[New Specialty in Cancer Care]

http://www.curetoday.com/currentissue/f ... index.html

In the recent issue of Cure, there is an interesting article, and it might be as well, for those who do not have a copy this magazine at hand.

ARTICLE:

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Palliative care is catching on in centers across the country, improving quality of life for patients along the way.

By Joanne Kenen

On November 11, 2000, Mark Quasius, then 37, learned that the strange sensation in his right ear was caused by a rare carcinoma in his upper sinuses.

After a variety of treatments, including multiple surgeries on his head, lungs, pancreas, and hip bones, the prognosis for his advanced adenoid cystic carcinoma is pretty good. After consultation with Andrew Putnam, MD, a palliative care specialist at Lombardi Cancer Center and Georgetown University Hospital, his life is pretty good too. Dr. Putnam brought Quasius’s unrelenting pain from the tumor behind his right eye under control after surgeons concluded that, for now, the risk of removing the tumor outweighed the benefits.

Quasius, now 44, can’t work at his old engineering job anymore. But he can still stroll down to the pond on his 30-acre farm south of Washington, D.C., still keep himself engaged with fun fix-up projects around his home, and still appreciate every day he has “with my wonderful, wonderful wife, Beth.”

That people are living longer with cancer as a chronic disease is well known. Because of the growing field of palliative care, people, like Quasius, are also living better.

Palliative care was once a scary word for hospice. Palliative care, the art of easing physical, emotional, or spiritual distress arising from a serious illness, is still the core of hospice care but it now takes place in many other settings—hospitals, nursing homes, and, now increasingly, in outpatient cancer clinics.

Unlike hospice, palliative care patients don’t have to have a life expectancy of six months or less. They don’t even have to be dying. And they don’t have to give up radiation, chemotherapy, or surgery in order to get “comfort care.” Doctors sometimes refer to palliative care as “concurrent care” or “a continuum of care” that can start early in treatment, sometimes even right at diagnosis. The idea is to give patients what they need when they need it, no matter what their ultimate prognosis.

That means both sophisticated medical management of symptoms, such as pain and fatigue, as well as enhanced communication about patient choices. This concept fits the biological principle that illness doesn’t turn from a treatable to terminal situation overnight, but may do so gradually, or even drift back and forth.

“When we walk in, it doesn’t mean we’re not going to treat your cancer anymore. It means that here is someone who is going to focus on the quality of your life, who is going to focus on other aspects of living beside the disease,” says Dr. Putnam. “The oncologist will focus on what the oncologists do best—and want to do. But you’ll also have someone who is going to concentrate and focus on the quality of life.”

Research is now providing the hard data to show the intervention works. A growing number of studies have reported benefit in quality of life for patients receiving palliative care. A recent study conducted by nurse-researcher Betty Ferrell, PhD, RN, and her colleagues at City of Hope in California found a better quality of life and fewer management barriers related to pain and fatigue among lung cancer patients receiving palliative care compared with those who did not receive the intervention.

Getting Access

When Heather Thomas, 34, of Vermont, fell on her kitchen floor a year ago, breaking eight vertebrae and three ribs, her doctors “wondered why I had bones that looked like an 80-year-old woman who never drank milk,” she says. The reason was metastatic breast cancer in her liver and bones. She knows her cancer won’t be cured, but it can be treated. Palliative care at Dartmouth-Hitchcock Medical Center in Lebanon, New Hampshire, is helping her keep her strength, her spirits, and her sanity.

“If something comes up that I don’t understand or I don’t know who to talk to, their only goal in life is to find the answer. It’s like trying to learn a whole other language when you get a cancer diagnosis. They are my translators,” Thomas says.

Some hospices, particularly larger ones, are developing community-based palliative care programs for cancer patients outside the traditional hospice model, either because death is not imminent or because they are not emotionally ready for hospice care. But they still have pain, symptoms, and emotional issues, and a palliative care team can fill the gap, smoothing the transition to hospice in those cases where it is eventually appropriate.

Some hospices have introduced an approach called “open access,” meaning the patient does fit the standard definition of a hospice patient, including the six-month prognosis, but doesn’t necessarily have to give up treatment, at least not immediately. Though some insurance companies, including Aetna and UnitedHealth, cover open access, it isn’t available everywhere, and it isn’t offered to every patient who may want it. But for some it is a gentle bridge over a chasm between aggressive curative care and what may feel like giving up.

“Open access has struck a chord,” says Carolyn Cassin, head of Continuum Hospice Care, a nonprofit in New York that offers it. “Everyone at the end of life has a right to specialized care, just like you are entitled to emergency room care if you are hit by a bus. The old-fashioned hospices defined themselves by what you could not have. They had relegated themselves to brink-of-death care. But if it’s only brink-of-death care, it’s not that useful. Open access provides a transition. That’s our core business—transition.”

Not every patient who needs palliative care gets it. Not every hospital offers it because of limited resources, and referral can come late. “There is still a mentality of cure, cut, and fix,” says Ferrell, who has been a national leader in training nurses in palliative medicine. “Too often we look at, say, the cancerous lung and forget about the rest of the person.” (Ferrell talks about barriers to palliative care in this issue’s Speaking Out.)

Yet it’s changing. At the major cancer centers around the country, from City of Hope to Memorial Sloan-Kettering Cancer Center in New York, palliative care has become a component of cancer care for inpatients and outpatients, and insurance

plans generally cover it. Some programs are more ambitious and far-reaching than others. But almost always the oncologist remains the primary doctor, with the palliative care team consulting just like any other medical specialist.

“When they asked me if I would be interested in seeing people from the palliative care unit, I didn’t know what to say,” recalls Patty Szostak, 53, who is being treated for a recurrence of non-Hodgkin’s lymphoma at Dartmouth-Hitchcock. “Is this

a death sentence? Are you telling me I’m terminal?” But once she understood palliative care, it made all the difference, not just in her physical comfort but in her emotional and spiritual health. The Dartmouth-Hitchcock team managed her physical symptoms, but also made sure Szostak, an artist and writer who meditates, does yoga, and tends to her horses in Vermont, got massages, Reiki, and even a serenade from a harpist.

Szostak’s response to treatment has been uneven; at one point she was very ill with the cancer infiltrating her brain. “There were two paths I could travel, a path to physical healing or another path that could lead to my death. And somewhere along the line, I realized palliative care was for either option.”

Pain as the Starting Point

Pain is usually what gets the patient to the palliative care team; that’s what initially brought Quasius to Dr. Putnam. But once patients walk through the door, palliative specialists often find other physical symptoms, such as severe fatigue, that the patient may have wrongly assumed were inevitable aspects of life with cancer. The specialist may also address the complicated family dynamics that can burden a cancer patient, or, sometimes, the rough decisions about how aggressively to pursue treatment.

“What palliative care does first of all is improve how you feel,” says Susan Lowell Butler, 64, a 10-year survivor of simultaneous breast and ovarian cancers who endured an arduous clinical trial and is now executive director of the DC Cancer Consortium advocacy group. “You tend to feel that everything you feel is a side effect of the cancer rather than of the treatment, when in fact most of those symptoms are perfectly manageable for most people. With palliative care you don’t have to fight the side effects, so you can just fight the cancer.”

Not every cancer patient will need to call in the palliative care cavalry; some cancers are easier to treat than others. “We get the more complicated constellations of physical symptoms, psychosocial, and spiritual needs,” says Janet Abrahm, MD, a palliative care physician who treats outpatients at Dana-Farber Cancer Institute and inpatients at Brigham and Women’s Hospital in Boston. “The [oncologist] has done the best he can but the person is suffering. Then they call us.”

Palliative medicine was recognized officially as a medical subspecialty in 2006 by the American Board of Medical Specialties, with growing training opportunities for physicians and nurses. Much of it involves administering state-of-the-art pain medication. Some clinics are using high-tech approaches, including various types of nerve blocks or pain pumps (see sidebar). But they also treat symptoms that cancer patients are all too familiar with, including neuropathy, fatigue, nausea, constipation, mouth sores, shortness of breath, and anxiety.

“We have more weapons in our armament for symptoms than the oncologist does,” says Dr. Putnam.

The palliative care team, which can involve doctors, nurses, social workers, chaplains, physical therapists, and nutritionists, can intervene in a crisis. But often palliative care can avert a crisis and let the patient avoid hospitalization and frantic trips to the emergency room, says Nessa Coyle, RN, a national leader in palliative care nursing at Sloan-Kettering. Some patients will only need palliative care during rigorous treatment; others will need ongoing assistance.

. . . . . . .

(Cure, Cancer Updates, Research & Education, Spring, By Joanne Kenen, 2008)

Disclaimer:

The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.

[Ten Things You Can Do to Reduce Your Cancer Risk]

http://www.prnewswire.com/cgi-bin/stori ... 886&EDATE=

Ten Things You Can Do to Reduce Your Cancer Risk

SEATTLE, April 4, 2008 /PRNewswire-USNewswire/ -- Most people assume that cancer is genetic and cannot be avoided. However, according to the American Cancer Society, healthy behaviors could prevent approximately half of cancer deaths. Below is a list of 10 lifestyle changes, all based on the latest research, which people can make to improve their odds of preventing cancer or catching it at its earliest, most curable stages.

-- Don't smoke or use any other tobacco products. Tobacco increases the risk for many cancers including those of the lung, bronchus, head and neck, colon, and bladder. If you smoke, stop. If you don't smoke, don't start. If you've tried to quit before, don't give up -- eventually something will work. Don't be afraid to ask for help from your physician, your family and friends, your employer, and even your insurance company. There are so many benefits to reducing smoking that many companies and insurance companies provide free help for quitting smoking.

-- Get screened for cancer regularly. Several tests can find cancer at a very early stage, sometimes even before a growth has turned cancerous. Finding cancer early can greatly increase your chance for a cure and reduce your risk of dying from the disease. Currently available cancer screening includes:

* Colon: Starting at age 50, all people should have a colonoscopy (or even younger if at high risk). The frequency of colon screening depends on

risk. A colonoscopy every 10 years is the norm for those with no personal or family history of colon cancer or high-risk polyps. Those at high risk

may need more frequent testing. Acceptable alternatives for people who are not at high risk for colon cancer include flexible sigmoidoscopy, CT

scanning and a test to check for hidden blood in the stool.

* Breast: Starting at age 40, all women should get an annual mammogram (or even younger if at high risk) and a breast exam performed by a clinician. Some women may be eligible for a breast MRI and ultrasound as recommended by their physician.

* Prostate: Starting at age 50 (or younger if at high risk), all men should have an annual physical exam (including a digital-rectal exam) and a

blood test to check for blood levels of prostate-specific antigen, or PSA, which when elevated can be an indication of prostate cancer.

* Cervix: Cervical-cancer screening (cervical sampling for Pap smear and human papillomavirus testing) should start as soon as a woman is

sexually active and should continue throughout life with frequency depending on the woman's risk and age.

* Skin: All adults should have a yearly skin exam by their primary care doctor. Those at high risk should have annual skin-cancer screening performed by a dermatologist. Persons at high risk for melanoma or other skin cancer should examine their own skin monthly.

-- Keep your alcohol consumption low. This means no more than two drinks per day for men and one drink per day for women. Alcohol use increases risk for several cancers including those of the breast,

esophagus, colon, pancreas, and head and neck. Keeping your alcohol intake to the minimum daily level doesn't mean that you can "save up" all your

drinks for a week and binge on Friday night with your weekly "allotment." This type of binge drinking is dangerous because it reduces your ability to

make rational decisions, and it increases your risk of injury and of acute heart failure.

-- Protect your skin from the sun. Use sunscreen every time you go outdoors (preferably one with an SPF of 30 or higher that protects against both UVA and UVB rays). Keep covered with a broad hat and sunglasses, keep the amount of exposed skin to a minimum and limit time in the sun when it is the strongest (usually 10 a.m. to 4 p.m.) Remember that sun rays penetrate car and other windows, so you should use sunscreen any time you'll be getting sun exposure through a window. Never use a tanning bed,

as they are as dangerous as sun exposure. If you want a tan without going outdoors, use a self-tanner, as such products do not cause skin cancer or

other skin damage.

-- Keep a physically active lifestyle. Research suggests that exercising three to four hours per week at moderate or vigorous levels reduces the risk of several cancers by 30 percent to 50 percent. Many

studies have shown that regular exercise lowers risk for breast and colon cancers, and studies now suggest that risks for endometrial and lung cancer

may also be lower in people who exercise regularly. You don't need to be an athlete to get the benefit of exercise. Activities like brisk walking, biking, dancing, or any exercise that raises your heart rate and makes you sweat will be beneficial.

-- Keep your weight in the normal range for your height. That means keeping to a body mass index (BMI) of 25 or less. (You can calculate you BMI with online calculators). People who are overweight or obese have increased risk of developing several cancers including those of the colon, breast, pancreas, liver, kidney and endometrium, and perhaps leukemia and lymphoma. There is also evidence that men who are obese are more likely to develop a deadly form of prostate cancer if they develop the disease. Keep your weight steady; don't gain pounds over time. Try to stay within 5 to 10 pounds of what you weighed at age 18. The best way to avoid weight gain and avoid overweight or obesity is to eat a diet high in vegetables and fresh fruit and low in high-calorie foods like sugared drinks, refined

carbohydrates and fatty foods.

-- Avoid taking menopausal hormone therapy. Menopausal hormone-replacement therapy increases risk for breast, endometrial and, possibly, ovarian cancer. If you have menopausal symptoms, try to handle them without hormone therapy including estrogens, progesterone, and testosterone. If you need to take hormones, limit your use to less than

five years.

-- Consider taking medications for reducing cancer risk. There are several medications that have been tested and found effective for reducing risk for cancer. Anyone considering using such medications should talk with their doctor about the pros and cons of these medications given their risk for the disease. These include:

* Breast: Tamoxifen and raloxifene both reduce the chance of developing breast cancer by half in women at increased risk for the disease. Women at increased risk include those over age 60, and women who have certain family histories of breast cancer or who have had certain types of benign breast

disease.

* Prostate: Finasteride has been shown to reduce the risk of developing prostate cancer by 25 percent. However, it increases risk for some types of advanced prostate cancer.

-- Avoid exposures to cancer-causing substances. Radiation exposures and some chemicals are known to cause cancer. Make sure that any physician who orders an X-ray for you, especially high-dose ones like CT scans, knows how many previous X-rays you have had. If it is not an emergency medical situation, ask whether there is an alternative examination that would work for you, such as ultrasound or MRI, which do not have radiation. Limiting X-ray exposure is especially important for children and teens. If you work in an industry or occupation where you are exposed to radiation or

chemicals, be very careful to follow the regulations of your company and the U.S. Occupational Safety and Health Administration.

-- Eat a cancer-risk-reducing diet. The role of diet in cancer is far from established, but research suggests that a plant-based diet is associated with reduced risks for several cancers, especially for colon cancer. Some general dietary guidelines for reducing cancer risk are:

* Keep your intake of red meat to a minimum. This means no more than 4 ounces of red meat per day on average. Four ounces of red meat is about as big as a deck of cards.

* Avoid processed meats such as sausages and bologna. The chemicals used to process such meats have been found to cause several kinds of cancer.

* Eat a variety of non-starchy vegetables and fruits every day. The National Cancer Institute recommends eating at least five servings of vegetables and fruit per day, but most experts on cancer and diet recommend at least double that amount. Experts further recommend that you eat a variety of brightly colored vegetables and fruits, as these contain the highest concentrations of vitamins. You can increase your intake of vegetables by putting them into your breakfast omelet, by snacking on carrots, and by mixing them into casseroles for dinner.

* Minimize your intake of high-calorie foods such as sugared drinks, juices, desserts and candies, refined breads and bagels, and chips. By lowering intake of these high-calorie foods and increasing your intake of non-starchy vegetables, you will be better able to keep your weight to a normal level and avoid gaining weight.

* Eat foods with high calcium and vitamin D levels such as fortified low- or nonfat milk and yogurt. If you don't get enough through your diet, you may want to take calcium and vitamin D supplements. Check with your doctor, who may want to check your blood level of vitamin D, because many Americans have been found to have a deficiency in this vitamin.

This news release was issued on behalf of Newswise. For more information, visit http://www.newswise.com.

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(NewWise, PRNewswire, Source: Fred Hutchinson Cancer Research Center, April 4, 2008)

Disclaimer:

The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.

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[Research Study: There May Be New Warhead Against Cancer]

http://www.recordnet.com/apps/pbcs.dll/ ... /-1/A_LIFE

ARTICLE:

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By The Record

April 05, 2008

The battle against cancer might have developed a new "warhead."

That's what two University of the Pacific chemistry professors are calling the model for a potential anti-cancer drug they have discovered.

"Often, cancer patients suffer severely from cancer treatments based on chemotherapy," said Elfi Kraka, who teamed with Dieter Cremer on the research project. "This new drug model has a lot of potential and could lead to a new, efficient anti-cancer drug with highly reduced side effects."

Kraka, the former chairman of Pacific's Chemistry Department, and Cremer published the results of their research in the March 6 edition of the American Chemical Society's Journal of Physical Chemistry B.

Their potential drug derives from enediynes, natural substances capable of cutting "like scissors" through a cell's DNA, said Kraka.

They used these enediynes - the "warheads" produced by microorganisms found in soil in Texas and Argentina in the 1980s - to attack the acidic nature of tumor cells.

Similar enediynes now used in some cancer treatments destroy healthy tissue as well as tumor cells, leading to unpleasant side effects.

Kraka and Cremer used a computer-assisted drug design to learn that - by combining enediynes with aminides, which occur naturally - a "warhead" can be created that only becomes active in acidic environments.

Unlike healthy cells, cancer cells generate such an acidic environment.

So, the enediyne can be "trained" as "warheads" that only would attack cancerous tumors, leaving healthy tissue alone and increasing the potential survival rate.

"Microorganisms have had 2 billion years more experience than humans have in figuring out how to fight toxic bacteria and viruses," Kraka said. "In this time, they have developed compounds such as enediynes. Now we have to learn how to adjus

nature's design to our needs."

"The breakthrough ... could have a tremendous impact on the treatment of one of the most significant diseases of our times," Pacific Provost Phil Gilbertson said.

Kraka and Cremer, who undertook key aspects of their research at Pacific, specialize in theoretical and computational chemistry, nanotechnology and computer-assisted drug design.

They said they are actively seeking a pharmaceutical company whose researchers would help further develop and test their drug model.

VIEW THE REPORTS

The cancer research report by University of the Pacific professors Kraka and Cremer, and Tell Tuttle, "Design of a New Warhead for the Natural Enediyne Dynemicin A.: An Increase of Biological Activity," is available at

http://dx.doi.org/10.1021/jp0773536.

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Disclaimer:

The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.

[CT or MRI which is better?]

Dear Tami,

Last year, Bill had a CT scan of the brain which denoted a single met to midbrain.

He had never had any previous symptoms except for an involuntary "flutter" in a muscle in his back. He has never been dizzy, has never had headaches, nor any other untoward effect.

A couple of weeks ago, he had a follow up scan of head and neck. It was to assess shrinkage from the chemo he is receiving.

I questioned the oncologist related to a statement I read on the scan report, about an area, possible in back of the sinuses.

I asked if it were brain related. He said, "Possibly." I asked him which was better, a CT or an MRI. He said, "MRI."

An MRI is scheduled for April 8. Holding steady until we know more.

The answer from Bill's oncologist told me that an MRI was superior to CT for the brain.

I'm sure you will feel much better having received attention by follow-ups, Tami. We discovered that vigilance is the name of the game.

Headaches do not mean brain mets, necessarily, but it is best to check these things out, so that we can keep on top of things.

Wishing you all the best, Tami. Let us know how things are going?

Barbara

[

[chronic]

Hello Bucky,

I don't know if it is a universal thing, but our oncologist, and radiation oncologist, plus the pulmonologist and Bill and I, are treating this as a chronic.

The oncologist works to find the best chemo appropriate to the situation, and we watch the reports of the scans (I read them with a fine-tooth comb). We watch for anything questionable and do ask these professionals to interpret.

Awareness is the name of the game. Having missed a few issues in the past, we have become vigilant to a fault.

We intend to be here as long as humanly possible. Hey, we like the planet. There are treatments, Bucky, and so far, the biggest side effect Bil has had is his fatigue with some.

He doesn't even count the loss of hair. After all, he always had more hair than any one guy ever needed.

Shampooing takes less time, shaving has become a quick run through (need electric razor due to Avastin).

Generally, summer's coming and it should feel cooler under the NYFD cap - which states on the rear - stay back 200 feet.

Barbara

"alexan"]Is Lung C allready consider and treated like a chronic desease???

thanks & hugs bucky

[This Is My RE-registration Arriving Back to Our Roots.]

Hello Carole

Yes, Carole, I have been posting the news here on LCSC for a short time now.

On the first page there are various categories. Scroll down and you will see "LUNG CANCER IN THE NEWS." There are news items from members which are very interesting, and up-to-date.

Just the other day, I received an email from Lori Hope, who gave me a "heads up" on a news article in which she was a subject.

Coincidentally, our son, William, who resides in New York, actually mailed the same article to us from a newspaper clipping.

(It is posted in "Lung Cancer in the News" [on the first page here by scrolling down to that category].)

I would love any item you might think is newsworthy. You can even post it here yourself, Carole.

There is a statement at the "Lung Cancer in the News" category which invites lung cancer news, or send it to me - either way - whichever you like.

Today, Bill and I are going to take one of our sons, Joe and our grandson out to lunch. We will be sitting at least 3 feet away, though, because Joe has a cold he brought up from Florida. Yikes! "It's always something..." (Gilda Radnor)

Bill's immune system is a bit compromised at this time, so Joe understands our being cautious.

Thank you for your very confidence-building posting to me. It was much appreciated.

Oh, btw, if you like there is a Private Message area here, PM at each posting window, as well, or email option.

All the best to you, Carole, and keep posting. These are wonderful, responsive people, as you will discover.

Barbara

[Gene Therapy Shows Promise in Treatment of Cancer]

http://www.newswise.com/articles/view/539458/

ARTICLE:

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Newswise — Thanks to the advances of molecular medicine and the mapping of the human genome, it is now certain that cancer is the result of defective or missing genes.

The Alliance for Cancer Gene Therapy (ACGT®) was created to support the extraordinary potential offered by gene therapy as a revolutionary model for effective and safe treatment of all types of cancer. To date, ACGT has awarded $18.8 million to fund 31 research projects in 25 prestigious medical institutions – all of which have shown promise in furthering the successful treatment of cancer.

“Molecular medicine is the new paradigm to treat and someday eradicate cancer,” said Edward Netter, co-founder and president, ACGT. “In the near future, ACGT is committed to devoting more grant awards in the hopes of encouraging researchers – especially young researchers - to move forward more rapidly, and eventually move their treatments into medical practice. We anticipate that gene therapy will someday make cancer a manageable disease with nominal side effects to patients.”

Currently, there are over 800 cancer gene therapy trials underway, according to the U.S. National Institutes of Health. ACGT has funded or facilitated 17 Basic Research/Laboratory Studies, five Pre-Clinical, eight Phase I Trials and one Phase II Trial.

“Gene therapy for cancer is revolutionary because it can lead to the eradication of tumors in ways that are distinct from existing treatment paradigms that include surgery, radiation, chemotherapy and antibody therapy,” said Savio Woo, PhD, professor, Mt. Sinai School of Medicine, chairman, ACGT Scientific Advisory Council. “This novel treatment can be used by itself and in conjunction with the existing therapies to achieve optimal outcome in patients including substantially prolonged survival.”

Research is being conducted on several approaches to gene therapy including:

replacing a missing or unhealthy gene with a functional and “healthy” gene;

immunotherapy which involves improving a patient’s own immune response to cancer;

inserting genes to improve the effectiveness of chemotherapy or radiation therapy;

inserting “suicide genes” into cancer cells (called apoptosis); and

inserting genes to strangulate cancer cells by cutting off their blood supply (called anti-angiogenesis).

Two-thirds of all gene therapy trials in the U.S. are for cancer and many of these are entering the advanced stage, including a Phase III trial for head and neck cancer and two different Phase III gene vaccine trials for prostate cancer and pancreatic cancer. Additionally, numerous Phase I and Phase II clinical trials for cancers in the brain, skin, liver, colon, breast and kidney among others, are being conducted in academic medical centers and biotechnology companies, using novel technologies and therapeutics developed on-site.

Specifically, ACGT has funded scientists including:

Dr. George Coukos, assistant professor and director of the Center for Research on Ovarian Cancer Early Detection and Cure of the University of Pennsylvania Abramson Family Cancer Research Institute, has worked in combating ovarian cancer by using “anti-angiogenic” gene therapy, which focuses on starving tumors from their supply of oxygen and nutrients by stopping the growth of new blood vessels. Additional therapies are underway, including development of tumor antigen vaccines. His lab has launched the first therapeutic vaccine trial for stage III and IV ovarian cancer. Dr. Coukos is a recipient of the ACGT Dr. Judah Folkman Angiogenesis Award for Cancer Gene Therapy.

Dr. Thomas Kipps, M.D., Ph.D., a professor in the Department of Medicine and Deputy Director for Research at the University of California, San Diego Moores Cancer Center, has developed a vaccine called Immune Stimulatory Factor 35 (ISF35), an active immune therapy product, or vaccine. Based on the results of previous studies, ISF35 has the potential to stimulate the immune system to act against Chronic Lymphocytic Leukemia cells and fight them naturally. Memgen, a biomedical company headquartered in Dallas, Texas, licensed the technology for the ISF35 molecule from UCSD and continues clinical development of the molecule.

A complete list of the research supported by ACGT can be found by visiting http://www.acgtfoundation.org

“Gene therapy research is rapidly moving along a continuum from basic scientific study to translational laboratory research, to clinical trials with both humans and domestic animals and ultimately to clinical application,” continued Mr. Netter. “We look forward to being on the front lines in funding the basic foundation in gene therapy research.”

About The Alliance for Cancer Gene Therapy (ACGT®)

The Alliance for Cancer Gene Therapy (ACGT) was founded in 2001 by Barbara and Edward Netter and is the only public charity in the nation dedicated exclusively to investing in research for cancer gene therapies. One hundred percent of all money raised goes to research grants with separate funding covering all administrative expenses. Based in Stamford Connecticut, ACGT is distinguished by its leadership, vision and the fusion of sound business principles and philanthropic investment with innovative scientific practice.

. . . . . . . . .

(NewsWise, Medical News, Source: Alliance for Cancer Gene Therapy, April 4, 2008)

Disclaimer:

The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.

[This Is My RE-registration Arriving Back to Our Roots.]

Hi Carole,

Welcome to LCSC and these warm and helpful people.

It was so comfortable to have been accepted here. I needed to have a lifeline to support and this is an answer to a special prayer.

When I recently re-arrived here, I believe I posted in the wrong place.

Bill's profile of treatments (signature) had been in my files, so that was easy to transfer, but shrinking it and filtering out the superfluous was another matter.

BUT, I received help. (Do not hesitate to ask anything here, they jump in and save the day.)

It takes a little while to adjust, but it is easier each day. Just seeing all the categories is very helpful.

One day, when I get my act together, I will post in "My Story." That way, the whole journey will be put into place. The only reason it is important is that it "may" help others to know that lung cancer affects actual human beings.

We are not just statistics.

It is sooo good to "see" you, Carole,

Sending you all our best,

Barbara

[Genetic Reprogramming: Epigenetics]

http://www.newswise.com/articles/view/539431/

ARTICLE:

. . . . . . . . .

Newswise — To radiation, chemotherapy, surgery and biological therapies deployed to wage war on cancer, M. D. Anderson researchers have added a new approach – diplomacy.

“In this instance, we’re not trying to kill cancer cells, rather we talk to cells and remind them of their regular programming. We persuade them to return to their normal behavior,” says Jean-Pierre Issa, M.D., professor in M. D. Anderson’s Department of Leukemia.

The instruments of persuasion are drugs that awaken cancer-suppressing genes in cancer cells by sweeping away chemical “off” switches connected to those genes. Methyl groups – which consist of a carbon atom surrounded by hydrogen atoms – silence genes by attaching at a certain spot, hanging off the gene like a tag or bookmark.

Issa and Leukemia Department Chair Hagop Kantarjian, M.D., are pioneers in the emerging field of epigenetics, the study of changes in gene expression and cellular behavior that are not caused by physical damage or mutation of the genes themselves. DNA methylation, for example, is epigenetic.

Issa and Kantarjian revived a failed chemotherapy, for instance, by turning it from attack to diplomatic mode. Using a low-dose, low-toxicity, longer-term approach, they showed that decitabine extends the life of some leukemia patients by demethylating, or turning on, genes.

Based on a clinical trial led by Kantarjian, the U.S. Food and Drug Administration last year approved decitabine (Dacogen™) for treatment of myelodysplastic syndrome, a lethal failure of the bone marrow to produce enough normal blood cells. The latest research by the group shows 70% of patients experienced some relief from MDS, with 35% experiencing complete remission. The median time of remission was 20 months.

Only the Beginning 


Before the development of decitabine and another epigenetic agent called azacytidine (Vidaza™), MDS was a disease “with no treatment,” Issa says. There was no chance of putting it in remission with a drug. Only supportive care, such as a blood transfusion, was available. Bone marrow transplants worked for a small number of patients.

“I see this as the beginning of the development of epigenetic therapy,” Kantarjian says. “FDA approval of decitabine was just the beginning. This is when the real research starts, when the drug becomes accessible to investigators in an easy manner so they can develop new concepts and new strategies to optimize the use of the drug as a single agent, in combinations and across many tumors.”

The leukemia group has a leading program, investigating epigenetic agents in 18 clinical trials. Four of those trials involve azacytidine, a drug that acts in a similar manner as decitabine. The two medications are the first epigenetic therapies approved for cancer.

Kantarjian, Issa, MDS Section Chief Guillermo Garcia- Manero, M.D., and colleagues have pressed ahead refining the optimal decitabine dosage for MDS, exploring its use in other leukemias, in combination with other drugs, and addressing how cancer becomes resistant to the drug. Azacytidine trials explore similar issues. Issa also collaborates with a team from Duke University on the use of decitabine for melanoma and renal cell carcinoma.

Nearly one-half of the 32 epigenetic trials at M. D. Anderson study decitabine. Not bad for a drug that was left for dead 25 years ago.

Drug Revival


Kantarjian’s and Issa’s work to revive decitabine is a classic example of the major role academic medical institutions play in drug discovery and development.

Decitabine was discovered in Czechoslovakia and tested against leukemia as traditional high-dose, cell-killing chemotherapy in Europe. The drug showed activity against the disease but was dogged by dangerous and unpredictable myelosuppression – the shutting down of blood production in the bone marrow.

This side effect caused the drug’s manufacturer, Pharmachemie BV of Europe, to shelve it in the 1980s.

Decitabine still intrigued Kantarjian, who was following the newborn field of epigenetics and suspected the drug had potential if used properly.

Pharmachemie was not interested in sponsoring any more clinical trials, but agreed to provide Kantarjian with decitabine. He filed his own investigational new drug application with the FDA and went to work. Kantarjian recalls that it was the early 1990s and he was the only physician in the United States working with the drug.

At the time, Issa was on the faculty at Johns Hopkins studying epigenetics. His research in DNA methylation led him to believe that decitabine might work epigenetically as a demethylating agent.

The two met in 1993 at a scientific meeting when Issa sought out Kantarjian and his poster on use of decitabine for chronic myelogenous leukemia. A collaboration was born.

They developed a Phase I clinical trial using decitabine intravenously for MDS at doses ranging from one-twentieth to one-fiftieth of the doses employed in the European trials. The trial showed that the drug was safe and active, with the lower dose preventing dangerous incidents of myelosuppression. Lab research indicated it worked by wiping out methyl tags.

Issa came to M. D. Anderson in 1999, where he and Kantarjian developed and led a pivotal Phase III multi-center trial in 2001. Results were reported early last year in the journal Cancer, citing that 17% of patients had some response, with responders having a median time to disease progression or death of 17.8 months, compared with 9.8 months for patients who didn’t respond.

By the time the FDA approved decitabine in May 2006, the drug had been held by four companies: Pharmachemie, TEVA, SuperGen and finally MGI Pharma, which purchased the drug from SuperGen in September 2004 and shepherded it through the FDA fast-track process. The frequent change of companies was another challenge in keeping decitabine alive, Kantarjian says.

Azacytidine, developed on a parallel track by a team at Mount Sinai Medical Center in New York, and owned by Pharmion, was approved by the FDA in 2004.

Decitabine, researchers note, is the more potent demethylating agent of the two.

Thinking Outside the Box


“Dr. Issa and Dr. Kantarjian brought a unique assimilation of scientific and clinical expertise that enabled them to think about developing decitabine in a different way,” says Mary Lynne Hedley, Ph.D., chief scientific officer of MGI Pharma. “And that’s really why decitabine ended up being so useful for patients.”

They upset three dogma of drug development and patient care, Hedley notes. First, they took a general cell-killing drug and by understanding its biological activity, transformed it into an early version of targeted therapy.

Second, they rejected the common practice of administering the maximum tolerated dose of a medication. And third, they focused on longer-term courses of therapy and disease management, rather than short courses of treatment.

The key to improved outcomes seen in the MDS follow-up study was prolonged treatment at low doses, Kantarjian says. “The best results with decitabine will be achieved by giving the drug to patients for one or two years, consisting of 20 to 24 courses of treatment, rather than three or four courses.”

Beyond MDS

Kantarjian leads a Phase III clinical trial of decitabine for acute myelogenous leukemia – the most common form of the disease in adults. Kantarjian notes that AML also is a leukemia that has shown the least improvement in treatment outcomes over the last 30 years.

A Phase II trial for decitabine as frontline therapy for AML in elderly patients, those with the grimmest prospects, also is under way.

Most patients over 65 go untreated, except for receiving supportive care, because of the toxicities associated with chemotherapy used against the disease. Their median survival is 1.7 months.

A poster presented by the team at the 2007 American Society of Clinical Oncology meeting showed how decitabine, with its low-intensity and minimal side effects, might help older AML patients. Total response rate was 52%, with 24% having complete remissions. Median survival time at the 20-month mark of the study was 12.6 months.

A study published this year comparing the effectiveness of decitabine to that of high-intensity chemotherapy in high-risk MDS patients showed comparable remission rates for each option, but those receiving decitabine had nearly doubled the mean survival time – 22 months versus 12 months. “Chemotherapy gets patients to remission, but it’s very toxic and remissions tend to be short-lived,” Issa says.

Other M. D. Anderson researchers also are testing epigenetic drugs alone or in combinations against solid tumors as well as myeloma and lymphoma.

David Stewart, M.D., professor in the Department of Thoracic/Head and Neck Medical Oncology, for example, is exploring in a Phase I trial the use of the drug for solid tumors and lymphomas that have resisted other treatment.

Some solid tumors, such as colon and head and neck cancers, are known to have a great deal of methylation. Issa notes that earlier clinical trials of decitabine against these cancers also failed, but they repeated the same mistake as the European trials, using maximum tolerated doses for short periods.

“This drug really hasn’t been properly tested at low doses over longer periods as a demethylating agent against those cancers,” Issa says.

More to Learn


There is still plenty to understand about how demethylating agents such as decitabine work. Their effect is global because they demethylate and switch on many genes. The research team is pinpointing specific cancer-suppressing genes that are silenced by methylation.

MDS eventually becomes resistant to decitabine. Issa says resistance starts as early as six months or as late as 3.5 years. The drug strips away all methyl tags, both normal and abnormal. The normal tags come back quickly, while the abnormal tags return more slowly. “If they come back, the drug stops working,” Issa notes.

Initial research in DNA methylation indicated that removing the tags might promote cancer by turning on oncogenes. However, Issa notes, subsequent research showed that methylation silenced hundreds of genes, inactivating those involved in tumor suppression and programmed cell death of cancerous cells.

Since tumors rely more on gene silencing to survive than normal adult cells do, the overall effect of demethylation is favorable for treatment.

Two for One


One potential answer to the problem of resistance is to combine agents, explains Garcia-Manero, M.D., an expert in epigenetics and associate professor of leukemia.

Garcia-Manero was lead author of a major study published in the journal Blood late last year. It combined decitabine with valproic acid, an anti-convulsant drug used for epilepsy.

Valproic acid hits a different epigenetic target, Garcia-Manero explains, inhibiting the removal of chemical “on” switches – acetyl tags – that activate genes.

Combining the two drugs in a group of 54 AML and MDS patients was shown to be safe and effective, Garcia-Manero notes. Methyl “off” switches were stripped from DNA, and two types of histone acetylation were achieved and an important tumor-suppressing gene was reactivated.

Of 10 elderly MDS and AML patients, five responded to the combination, with four of them experiencing remission. Overall, 22% of patients got some relief from the combination, with 19% having complete remission. While the study was too small to draw conclusions about the drugs’ effectiveness, it points to the need for follow-up clinical trials.

“We’re testing a number of epigenetic agents that have exciting potential,” Garcia-Manero notes. His team has a paper pending in Blood that shows promising results with the combination of valproic acid, azacytidine and all-trans retinoic acid for AML and MDS patients. Overall, 42% of 53 patients showed some response to the three-drug combination, with 22% having complete remissions.

Garcia-Manero also is testing three other epigenetic agents, all of which protect acetyl “on” switches: vorinostat, MGCD0103 and LBH589.

Razelle Kurzrock, M.D., professor in the Department of Experimental Therapeutics and director of M. D. Anderson’s Phase I Clinical Trials Program, leads a clinical trial testing azacytidine and valproic acid in advanced metastatic cancers.

Issa remembers presenting a research poster on epigenetics to the 1992 annual meeting of the American Association for Cancer Research, “There was one other poster on the subject out of 4,000,” he says.

At this year’s AACR meeting, there were 500 posters on epigenetic approaches – genetic diplomacy marches on.

Genes Misbehaving


Cancer remains a disease of genes and genetic mutations, changes that drive cancer and make it hard to treat. But it’s also a disease of genetic expression – genes behaving badly – and that, Jean-Pierre Issa, M.D., explains, is where epigenetics comes in.

To understand epigenetics, you have to start at the beginning, at the embryonic stage. An embryo’s cells all have an identical set of genes. Its next job is to use those genes to differentiate cells into varied organs and tissues to build the body. This is accomplished with epigenetic signals that turn on the genes needed to create an organ while blocking other genes, explains Issa, professor in M. D. Anderson’s Department of Leukemia.

The crucial actors here are methyl groups (off switches) and acetyl groups (on switches). Methyl tags attach to specific areas of genes. Acetyl tags have a more complex story, connecting with histone proteins to turn genes on.

Histones wrap around DNA. This histone-DNA combination forms the chromatin complex, which in turn composes chromosomes. When acetyl groups attach to histones, they turn on the accompanying gene. When acetyl tags are removed, the histone tightens around genes, turning them off.

Epigenetic drugs wipe out the methyl groups temporarily or block the stripping of acetyl groups from histones.

While some cancers are tied to inherited genetic variations, others are launched by damage to DNA. Mutated or damaged genes generally are impervious to repair by treatment. Therapies generally target these cells for death. Genes that are suppressed, Issa notes, can be manipulated through epigenetics – a more diplomatic approach.

“Our genome is set. It can’t be modified. Our epigenome is more dynamic. It’s something we can affect with epigenetic drugs or by our behavior,” Issa says.

Think of genes as hardware and epigenetics as the operating system software, explains Cheryl Lyn Walker, Ph.D., professor in M. D. Anderson’s Department of Carcinogenesis at the Virginia Harris Cockrell Cancer Research Center in Smithville, Texas.

External carcinogenic factors such as diet, tobacco use or environmental toxins can cause cancer both via direct DNA damage and epigenetic effects, Walker says. She and her colleagues are focusing on all suspects that turn normal cells into cancer cells.

Walker, for example, studies genetic predisposition to cancer and how cancer-causing chemicals, or carcinogens, interact with genetic factors to cause cancer.

She examines the impact of xenoestrogens – chemicals present in our environment that act like estrogens – which are taken in through environmental exposures or in food, such as a plant phytoestrogen that is present in soy. Walker studies how exposure to xenoestrogens affects the development of uterine fibroids. Fibroids occur in upwards of 50% to 75% of women, and these tumors are the principal reason for hysterectomy in women of reproductive age.

Working in a rodent model, Walker found that those with a genetic predisposition to develop fibroids and who are exposed to environmental estrogens at crucial times during development have dramatically increased risk of developing tumors later.

“This is called developmental reprogramming. When you disrupt a tissue while it’s developing, you worsen the risk of disease in adulthood,” Walker says. “We’re finding that for this type of environmental exposure, it’s all about timing.”

Reprogramming probably is accomplished through an epigenetic mechanism, Walker says, and so may be susceptible to epigenetic treatment.

Interestingly, Issa has found that methyl tags accumulate over time, shutting down genes. It’s a tantalizing possible connection to aging, he says, but that’s another story.

Epigenetics — By Definition:

Acetylation: a reaction that introduces an acetyl group into a molecule of an organic compound. Acetyl tags work by connecting to specific proteins and act as a genetic on switch.

Demethylation: the chemical process of removing a methyl group from a molecule, which, in turn, can reactivate tumor-suppressor genes that are silenced by methylation.

Epigenetics: the study of changes in gene expression and cellular behavior that are not caused by physical damage or mutation of the genes themselves.

Methylation: an enzyme-mediated chemical modification that adds methyl groups at selected sites on proteins, DNA and RNA. Methyl tags work by attaching to specific areas of genes and act as a genetic off switch.

. . . . . . . . .

(NewsWise, Medical News, Source: University of Texas MD Anderson Cancer Center, April 3, 2008)

Disclaimer:

The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.

[New Dawn for Research: Surviving Cancer, Living with Pain?]

http://www.newswise.com/articles/view/539433/

ARTICLE:

. . . . . . . . .

Newswise — With two out of three adult cancer patients surviving their disease, researchers are finding they need to widen their focus beyond effective, life-saving treatments. Surviving with poor quality of life and heavy symptom burden is increasingly unacceptable in a world in which 22.4 million people have survived cancer.

Fatigue, cognitive deficit, sleep disturbance and neuropathic pain are just some of the side effects with which survivors must deal. Yet, historically, there has been little research to understand the biologic mechanisms that cause them, the patients who are most susceptible to developing them or what kind of interventions might alleviate them.

“The problem is that many areas of importance to patients, especially side effects, have not been funded by the National Cancer Institute or the National Institutes of Health,” says Charles Cleeland, Ph.D., chair of the Department of Symptom Research at M. D. Anderson.

Paving way for new studies

This situation has brought about new opportunities for cancer research: a recent alliance between a pharmaceutical company, AstraZeneca, and a research-oriented cancer center, M. D. Anderson, in which “AstraZeneca has given us full freedom to design these studies,” says Cleeland, who is co-principal investigator on this multifaceted study.

In the best of all worlds, these two entities would have joined hands long ago and worked in tandem to study and discover new treatments for cancer and the side effects of its treatments. However, collaborations between for-profit companies and non-profit institutions usually brought up the potential for conflict of interest.

So what has changed?

“Today, in the face of limited federal funding and squeezes on the NIH’s budget, research grants, especially in the area of reducing or preventing symptoms, are harder to obtain than ever before. Collaborating with AstraZeneca allows us to continue working toward helping our patients. But rest assured, M. D. Anderson and The University of Texas System have put extensive safeguards and conflict-of-interest policies and committees in place to help carefully cultivate relationships with the pharmaceutical industry,” Cleeland says.

The development of strategic alliance relationships such as this one between

M. D. Anderson and AstraZeneca helps to combine the unique strengths of both partners to more effectively bring the newest drugs to patients faster.

The pharmaceutical industry benefits by obtaining early input on clinical needs, insight on research and drug development and access to academe’s faculty expertise. Likewise, M. D. Anderson also benefits by gaining access to various resources as well as some of the industry’s top neuroscientists within the company.

Filling a critical need

One of the foremost side effects to be studied under the terms of this agreement is chemotherapy-induced neuropathy, a common problem for patients receiving certain kinds of chemotherapy, such as paclitaxel, docetaxel, cisplatin, oxaliplatin, vincristine, thalidomide and bortezimib. If two or more of these agents are given in combination, the toxicity and potential for nerve damage increases.

“For up to 40 percent of patients who experience this distressing problem, it may: a) limit the amount of chemotherapy he or she can receive, and become a chronic pain problem for some smaller percent of those patients,” says Allen Burton, M.D., professor and clinical medical director of M. D. Anderson’s Pain Management Center.

Together, he and Patrick Dougherty, Ph.D., professor in the Department of Anesthesiology and Pain Medicine, hope to identify neurobiologic differences between cancer patients who develop neuropathy and those who have little or no pain. This could give them a better understanding of the biologic mechanisms that cause this peripheral nerve damage, then help them design appropriate interventions.

“If we can limit toxic effects on the nervous system and thereby give full chemotherapy regimens, we may increase a patient’s survival, and hopefully also eliminate the long-term chronic symptoms that survivors deal with,” say Dougherty, co-principal investigator with Cleeland on these studies.

Reducing the symptom burden

This project also will study such treatment-related symptoms as cognitive deficit, fatigue and sleep disturbance, and explore potential common biologic mechanisms that may underlie these distressing symptoms.

This research also could lead to new treatments to prevent pain, extending the therapeutic value of current chemotherapies, as well as help in the development of new chemotherapies with less severe pain-related side effects.

“Our collaboration with AstraZeneca presents a unique opportunity to study ways of making cancer therapy much more tolerable,” Cleeland says. “Our overarching goal is to reduce the symptom burden of survivorship.”

. . . . . . . . .

(NewsWise, Source: University of Texas, MD Anderson Cancer Center, April 3, 2008)

Disclaimer:

The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.

[budget cuts and Less research Money!]

Randy,

First, let me thank you for posting this. You are amazingly perceptive.

This news is "business as usual." I have been reading here and there, and everywhere that funding crunches have been in the mix for ever so long.

Of course, we hate hearing this. It's an abomination. Mainly, this is so abhorrent due to it having gone on for ever so very long in the case of lung cancer research.

Lung Cancer is the "anathema" of cancers. Public perception is that those who develop it are the initiators of their own illness. What a cop-out not to fund research.

This has got to change. Where are the public entertainers out there to push the judgemental-ism out of the picture?

They did it for HIV/AIDS. They were the "changers of public opinion". Where are they for those with lung cancer? Come on guys, help us out with this killer.

NO ONE DESERVES LUNG CANCER.

Barbara

[Nano-sized Technology Has Super Effect on Tumors]

http://www.newswise.com/articles/view/539380/?sc=dwhn

ARTICLE:

. . . . . . . . .

Newswise — Anyone facing chemotherapy would welcome an advance promising to dramatically reduce their dose of these often harsh drugs. Using nanotechnology, researchers at Washington University School of Medicine in St. Louis have taken a step closer to that goal.

The researchers focused a powerful drug directly on tumors in rabbits using drug-coated nanoparticles. They found that a drug dose 1,000 times lower than used previously for this purpose markedly slowed tumor growth.

"Many chemotherapeutic drugs have unwanted side effects, and we've shown that our nanoparticle technology has the potential to increase drug effectiveness and decrease drug dose to alleviate harmful side effects," says lead author Patrick M. Winter, Ph.D., research assistant professor of medicine and biomedical engineering.

The nanoparticles are extremely tiny beads of an inert, oily compound that can be coated with a wide variety of active substances. In an article published online in The FASEB Journal, the researchers describe a significant reduction of tumor growth in rabbits that were treated with nanoparticles coated with a fungal toxin called fumagillin. Human clinical trials have shown that fumagillin can be an effective cancer treatment in combination with other anticancer drugs.

In addition to fumagillin, the nanoparticles' surfaces held molecules designed to stick to proteins found primarily on the cells of growing blood vessels. So the nanoparticles latched on to sites of blood vessel proliferation and released their fumagillin load into blood vessel cells. Fumagillin blocks multiplication of blood vessel cells, so it inhibited tumors from expanding their blood supply and slowed their growth.

Human trials have also shown that fumagillin can have neurotoxic side effects at the high doses required when given by standard methods. But the fumagillin nanoparticles were effective in very low doses because they concentrate where tumors create new blood vessels. The rabbits that received fumagillin nanoparticles showed no adverse side effects.

Senior author Gregory M. Lanza, M.D., Ph.D., associate professor of medicine and of biomedical engineering, and Samuel A. Wickline, M.D., professor of medicine, of physics and of biomedical engineering, are co-inventors of the nanoparticle technology. The nanoparticles measure only about 200 nanometers across, or 500 times smaller than the width of a human hair. Their cores are composed mostly of perfluorocarbon, a safe compound used in artificial blood.

The nanoparticles can be adapted to many different medical applications. In addition to carrying drugs to targeted locations, they can be manufactured to highlight specific targets in magnetic resonance imaging (MRI), nuclear imaging, CT scanning and ultrasound imaging.

In this study, researchers loaded blood-vessel-targeted nanoparticles with MRI contrast agent and were able to make detailed maps of tumor blood vessel growth using standard MRI equipment. The MRI scans showed that blood vessel formation tended to concentrate in limited areas on the surface at one side of tumors instead of dispersing uniformly, which was a surprise.

"Using the blood-vessel targeted nanoparticles, we get a far more complete view of tumor biology than we would get with any other technique," Winter says. "If you followed a tumor over a period of time with the nanoparticles and MRI scans, you would have a much better understanding of the tumor's reaction to treatment."

The researchers say they believe nanoparticle technology will be very useful for monitoring cancer treatment results in both the short and long term.

"It gives you a way of determining whether you should continue treatment, change the dose or even try a different treatment altogether," Lanza says.

Prior work has shown that the nanoparticles can be loaded with many kinds of drugs. The researchers used fumagillin nanoparticles in these experiments to demonstrate the feasibility of this approach, but they plan further investigations with other versions of the nanoparticles.

"What this report clearly demonstrates is that our nanoparticles can carry chemotherapeutic drugs specifically to tumors and have an effect at the tumor site," Lanza says. "Sometimes when I give presentations about our nanotechnology, people react as if it was science fiction or at best a technology of the distant future. But we've shown that the technology is ready for medical applications now."

The nanoparticles will be tested this year in preliminary human clinical trials to determine the optimal method for using them as imaging agents. These studies will lay essential groundwork for using the nanoparticles as therapeutic agents.

Winter PM, Schmieder, AH, Caruthers SD, Keene JL, Zhang H, Wickline SA, Lanza GM. Minute dosages of αvβ3-targeted fumagillin nanoparticles impair Vx-2 tumor angiogenesis and development in rabbits. The FASEB Journal. March 24, 2008 (advance online publication).

The nanotechnology is owned by Barnes-Jewish Hospital and Washington University and licensed to Kereos Inc, a St. Louis-based company. Gregory M. Lanza and Samuel A. Wickline are scientific cofounders of Kereos.

Funding from the National Cancer Institute, the National Heart, Lung, and Blood Institute, the National Institute for Biomedical Imaging and Bioengineering, Philips Medical Systems and Philips Research supported this research.

Washington University School of Medicine's 2,100 employed and volunteer faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Children's hospitals. The School of Medicine is one of the leading medical research, teaching and patient care institutions in the nation, currently ranked third in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Children's hospitals, the School of Medicine is linked to BJC HealthCare.

. . . . . . . . .

(NewsWise, Medical News, Source: Washington University in St. Louis, April 2, 2008)

Disclaimer:

The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.

[One Year On Tarceva!]

Deanne,

I LOVED your posting about you and your husband. What a wonderful celebration you must be having!

Congratulations, and continued success. You are a lovely couple and I especially admire your tenacity. Great going there. This stuff is food for the soul.

It definitely lifted my spirits.

Excelsior,

Barbara

[Metatistatic Lung Cancer]

"John Caskey"]Greetings, my name is John

Hello John,

I welcome you to a truly informative, warm and caring group. This is a very responsive message board, knowledgeable, as well.

Please let us know how it is going with your wife. My husband is a Stage IV survivor (3yrs. 4 mos. since diagnosis).

We are LIVING with lung cancer.

Gambaru (Japanese for never, never, never, never ... give up even when told "impossible")

Barbara

[Scientists Solve Mystery of Polyketide Drug Formation]

http://www.sciencedaily.com/releases/20 ... 112350.htm

ARTICLE:

. . . . . . . . .

ScienceDaily (Apr. 1, 2008) — Many top-selling drugs used to treat cancer and lower cholesterol are made from organic compounds called polyketides, which are found in nature but historically difficult for chemists to alter and reproduce in large quantities.

For the first time, scientists at UC Irvine have discovered how polyketides form their ringlike shape, making it easier for chemists to manipulate them into new drugs.

The key, they found, is an enzyme called aromatase/cyclase, which forms a C-shape mold in which polyketides can form one molecule at a time. By changing this mold, chemists can control the size and shape of the polyketide, resulting in the formation of new drugs.

“Almost every polyketide has rings in its chemical structure, and if we can control ring formation, we can produce more polyketide drugs,” said Sheryl Tsai, lead author of this study and an assistant professor of molecular biology and biochemistry and chemistry at UCI. “Until now, polyketide ring formation was a mystery that hampered our efforts to produce new drugs.”

Polyketide-based drugs and products account for more than $35 billion in sales annually. They include antibiotics that can cure a bacteria infection (tetracycline and erythromycin); anti-cancer drugs used in chemotherapy (doxorubicin and mithramycin); anti-oxidants that help prevent cancer and promote heart strength (EGCG and resverastrol); and drugs that lower cholesterol levels (Zocor). Green tea and red wine also contain beneficial polyketides.

Polyketides are made naturally by bacteria, fungi, plants and marine animals. Those organisms produce polyketides to kill their predators, be it another bacteria or fungi. They can produce different types of polyketides that kill different types of enemies.

“Because bacteria do not have arthritis or diabetes, they would not evolutionally select polyketides that could be used for arthritis or diabetes treatment,” Tsai said. “But we can coax the bacteria to do precisely that, if we can control the ring formation in the polyketides.”

Prior to this study, it was not known how nature controls the polyketide ring shape, which is essential for antibiotic and anti-cancer properties.

By using molecular cloning and chemical biology techniques, Tsai and her scientific team discovered that the aromatase/cyclase enzyme has a pocket that shapes the polyketide, promoting a unique ring pattern.

Said Tsai: “We hope this will lead to the development of new drugs in such areas as cancer therapeutics, obesity treatment and stem cell research.”

The research appears online in the Proceedings of the National Academy of Sciences. UCI scientists Brian Ames, Tyler Korman, Peter Smith, Thanh Vu, along with UCLA researchers Yi Tang and Wenjun Zhang, also worked on this study, which was funded by the Pew Foundation and the National Institutes of Health.

Adapted from materials provided by University of California - Irvine.

. . . . . . . . .

(Science Daily, Latest Research News, Source: University of California - Irvine, April 1, 2008)

Disclaimer:

The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.

[Bill Just Completed Third Round]

Dear Sharon,

Keep that positive thinking going. That is key. Without it, we have negativity, which can compromise the immune system.

Just to put my imprimater on my statement, I can develop a cold sore on my lip when under stress, and/or shingles when under severe stress.

We know this inately, but we are human, and fall prey to doubts. Yes, they are there, but not being given too much headway. We are LIVING with lung cancer.

Those prayers are so very appreciated. There is power in that - lots of power, and we need them.

We will keep doing what we are doing. This week it's getting up every morning to get over to the cancer center for Bill's Neupogen injection.

Today following that, we made a swing over to our son's house to give him his birthday present, and then on home to feed the cats (two), and complete some errands.

We are being strong.

Many blessings are wished for you, Sharon,

Barbara

[Bill Just Completed Third Round]

Hello Linda,

I am so glad that you are able to reply and work the message board. You need the support as I know I do. Receiving answers and suggestions during this is crucial.

It is the connection to others who have walked this walk that helps immeasurably.

Please keep posting, Linda, and letting others know the remarkable journey you have experienced, and it is truly remarkable.

Thank you for giving me a "hello." I appreciate your thoughtfulness. It gave me a smile.

Love you,

Barbara

[How to Support a Loved One with Lung Cancer]

http://online.wsj.com/article/SB120700289277678397.html

Article:

. . . . . . . . .

How to Support a Loved One

Reeling From Cancer Diagnosis

By ELIZABETH BERNSTEIN

April 1, 2008; Page D1

A few years ago, my sister called to tell me my mother had just been diagnosed with leukemia. After we hung up and I prepared to call my mom, I realized I had absolutely no idea what to say to her. It took me four hours to make the call.

I learned a lasting lesson that day: There isn't anything correct to say to someone reeling from the shock of a cancer diagnosis. But in helping my mom through her illness, I also discovered that some ways of showing support are better than others. And while there's no right approach, there may indeed be wrong things to say or do.

Even as the medical community has gotten better at detecting and treating cancer early -- allowing many patients to live longer -- people are understandably overwhelmed by the devastating news of a diagnosis. So family and friends grapple with how to best offer comfort.

Not every cancer patient wants the same type of support. Some want to talk about their illness and accept help willingly. Others struggle to preserve their independence and behave, at least outwardly, as if nothing is wrong.

So how do you know how best to offer assistance to someone struggling with a serious illness? I posed this question to oncologists, psychologists and patients.

"Loved ones don't know what to do, and they don't want to make a terrible error," says Marisa Weiss, an oncologist and founder of Breastcancer.org, a nonprofit organization. "This fear keeps people from doing anything."

While that's the worst mistake you can make, experts say, there are a number of other slip-ups. Well-meaning friends and family members often ask inappropriate questions, such as the patient's prognosis. They offer theories on why their loved one got sick, give unsolicited advice or insist that "everything is going to be just fine."

When Lori Hope was diagnosed with lung cancer in 2002, she says many people asked her if she had been a smoker. Some told her of people they knew who had died of cancer. One friend asked why she was going on vacation since she would probably worry the whole time. "People tend to rush in without thinking," she says.

In response, Ms. Hope wrote a book, "Help Me Live: 20 Things People with Cancer Want You to Know." Her advice: Admit you don't know what to say. Apologize in advance for doing or saying anything upsetting. Then be sure to tell your friend you will be there for her.

"Bumbling is OK," says Susan Brace, a psychologist in Evergreen, Colo., whose specialty is treating terminally ill patients. "You're in a situation you've never been in before, so you make up the rules as you go along."

In general, experts say, you should take your lead from the person who is sick. If she wants to talk about her illness, then listen. Don't be afraid of emotions. "Being there, listening and being supportive is a powerful role," Dr. Weiss says. "If the person feels comfortable crying in front of you, be honored, because you fulfilled a really important need."

It's critical not to treat your friend just as a patient. So remember to ask about other aspects of her life, such as her children. Ask her permission before you share news of her illness with others. Don't recommend books or treatments without first inquiring if she'd like to hear about them.

You should also ask exactly what type of help your loved one needs. You can offer to pick up groceries, provide transportation or return phone calls. And don't be deterred if your offer of help is declined. People who are diagnosed with a major illness often don't know what they will need at first. In addition, accepting help can be frightening for people accustomed to being independent. Keep offering help.

And if your friend, co-worker or family member isn't returning calls, don't take it personally. She may not have the energy or time to call you back. Stay in touch anyway.

As cancer awareness has grown in recent years, so have the resources to help people offer support to patients. Web sites for the American Cancer Society (www.cancer.org) and the National Cancer Institute (www.cancer.gov) offer information for caregivers, family and friends. There are books, too: "Help Me Live," by Ms. Hope; "What Can I Do to Help," by Deborah Hutton; "Cancer Etiquette," by Rosanne Kalick; "The Etiquette of Illness," by Susan P. Halpern.

In short, there is help for people who want to help their friends and loved ones. "You should be there for your friends," says Howard Leventhal, professor of psychology at Rutgers University and director of the Center for the Study of Health Beliefs and Behavior. "And being there doesn't require much more than enduring their pain and trying to be useful."

. . . . . . . . .

(WSJ, Health Journal, Elizabeth Bernstein, April 1, 2008)

Disclaimer:

The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.

[connect with survirvors with similar condition]

Hello Margot ,

I offer you a warm welcome. You have come to a very caring and informative community.

All the best,

Barbara

[Study: Scientists Pinpoint Genetic Link to Tobacco Addiction]

http://www.courierpostonline.com/apps/p ... 006/news01

. . . . . . . . .

Researchers find 'double whammy' gene tied to smoking dependency

WASHINGTON (AP) -- Scientists have pinpointed a genetic link that makes people more prone to get hooked on tobacco, smoke more cigarettes longer, and develop deadly lung cancer.

The discovery by three separate teams of scientists makes the strongest case so far for the biological underpinnings of the addiction of smoking and how genetics and cigarettes combine in cancer, experts said. And it may lay the groundwork for more tailored quit-smoking treatments.

"This is kind of a double whammy gene," said Christopher Amos, a professor of epidemiology at the M.D. Anderson Cancer Center in Houston and author of one of the studies. "It also makes you more likely to be dependent on smoking and less likely to quit smoking."

A smoker who inherits this genetic variation from both parents has an 80 percent greater chance of lung cancer than a smoker without the variants, the researchers reported. And that same smoker on average lights up two extra cigarettes a day and has a much harder time quitting than smokers who don't have these genetic differences.

The three studies, funded by governments in the U.S. and Europe, is being published Thursday in the journals Nature and Nature Genetics.

The scientists surveyed genetic markers in more than 35,000 people in Europe, Canada and the United States, zeroing in on the same set of genetic differences. They aren't quite sure if what they found is a set of variations on one gene or on three closely connected genes. But they said the result is the same: These genetic quirks increase the risk of addiction and lung cancer.

The studies' authors disagreed on whether the set of variants directly increased the risk of lung cancer or did so indirectly by causing more smoking that led to the cancer.

The genetic variations, which encode nicotine receptors on cells, could eventually help explain some of the mysteries of chain smoking, nicotine addiction and lung cancer that can't be chalked up to environmental factors, brain biology and statistics, experts said. These oddities include why there are 100-year-old smokers who don't get cancer and people who light up an occasional cigarette and don't get hooked.

In the last 40 years, the rate of adult Americans smoking has been cut from 42 percent in 1965 to less than 21 percent now.

The new studies point to surprising areas of the genes not associated with pleasure and addiction rewards. That may help explain why people have trouble quitting, said Dr. Nora Volkow, director of the National Institute of Drug Abuse in Bethesda, Md., which funded one of the studies. Eventual testing for the genetic variants could lead to custom treatments for quitting smoking.

"This is really telling us that the vulnerability to smoking and how much you smoke is clearly biologically based," said psychiatry professor Dr. Laura Bierut, of Washington University in St. Louis, and a genetics and smoking expert who did not take part in the studies. She praised the research as "very intriguing."

The studies mostly looked at smokers and ex-smokers -- although two of the studies also looked at several hundred nonsmokers. The research only involved white people of European descent. People of Asian and African descent will be studied soon and may yield quite different results, scientists said. Smoking-related diseases worldwide kill about one in 10 adults, according to the World Health Organization.

The studies show on average the consequences of the set of variations in the alphabet of genetic code that people inherit from each parent:

-- Smokers who get the set of variants from only one parent see a risk of lung cancer that is about one-third higher than people without any variants. They also smoke about one more cigarette a day on average than other smokers. This group makes up about 45 percent of the population studied.

-- Smokers who inherit the variants from both parents have almost a one in four chance of developing lung cancer. Their risk is between 70 and 80 percent higher than the cancer risk of other smokers without the genetic variants. They smoke on average of two extra cigarettes a day, and have a 45 percent higher risk of peripheral artery disease. This group accounts for about one in nine people of European descent.

-- Smokers who don't have the variants are still more than 10 times more likely to get lung cancer than nonsmokers. Smokers without the variant overall have about a 14 percent risk of getting lung cancer. By comparison the risk of lung cancer for people who have never smoked is less than 1 percent, said another study author, Paul Brennan of the International Agency for Research on Cancer in Lyon, France.

Brennan and Amos, working on different teams, linked the genetic variation itself -- when triggered by smoking -- directly to lung cancer. Brennan said the nicotine receptors that the variants act on also can stimulate tumor growth.

Brennan's study also found that lung cancer risk for nonsmokers with the variants was higher than for those without the variants. However, his small sample size of nonsmokers requires further study. Amos' study didn't find increased lung cancer risk for people with the set of variants who have never smoked.

But Kari Stefansson, lead author of the largest of the three studies and chief executive of deCode Genetics of Iceland, said the increased lung cancer risk was indirect, and that the variant caused more addiction and more smoking. It was the extra cigarettes from increased daily smoking and the inability to quit that contributed to the higher cancer risk, Stefansson said.

"It's very likely that in the end there's going to be a test and this is going to be folded into a panel of tests for the risk of cancers," said Stefansson, whose company already does prostate cancer genetic tests. The tests will lead to better treatments, but probably not prevention of smoking, he said.

Stefansson and others emphasize that people without the variants should not take that genetic finding as a green light to smoke. There are other smoking-related diseases and they would still be at high risk of lung cancer.

For Stefansson, the research hits home. His father, a smoker, died of lung cancer. And Stefansson, who doesn't smoke, frequently lectures his 23-year-old daughter "who smokes like a chimney." She acts like she is immortal and smoking can't kill her, Stefansson said. But his own research shows that her genes are probably stacked against her.

. . . . . . . . .

(CourierPostOnline.com, South Jersey, Seth Borenstein, AP, April 2, 2008)

Disclaimer:

The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.

[Study: Researchers Develop New Way to Test for Lung Cancer]

http://www.eurekalert.org/pub_releases/ ... 040108.php

Boston University

"Researchers develop new method to test for lung cancer

Boston, MA--Researchers from Boston University School of Medicine have developed a new “clinicogenomic model” to accurately test for lung cancer. The model combines a specific gene expression for lung cancer as well as clinical risk factors. These findings currently appear on-line in the journal Cancer Prevention Research.

Lung cancer is the leading cause of cancer death in the United States and the world, with more than one million deaths worldwide annually. Eighty-five to 90 percent of subjects with lung cancer in the United States are current or former smokers with 10 to 20 percent of heavy smokers developing this disease.

A previous study by the same researchers reported a gene expression biomarker capable of distinguishing cytologically normal large airway epithelial cells from smokers with and without lung cancer. However, the biomarker has limited sensitivity depending on the stage and the location of the cancer.

Studying current and former smokers undergoing bronchoscopies for suspicion of lung cancer, the researchers compared the likelihood of the subjects having lung cancer using the biomarker, the clinical risk factors and a combination of the two -- clinicogenomic model. They found patients using the clinicogenomic model had increased sensitivity, specificity, positive value and negative predictive value of their cancer compared to the other methods.

“Our data suggests that the clinicogenomic model might serve to identify patients who would benefit from further invasive testing, thereby expediting the diagnosis and treatment for their malignancy,” said senior author Avrum Spira, MD, an assistant professor of medicine and pathology at Boston University School of Medicine.

According to the researchers, it is hoped this prediction model will expedite more invasive testing and appropriate therapies for smokers with lung cancer as well as reduce invasive diagnostic procedures for individuals without lung cancer.

###

Funding for this study was provided by the Doris Duke Charitable Foundation and National Institutes of Health and National Cancer Institute grants.

Spira is a pulmonary and critical care medicine physician at Boston Medical Center and is one of the founders of Allegro Diagnostics Inc., a molecular diagnostics company that plans to market the gene expression biomarker."

(Eureka Alert, Press Release, April 1, 2008)

Disclaimer:

The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.

[Ongoing Research Study: The Silver Shield]

http://www.newswise.com/articles/view/539044/?sc=dwhn

"Warning: FOR CLINICIANS AND PATIENTS

Fasting before chemotherapy has unknown risks and benefits for humans, Longo cautioned. Only clinical trials can establish the effectiveness and safety of fasting before chemotherapy.

“Don’t try and do this at home. We need to do the studies,” said Quinn, the USC Norris oncologist."

ARTCLE: Contains Video.

"Newswise — Fasting for two days protects healthy cells against chemotherapy, according to a study appearing online the week of Mar. 31 in PNAS Early Edition.

Mice given a high dose of chemotherapy after fasting continued to thrive. The same dose killed half the normally fed mice and caused lasting weight and energy loss in the survivors.

The chemotherapy worked as intended on cancer, extending the lifespan of mice injected with aggressive human tumors, reported a group led by Valter Longo of the University of Southern California.

Test tube experiments with human cells confirmed the differential resistance of normal and cancer cells to chemotherapy after a short period of starvation.

Making chemotherapy more selective has been a top cancer research goal for decades. Oncologists could control cancers much better, and even cure some, if chemotherapy were not so toxic to the rest of the body.

Experts described the study as one of a kind.

“This is a very important paper. It defines a novel concept in cancer biology,” said cancer researcher Pinchas Cohen, professor and chief of pediatric endocrinology at the University of California, Los Angeles.

“In theory, it opens up new treatment approaches that will allow higher doses of chemotherapy. It’s a direction that’s worth pursuing in clinical trials in humans.”

Felipe Sierra, director of the Biology of Aging Program at the National Institute on Aging, said: “This is not just one more anti-cancer treatment that attacks the cancer cells. To me, that’s an important conceptual difference.”

Sierra was referring to decades of efforts by thousands of researchers working on “targeted delivery” of drugs to cancer cells. Study leader Longo focused instead on protecting all the other cells.

Sierra added that progress in cancer care has made patients more resilient and able to tolerate fasting, should clinical trials confirm its usefulness.

“We have passed the stage where patients arrive at the clinic in an emaciated state. Not eating for two days is not the end of the world,” Sierra said.

“This could have applicability in maybe a majority of patients,” said David Quinn, a practicing oncologist and medical director of USC Norris Hospital and Clinics. He predicted that many oncology groups would be eager to test the Longo group’s findings, and advised patients to look for a clinical trial near home.

Longo, an anti-aging researcher who holds joint appointments in gerontology and biological sciences at USC, said that the idea of protecting healthy cells from chemotherapy may have seemed impractical to cancer researchers, because the body has many different cells that respond differently to many drugs.

“It was almost like an idea that was not even worth pursuing. In fact it had to come from the anti-aging field, because that’s what we focus on: protecting all cells at once,” Longo said.

“What really was missing was a perspective of someone from the aging field to give this field a boost,” UCLA’s Cohen said.

The idea for the study came from the Longo group’s previous research on aging in cellular systems, primarily lowly baker’s yeast.

About five years ago, Longo was thinking about the genetic pathways involved both in the starvation response and in mammalian tumors.

When the pathways are silenced, starved cells go into what Longo calls a maintenance mode characterized by extreme resistance to stresses. In essence the cells are waiting out the lean period, much like hibernating animals.

But tumors by definition disobey orders to stop growing because the same genetic pathways are stuck in an “on” mode.

That could mean, Longo realized, that the starvation response might differentiate normal and cancer cells by their stress resistance, and that healthy cells might withstand much more chemotherapy than cancer cells.

The shield for healthy cells does not need to be perfect, Longo said. What matters is the difference in stress resistance between healthy and cancerous cells.

During the study, conducted both at USC and in the laboratory of Lizzia Raffaghello at Gaslini Children’s Hospital in Genoa, Italy, the researchers found that current chemotherapy drugs kill as many healthy mammalian cells as cancer cells.

“(But) we reached a two to five-fold difference between normal and cancer cells, including human cells in culture. More importantly, we consistently showed that mice were highly protected while cancer cells remained sensitive,” Longo said.

If healthy human cells were just twice as resistant as cancer cells, oncologists could increase the dose or frequency of chemotherapy.

“We were able to reach a 1,000-fold differential resistance using a tumor model in baker’s yeast. If we get to just a 10-20 fold differential toxicity with human metastatic cancers, all of a sudden it’s a completely different game against cancer,” Longo said.

“Now we need to spend a lot of time talking to clinical oncologists to decide how to best proceed in the human studies.”

Edith Gralla, a research professor of chemistry at UCLA, said: “It is the sort of opposite of the magic bullet. It’s the magic shield.”

Funding from the study came from NIA (part of the National Institutes on Health), the USC Norris Cancer Center and the Associazione Italiana per la Lotta al Neuroblastoma.

USC graduate student Changhan Lee and Gaslini’s Raffaghello performed key experiments. The other authors were Fernando Safdie, Min Wei and Federica Madia of USC, and Giovanna Bianchi of Gaslini.

Longo has been studying aging at the cellular level for 15 years, and has published in the nation’s leading scientific journals. He is the Albert L. and Madelyne G. Hanson Family Trust Associate Professor in the USC Leonard Davis School of Gerontology with joint appointments as associate professor of biological sciences in the USC College of Letters, Arts and Sciences, and in the Norris Cancer Center."

(NewsWise, Medical News, Source: University of Southern California, March 31, 2008)

Disclaimer:

The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.

[Bill Just Completed Third Round]

"alexan"]Hey barbara Ellen, welcome bCK. i USED TO REAd your Blogs & answers in the othe one. You are a such a wonderfull & helpfull person tha eerybody will love both of you here

hugs bucky

Hello Bucky ,

Thank you for the very kind and positive welcome. As you may imagine, I am very happy to be here.

I feel connected to support again. Being out there with no safety line, even for a little bit, was unsettling.

Thanks again to you, and all for throwing me the lifesaver.

Hugs to you, Bucky,

Barbara

[Update on my mom]

"Robbi"]My mom passed away at 9:15 this morning. I can't believe how fast the time went from her diagnosis. I am so sad, but realize she is in a better place AND is now reunited with my dad.

Thank you for your prayers

Robbi

Dear Robbi,

Please accept my condolences. You and your family are in my thoughts and my prayers.

I am so very sorry for your loss.

Barbara

[FDA Alerting about Chantix (varenicline) Stop Smoking Drug]

http://www.accessdata.fda.gov/scripts/c ... ?show=74#3

FDA is alerting healthcare professionals about new safety warnings for Chantix (varenicline), a drug used to help people stop smoking.

Chantix has been linked to serious neuropsychiatric problems, including changes in behavior, agitation, depressed mood, suicidal ideation and suicide. The drug can cause an existing psychiatric illness to worsen, or an old psychiatric illness to recur. The symptoms can occur even after the drug is discontinued.

People who are trying to give up smoking often experience mood swings, irritability and other changes in behavior. But as the reports accumulate, it becomes clearer that there is a link with the drug. For example, some of the patients who experienced these psychiatric symptoms hadn't actually quit smoking.

Physicians and patients have to make an informed decision about whether Chantix is suitable, but in order to do that, it's important that they exchange some important information. For example, physicians should inquire about past psychiatric illnesses before they prescribe Chantix, and patients should be educated to volunteer this information. The premarketing studies of Chantix did not include patients with serious psychiatric illnesses, so the safety of Chantix in these patients hasn't been established.

It is also important for everyone involved in the patient's care (including family members and caregivers) to be vigilant about changes in mood and behavior during the treatment. Things to watch out for include anxiety, nervousness, depressed mood, vivid or unusual dreams, and thinking about or attempting suicide. These changes should be immediately reported to the physician.

Patients should also know that the drug can impair their ability to drive or operate heavy machinery.

To help educate patients about all of these issues, FDA is working with Pfizer, the manufacturer of Chantix, to develop a Medication Guide that will be dispensed with each prescription.

(FDA Alert, April 2008)

Additional Information:

FDA MedWatch Safety Alert. Varenicline (marketed as Chantix). February 1, 2008.

http://www.fda.gov/medwatch/safety/2008 ... arenicline

FDA Press Release. FDA Issues Public Health Advisory on Chantix. February 1, 2008.

http://www.fda.gov/bbs/topics/NEWS/2008/NEW01788.html

Disclaimer:

The information contained in these articles may or may not be in agreement with my own opinions. They are not posted as medical advice of any kind.