapy, or HRT, could protect women from chronic diseases, especially heart disease.

But use of the drugs plunged after 2002 when the large Women's Health Initiative study was stopped after finding that HRT could raise the risk of breast and ovarian cancer, strokes and other serious conditions.

Tobacco smoking is the leading cause of lung cancer. About 85 percent to 90 percent of lung cancer deaths are directly caused by smoking, according to the American Cancer Society.

Among smokers, the use of HRT could be particularly problematic because they already have an increased risk of developing disease, researchers said.

"Women almost certainly shouldn't be using combined hormone therapy and tobacco at the same time," said Dr. Rowan Chlebowski, a medical oncologist at Harbor-UCLA Medical Center in Los Angeles and lead author of the study, which analyzed data from the Women's Health Initiative.

Lung cancer is the leading cause of cancer death in U.S. women.

The trial studied the use of Wyeth's (WYE.N) combined estrogen/progestin hormone-replacement therapy, Prempro.

Since 2001, sales of Wyeth's hormone products have plunged by about 50 percent to around $1 billion a year, and the bulk of sales are now estrogen-replacement drug Premarin and cream formulations, said Joseph Camardo, head of medical affairs at Madison, New Jersey-based Wyeth.

"Practice has already changed significantly," he said. "Guidance and the label have changed ... use has shifted toward much shorter duration and lower doses."

The Wyeth official noted that the average age of women in the Women's Health Initiative was 63, and the participants used high doses of Prempro over long periods of time.

Chlebowski said previous research suggested that hormones play a role in non-small cell lung cancer, the most common form of the disease, because women tend to have higher survival rates than men and respond better to certain therapies.

His study, presented here at a meeting of the American Society of Clinical Oncology, was the first to show a correlation in a randomized clinical trial setting.

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http://www.google.com/hostednews/ap/art ... AD98GOFO02

Immune system taught to fight deadly skin cancer

By MARILYNN MARCHIONE – 59 minutes ago

ORLANDO, Fla. (AP) — For the first time, a novel treatment that trains the immune system to fight cancer has shown a modest benefit in late-stage testing against the deadly skin cancer melanoma.

The approach is called a cancer vaccine, even though it treats disease rather than prevents it as most vaccines do.

Doctors say that in a study of 180 patients already getting standard treatments, the vaccine doubled the number of patients whose tumors shrank, and extended the time until their cancer worsened by about six weeks.

Results were reported Saturday at a cancer conference in Orlando.