Barb73

Thank you for posting to let us know about this, Randy, It is a beautiful idea. In fact, it would be an excellent gift for any occasion of celebration. It has given me a few ideas for gifts for the special women in our lives. Barbara

http://seattlepi.nwsource.com/local/357 ... apy07.html ARTICLE: . . . . . . . . . By TOM PAULSON P-I REPORTER Researchers at the University of Washington and the Fred Hutchinson Cancer Research Center are trying to trick a strain of the cold virus into killing several kinds of cancer, including a notoriously difficult-to-treat brain tumor. "There are not many options out there for these patients," said Dr. Hans-Peter Kiem at Fred Hutch, noting that most people with this kind of tumor, glioblastoma multiforme, die within a year of diagnosis. So far, the scientists have only been able to use the viruses to attack the brain tumors in mice. The concept of employing viruses as biological anti-cancer smart bombs, though it may sound bizarre, has been around for quite a while. "It's not a new idea," said Dr. Andre Lieber, a researcher at the University of Washington and a leader in this field. But Lieber and others are using innovative genetic techniques to retrain the common cold virus, known as adenovirus. Some say the notion of enlisting infections to fight cancer first took hold back in 1912, when a rabid dog bit an Italian woman who had advanced ovarian cancer. Italian doctors injected the woman with a weakened rabies virus, a vaccine, to protect her against the deadly infection. And after the immunization, to everyone's surprise, her aggressive ovarian tumor also shrank back. This is often cited as the first scientific report of the possibility that viral infections or vaccinations might somehow work against cancer. There had been earlier anecdotal stories about people with cancer being cured after getting this or that bug, but not much hard evidence. "It wasn't until the 1950s and '60s that it really took off," Lieber said. Scientists in the '50s and '60s tried injecting cancer patients with all sorts of live viruses such as mumps or the cold virus, he said, but without really knowing exactly what was going on inside the body. If you consider what cancer really is and what viruses do, it makes perfect sense. Cancer is the uncontrolled proliferation of cells in the body. Viruses selectively kill cells. "The trick is to make them kill only the cells you want them to kill, the cancer cells," Lieber said. Lieber, Kiem and their colleagues have focused on a strain of cold virus, adenovirus serotype 5 (or Ad5). The cold virus achieves its purpose in nature by injecting its genes into our cells, forcing our nasal passage cells or whatever else is infected to produce new viral offspring. Eventually the nose or lung cells that are infected burst, which helps explain why we cough and our noses turns red. Catching a cold means your cells have been hijacked. Lieber and Kiem, in turn, are hijacking the cold virus to redirect it against cancer. "Andre has modified the viruses so they can selectively target the tumor cells, replicate inside them and kill them," Kiem said. "And they can only replicate inside the tumor cells." Though the research is limited to mice in the U.S., Lieber is working with British researchers to do clinical testing soon of his modified cold virus in a dozen people with late-stage, incurable colon cancer. There are still plenty of obstacles, however, to making this an approved cancer therapy -- beginning with the immune system's tendency to fiercely attack and destroy viruses. "That's a big problem," Lieber said. One way to get around it, he said, is to use immune-suppressing drugs until the anti-cancer virus finishes its attack on the tumor. Another concern is that the virus could stimulate an adverse immune response in the patient, he said, or that the altered virus would evolve and revert to its disease-causing natural "wild type" -- or perhaps turn into something even worse. "Andre is an incredibly creative guy, but he does tend to focus on problems," joked Dr. Stephen Russell, a researcher at the Mayo Clinic in Rochester, Minn., widely considered one of the world leaders in the field known as oncolytic (cancer-killing) virotherapy. Russell and his team have altered measles viruses to attack ovarian cancer, multiple myeloma and glioblastoma, and have recently launched early stage human trials. "It's no longer a question of whether virotherapy will work so much as it is a question of what we still need to do to make it work better," Russell said. After the field's long history of fits and starts, the Mayo Clinic scientist is nevertheless concerned about anything that might once again send this avenue of inquiry back into hibernation. When his 17-year-old daughter came home one night to report that she just saw the movie "I Am Legend," in which Will Smith is a scientist who alters a measles virus that creates zombies and kills everyone in Manhattan, Russell was concerned. "I thought, 'Oh no, here we go,' " he said. "We're at a very vulnerable stage in development, just moving into early stage human trials." Russell and his colleagues monitored the Internet to see what people said about this Hollywood movie that had the altered measles virus creating zombies and depopulating New York City. Fortunately, few saw any reason to storm the Mayo Clinic and demand that the science stop. "It may have helped that the movie was pretty cheesy," Russell said. Despite his reputed tendency to see most glasses half empty, Lieber believes the new genetic and molecular biological techniques available today do promise to finally make virotherapy an effective, incredibly accurate and safe way to rid the body of cancer. "These viruses have evolved over millions of years to figure out how to get into cells," he said. "They have an inherent ability to take over specific cells and kill them." . . . . . . . . . (Seattlepi.com, By Tom Paulson, PI Reporter, April 6, 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.

http://www.primenewswire.com/newsroom/n ... l?d=139597 ARTICLE: . . . . . . . . . Hana Biosciences (Nasdaq:HNAB), a biopharmaceutical company focused on strengthening the foundation of cancer care, today announced that active cancer patient dosing has commenced in the company's Phase 1 clinical trial of topical menadione lotion for the treatment and/or prevention of the rash associated with Epidermal Growth Factor Receptor Inhibitors (EGFRIs). Currently, there are no products or therapies approved by the U.S. Food and Drug Administration (FDA) to treat this pervasive skin toxicity that may cause the reduction, interruption or discontinuation of the EGFRI treatment. "EGFRIs have proven to be very effective in the fight against numerous types of cancer and are used in over 100,000 patients annually. However, a majority of patients develop the rash associated with these therapies, affecting their quality of life and leading to possible reduction or cessation of their anticancer therapy, which can affect survival. I am excited to work with Hana Biosciences in the clinical evaluation of topical menadione, which may have the potential to offer relief from this terrible side-effect to patients during their cancer treatment," said Mario Lacouture, M.D., Assistant Professor of Dermatology at Northwestern University's Feinberg School of Medicine, and the principal investigator for this study. "Initiating this Phase 1 trial of menadione represents an important opportunity for Hana Biosciences. It is a first-in-class, locally-targeted formulation that may play a major role in the management of a large and growing population of cancer patients. The ability to obtain patient data so early in development will help us to push forward with an aggressive development timeline," stated Steven R. Deitcher, M.D., President and CEO of Hana Biosciences. "We look forward to working with Dr. Lacouture and other investigators in this Phase 1 clinical study and potentially reach proof-of-concept in the second half of this year." The primary objective of the Phase 1 study is to evaluate the systemic absorption of menadione topical lotion as an emergent and pre-emergent (prophylactic) treatment for EGFR inhibitor-associated rash. Additionally, the study will evaluate the efficacy and safety of menadione topical lotion in both treatment emergent and prophylaxis patients. The Phase 1 trial is designed to enroll a total of 24 adult subjects who are about to begin treatment with an approved EGFRI for cancer. Subjects will be divided into two cohorts, run sequentially. The first cohort will consist of subjects who develop the first signs and symptoms of EGFRI-associated rash on the face, neck, and/or upper chest following the initiation of their cancer treatment. In the second cohort, subjects will receive menadione lotion prophylactically, starting one day prior to beginning their EGFRI therapy. In both cohorts, subjects will serve as their own control and apply menadione lotion on one side of the treatment area and placebo lotion on the other side, in a blinded fashion. Treatment duration will last approximately one month. There are currently four approved EGFRIs on the market: cetuximab (Erbitux®; Bristol-Myers Squibb/Imclone), panitumumab (Vectibix; Amgen), erlotinib (Tarceva®; Genentech/OSI Pharmaceuticals), and gefitinib (Iressa®; AstraZeneca). For Hana's Phase 1 study, there are no restrictions on the brand of EGFRIs administered to patients. The Phase 1 clinical trial is currently open and enrolling in Chicago, Illinois at Northwestern University's Feinberg School of Medicine by Dr. Mario Lacouture. About Menadione Topical Lotion Menadione, a small organic molecule, has been shown to activate the Epidermal Growth Factor Receptor (EGFR) signaling pathway by inhibiting phosphatase activity. EGFR inhibitors, or EGFRIs, are currently used to treat over 100,000 patients per year with a variety of cancers including non-small cell lung cancer, pancreatic, colorectal, and head & neck cancer. The majority of patients taking EGFRIs develop an associated skin rash. Loss of EGFR signaling has been hypothesized as a mechanism of skin toxicity in patients receiving EGFRIs. In vitro studies have suggested that topically-applied menadione may restore EGFR signaling, specifically in the skin of patients treated systemically with EGFRIs. Currently, there are no FDA-approved products or therapies available to treat these skin toxicities. Hana Biosciences in-licensed topical menadione from the Albert Einstein College of Medicine in New York in October 2006. . . . . . . . . . (News Release, Source: Hana Biosciences, Inc., South San Francisco, California, PrimeNewsWire, April 7, 2008 [Contains Forward-looking Statments]) 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.

http://www.boston.com/news/local/articl ... ave_lives/ ARTICLE: . . . . . . . . . A screening that would save lives By Beverly Beckham, Globe Columnist | April 6, 2008 She is angry, but who can blame her? Her sister - "my beloved sister" - died of lung cancer, writes a reader named Barbara. Her sister was diagnosed in April 2004 with lung cancer. She thought she had a cold. She died two years later. Whatever the cause - radon? cigarettes? asbestos? pesticides? pollution? - nobody knows. What is known is that her sister might not have died if her cancer had been detected sooner. A test exists, a simple test, that could save lives, advocates insist, and that test is not being given. Mammograms, colonoscopies, screenings for prostate cancer - these are routine. But a simple low-cost, low-level CAT scan that detects lung cancer in its earliest stages is not. This, says Barbara, is what makes her angry. And this is what state Senator Susan Fargo, a Democrat from Lincoln, is working to change. Last November she filed legislation to establish the nation's first Lung Cancer Early Detection and Treatment Research Fund, using money from existing cigarette taxes to pay for screening for high-risk people and to research the incidence of this disease. Here's what's startling about this initiative: It would be the first ever. How can this be? Lung cancer, according to the National Cancer Institute, is the leading cause of cancer deaths in the United States. It will kill more people this year than breast, prostate, colon, liver, kidney, and skin cancers combined. It will kill nearly twice as many women as breast cancer and three times as many men as prostate cancer. But if found early, lung cancer can be treated. The five-year survival rate is only 15 percent (compared with 88.5, 99.9, and 64.1 percent for breast, prostate, and colon cancers) because 70 percent of lung cancers are not found until the cancer has spread, according to the Lung Cancer Alliance. And they're not found because even people who are most at risk - smokers and ex-smokers, veterans, African-American men - are not screened. Startling, too, is that Massachusetts uses just 1.8 percent of all the revenue it gets from cigarette taxes and tobacco settlements to reduce tobacco use. And not a single penny for lung cancer detection or research, according to the Campaign for Tobacco-Free Kids. Massachusetts is not alone. Lung cancer research is underfunded nationwide. In fiscal year 2006, the Centers for Disease Control budgeted $204 million for breast and cervical cancer research, $14 million for prostate cancer research, and $14.6 million for colon cancer research. And, the Lung Cancer Alliance says, nothing for lung cancer research. Those who get lung cancer are often blamed for their illness. "Did they smoke?" people ask. And the answer? Sometimes, yes. Sometimes no. "You cannot discuss lung cancer without discussing discrimination," Joanne O'Connor, cochairwoman of the Massachusetts Lung Cancer Alliance, explained in her testimony supporting Senate Bill 2454. "Unlike other diseases, lung cancer and its victims have the added burden of stigma and shame. . . . If you smoked, you brought it on yourself. "My sister Kathy felt the shame," testified O'Connor. She wanted friends and family to be told she had breast cancer, the acceptable women's cancer. Kathy was diagnosed with Stage 4 lung cancer in January 2006 and died six months later. Cigarettes cause lung cancer. We know this. But what most people don't know is that 60 percent of lung cancers are being diagnosed in former smokers, many who quit decades ago, and in people who have never smoked at all. National Cancer Institute statistics are clear. Black men have a 37 percent higher rate of lung cancer than white men, though they smoke less. Veterans, who have been exposed to toxins and who, until 1976, got cigarettes free as part of their K-rations, have a significantly higher rate of lung cancer than nonveterans. And women under 50, who've never smoked at all, are now being diagnosed with this disease. The National Cancer Institute also cites studies showing that when lung cancer is found early, there is a 92 percent 10-year survival rate. Compare this with late detection and just a 15 percent survival rate, and it's clear that screening saves live. Fargo's bill, if it survives the legislative process and becomes law, will be the first in the nation. It will not help everyone. It's modest. It focuses on people who are high risk. But it's a noble start, a small step in the right direction. Equally important, it says to people with lung cancer: You count. Beverly Beckham can be reached at bevbeckham@aol.com. Listen to Beverly read and talk about her columns in her weekly podcast at boston.com/news/podcasts. . . . . . . . . . (The Boston Globe, By Beverly Beckham, Globe Columnist, April 6, 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.

http://www.cancernews.com/data/Article/589.asp ARTICLE: . . . . . . . . . UCLA researchers have developed a novel type of nanomachine that can capture and store anticancer drugs inside tiny pores and release them into cancer cells in response to light. Known as a "nanoimpeller," the device is the first light-powered nanomachine that operates inside a living cell, a development that has strong implications for cancer treatment. UCLA researchers reported the synthesis and operation of nanoparticles containing nanoimpellers that can deliver anticancer drugs March 31, 2008, in the online edition of the journal Small. The study was conducted jointly by Jeffrey Zink, UCLA professor of chemistry and biochemistry, and Fuyu Tamanoi, UCLA professor of microbiology, immunology and molecular genetics and director of the signal transduction and therapeutics program at UCLA's Jonsson Comprehensive Cancer Center. Tamanoi and Zink are two of the co-directors for the Nano Machine Center for Targeted Delivery and On-Demand Release at the California NanoSystems Institute. Nanomechanical systems designed to trap and release molecules from pores in response to a stimulus have been the subject of intensive investigation, in large part for their potential applications in precise drug delivery. Nanomaterials suitable for this type of operation must consist of both an appropriate container and a photo-activated moving component. To achieve this, the UCLA researchers used mesoporous silica nanoparticles and coated the interiors of the pores with azobenzene, a chemical that can oscillate between two different conformations upon light exposure. Operation of the nanoimpeller was demonstrated using a variety of human cancer cells, including colon and pancreatic cancer cells. The nanoparticles were given to human cancer cells in vitro and taken up in the dark. When light was directed at the particles, the nanoimpeller mechanism took effect and released the contents. The pores of the particles can be loaded with cargo molecules, such as dyes or anticancer drugs. In response to light exposure, a wagging motion occurs, causing the cargo molecules to escape from the pores and attack the cell. Confocal microscopic images showed that the impeller operation can be regulated precisely by the intensity of the light, the excitation time and the specific wavelength. “We developed a mechanism that releases small molecules in aqueous and biological environments during exposure to light,” Zink said. “The nanomachines are positioned in molecular-sized pores inside of spherical particles and function in aqueous and biological environments.” “The achievement here is gaining precise control of the amount of drugs that are released by controlling the light exposure,” Tamanoi said. “Controlled release to a specific location is the key issue. And the release is only activated by where the light is shining.” “We were extremely excited to discover that the machines were taken up by the cancer cells and that they responded to the light. We observed cell killing as a result of programmed cell death,” Tamanoi and Zink said. This nanoimpeller system may open a new avenue for drug delivery under external control at specific times and locations for phototherapy. Remote-control manipulation of the machine is achieved by varying both the light intensity and the time that the particles are irradiated at the specific wavelengths at which the azobenzene impellers absorb. “This system has potential applications for precise drug delivery and might be the next generation for novel platform for the treatment of cancers such as colon and stomach cancer,” Zink and Tamanoi said. “The fact that one can operate the mechanism by remote control means that one can administer repeated small-dosage releases to achieve greater control of the drug's effect.” Tamanoi and Zink say the research represents an exciting first step in developing nanomachines for cancer therapy and that further steps are required to demonstrate actual inhibition of tumor growth. . . . . . . . . . (Cancer News, Cancer Information, Source: UCLA's Jonsson Comprehensive Cancer Center, 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.

Hello Deb, and welcome, but sorry for the reason. Over three years ago, my husband was diagnosed with lung cancer (after being delayed through non-diagnosis - 2 digital X rays and several tests - through a pulmonologist). But, the diagnosis was made after a our GP found it through a CT scan months later. Bill received the carbo/taxol/radiation treatment/, a concurrent regimen. Once that was established, Deb, things went pretty smoothly. It does make a difference when a plan of action is established, and treatment is in place. We quickly learned that spending hours at the Cancer Center can be very doable. I brought extra liquid for Bill to drink - hydration is crucial. It helps to flush the chemo out of the kidneys. The nutritionist and nurses kept stressing that. Pretty soon, I brought a bag with some food (They did serve a lunch for Bill.) but he is a snacker, so .... I became a bag-lady. He managed all of that for over 5 weeks (chemo part was once a week) and had no untoward side effects. However, we were told that if there was any nausea there were meds for that, and they gave us a prescription. It never occurred, but we wanted to be prepared. There are so many here if you need. This was the first site I came to when first hit with the scary news. Feel free to "sing out." Keep posting and let us know how it is going? Barbara

Hello Again, Carole, I am soooo glad to see you here. Your attitude is fantastic, and I hope it is contagious. Please keep posting. People with your zest for life give us a bolstering. Sending you a warm welcome, Barbara

Yes, Ned, That is in the neighborhood of what I was thinking when I read it. I'm glad they are moving in a positive direction with thought to more personalized care, and using the words "either/or option" as a saving grace. I also like your idea about spending energy and the immune system. Barbara

Carole, I appreciate your sense of humor. Bill and I love to laugh. Did you know that it helps the immune system? Ok, Joe did not even have to sit across the room - we visited out-of-doors. Our grandson, Joseph, has grown so tall that I sm now feeling very short (I began as 5' 6 1/2," but have lost an inch over the years). Of course, he hasn't reached his Grandpa's height yet - that of 6 feet, but he will get there, or close to it. I will PM you with a few sites to watch - but do not worry about these things. It always gives me a kick to read all this stuff. Of course, then I often discover some of it is so dry and scientific, that it makes my eyes cross. You could say that anything you find which seems you find interesting would, no doubt, be intersting to others. I thank you so much Carole, for your offer of help. You are wonderful. PS: You will find that those buttons at the top of the posting window are very helpful. Quote: reply PM: private message email speaks for itself. Luv ya, Barbara ]

Or, Randy, we could walk around in a filtered bubble? Who knows? We may not be too far from that. Barbara

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: . . . . . . . . . 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.

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. . . . . . . . . . (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. -----------------------------------------------------

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

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 [

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

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

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

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

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.

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.

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

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.

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

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

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.