Barb73

http://dsc.discovery.com/news/2008/04/1 ... ancer.html ARTICLE: . . . . . . . . . April 14, 2008 -- A new nanodevice loaded with powerful cancer-killing drugs can operate inside a living cell to zap cancer cells in response to light. The nanomachine, created by researchers in California, is called a nanoimpeller and is the first of its kind. "We have developed a machine to deliver the cancer drugs only in the cancer cells and not normal cells," said Fuyuhiko Tamanoi, a study author and scientist at the University of California, Los Angeles. "Our research is the first demonstration of controlled and on-demand release of anticancer drugs using mechanized anopartilces in living cells," said Tamanoi. The nanoimpellers are actually tubes made of light-sensative silica. When light strikes the silica, tiny tails on the inside of the tubes wag back and forth, creating a current that propels the drugs out of their cyllindrical home. The more light is directed at the silica, the more drugs they deliver. For initial tests the researchers loaded their nanomachines with camptothecin, a chemotherapy drug commonly used to treat pancreatic and colon cancer. The nanoparticles were then injected into human cancer cells in vitro and taken up in the dark. When a light source was turned on for five minutes, the drugs, which trigger cell suicide or apoptosis, were released and shrank the tumors. Since the drug release is only activated in locations where the light is shining, scientists can direct the drug release within cancer cells. The researchers note that they could load other drugs into the nanoimpellers to treat other diseases that are specific to certain locations and not spread out across the entire body. The nanoimpeller drug delivery system will take several years before it is approved for human use, but Tamanoi says he expects a "clear path" toward approval. If it is approved, patients wouldn't need to worry about inadvertently activing the nanoimpellers by stepping outdoors. The devices only respond to a very specific wavelength of light. "This is a highly significant application of these light activated materials," said Darren Dunphy, a nanomaterials scientist at the University of New Mexico who was not involved in the research. ''This is beyond proof of concept and at some point could be applied to people." . . . . . . . . . (DISCOVERY News, By Eric Bland, April 14, 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.msnbc.msn.com/id/24108228/ ARTICLE: . . . . . . . . . Reuters April. 14, 2008 WASHINGTON - Damage to cells lining the mouth can predict similar damage in the lungs that eventually leads to lung cancer in smokers, U.S. researchers reported. They hope it may be possible to some day swab the mouths of smokers to predict who is developing lung cancer — saving painful and dangerous biopsies of the lung. The process may also lead to tests that will predict other cancers, said Dr. Li Mao, an expert in head, neck and lung cancer at the University of Texas M.D. Anderson Cancer Center in Houston. “Our study opens the door to enhancing our ability to predict who has higher probability of getting tobacco-related cancers,” Mao said in a statement. “Not only lung cancer, but pancreatic, bladder and head and neck cancers, which also are associated with tobacco use.” Smoking is the leading cause of lung cancer, but only about 10 percent of smokers ever get it. It causes few symptoms until it is advanced, which means patients are rarely diagnosed or treated until it is too late for a cure. Mao’s team wanted to find a way to monitor patients taking a drug — the COX-2 inhibitor celecoxib, sold by Pfizer under the brand name Celebrex — in the hopes of preventing lung cancer. They looked at two genes known to help prevent the development of cancer — p16 and FHIT. “There is substantial damage (to the two genes) long before there is cancer,” Mao said. Speaking to a meeting of the American Association for Cancer Research in San Diego, they said they looked for specific damage to these genes in both lung samples and mouth samples from 125 long-time smokers. “We are talking about just a brushing inside of the cheek to get the same information we would from lung brushings obtained through bronchoscopy,” said Dr. Manisha Bhutani, who works with Mao. The p16 gene was shut down via a process called methylation in the lungs of 23 percent of the volunteers, while FHIT was affected in 17 percent. In the mouth, p16 was silenced in 19 percent of the smokers and FHIT in 15 percent of them. In 95 percent of those whose genes were affected, they were affected in both the mouth and the lung, Mao and Bhutani said. This would make an easier test for pre-lung cancer than having to access the lung, the researchers said. This could be useful in monitoring for lung cancer and also looking to see if prevention measures might work. “This could have strong implications for further lung cancer prevention trials,” they wrote in a summary submitted to the conference. At least one other group is working on a saliva test for breast cancer, one that looks for a mutated version of the HER-2 protein linked to some breast cancers. . . . . . . . . . (MSNBC, Reuters, April 14. 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 Gail, This is a fascinating story. It reminds me of the tenacity and strong will to accomplish that the parents in "Lorenzo's Oil" had. Mr. Kanzius is motivated. May God bless him, and I hope he gets to see his invention help people. Excelsior! Barbara

http://www.kten.com/Global/story.asp?S=8152072 ARTICLE: . . . . . . . . . What if we could find the off switch in cancer cells and a way to halt these rapidly dividing cells from the inside. Well researchers may have done just that KTEN's Whitney Allen has the story. Researchers in the lab at The OU Cancer Institute may be closing in on a powerful new cancer treatment. Dr. Courtney Houchen and his associates have found a way to turn off a protein in cancer cells, which in return will keep tumors from growing. The protein is called musahshi and until now scientist believed it was only located in adult stem cells in the intestinal tract. Researchers decided to test a hunch and found the protein inside the stem cells cancerous tumors too. Dr. Courtney Houchen says, "Our next step was to determine whether blocking this protein would cause a reduction in tumors." Houchen and colleagues found it did just that, halting the tumor's growth. Perhaps just as importantly the research provides a target for adults stem cells inside cancerous tumors. Cells that seem to elude the cancer killing power of current treatments and may be responsible for cancer coming back. Dr. Houchen goes on to say, "I've used the analogy killing cancer is like cutting your hair. If you don't get the root the hair will just grow back." The research team believes their findings point to a new way to target those stem cell in cancer. . . . . . . . . . (World Now and KTEN, News, By Whitney Allen, KTEN, April 11, 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/p/articles/view/539690/ ARTICLE: . . . . . . . . . The following summary is based on an abstract scheduled for presentation at the American Association for Cancer Research (AACR) Annual Meeting, April 12 - 16 in San Diego, CA. Newswise — Preliminary data from one of the first clinical trials to test a stem cell-targeting drug in cancer patients shows that while the drug did not prolong survival, its suppressing effect on patients’ stem cells was impressive enough to send investigators looking for a better drug to try. As an emerging field of study in cancer research, stem cells are believed to sprout cancer much like the hidden roots of weeds that elude efforts to get rid of them. Rituximab, a drug currently approved to treat B-cell lymphomas, plus a common chemotherapy agent, cyclophosphamide, were given to 21 patients whose multiple myeloma, a cancer of the bone marrow, had relapsed or was defined as high-risk first remission. A previous study using the drug alone in multiple myeloma patients suggested that the disease in some participants progressed more slowly. During the study, the Johns Hopkins team examined the stem cells under the microscope. “We found cancer stem cells coated with rituxumab, but the drug wasn’t killing them,” said Carol Ann Huff, M.D., assistant professor of oncology. “We think the idea is correct, but the drug itself wasn’t the right one.” Rituximab is sold under the trade name Rituxan. Huff and her team believe that several therapies are required to kill cancer - one to get rid of the bulk of the tumor, like mowing the lawn, and another to hit the root of the cancer, its stem cells. “We think one reason that cancer comes back is because stem cells, which are resistant to chemotherapy, repopulate the body with new cancer cells,” says William Matsui, M.D., assistant professor of medicine at the Johns Hopkins Kimmel Cancer Center. Their test of the rituximab-cyclophosphamide combo showed up to a 1000-fold reduction in cancer stem cells during the initial treatment. However, stem cell quantities eventually crept back up and led to a progression of disease. Investigators were able to predict when patients’ disease would recur by tracking the number of stem cells they had. The average advance notice was two months. Since the study began in early 2005, four patients have died from their disease, three remain progression-free, and the rest have disease that has progressed. Matsui and Huff are currently testing drugs that block an enzyme called telomerase, which may give cancer stem cells longevity, and other drugs that block a stem cell-signaling pathway called hedgehog. Other promising therapies, according to the scientists, include a combination of the drugs, interleukin-6 and interferon-alpha, which may prematurely age stem cells. Funding for the study was provided by the National Cancer Institute, American Society of Clinical Oncology, the Commonwealth Foundation, and Genentech. In addition to Matsui and Huff, these Johns Hopkins scientists participated in the study: Q Wang, K Rogers, M Jung, Javier Bolanos-Meade, Ivan Borrello, and Richard Jones. On the Web: http://www.hopkinskimmelcancercenter.org http://www.aacr.org . . . . . . . . . (NewsWise, John Hopkins Kimmel Cancer Center, April 13, 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.kfyrtv.com/News_Stories.asp?news=17491 ARTICLE: . . . . . . . . . Sometimes cancer takes a long time to run its course, sometimes it strikes fast. Being told you have 30 days to live would be earth shattering for most people, but one man has turned it into a personal mission. This year, about a half-million Americans are expected to die of cancer, That`s more than 1,500 people a day. And while most of them rely solely on medication, some believe that what is on the inside can make a huge difference. "People need to hear this message," says Sally May, of Minot. "People need to hear that there`s hope, people need to know that they have choices and that can empower them to live well." Cancer Recovery Foundation founder Greg Anderson was told that he had only 30 days to live when he was diagnosed with stage 4 lung cancer. That was over 20 years ago. Now he tours the country empowering people to live by the new cancer pyramid - medical, nutrition and exercise, attitude, support and spiritual, embracing the whole self. "In addition to medicine, not in place of it, but in addition to medicine there are things you can do in terms of diet, certainly exercise, we believe that the mind affects the body, we also believe that our relationships have an impact on health," Anderson says. "If people aren`t willing to extend you hope and be a part of your betterment, then you need to readjust your team," says Sandy Larson, a cancer survivor. "You need to do everything you can to help your spirit, your heart and your health grow. That`s important." Larson would know. A survivor of colon cancer, she fired her first doctor after he told her and her medical staff that she was going to die that day in the hospital. Now she is now a spokesperson for colon cancer and speaks to doctors on patient relations and working with the patient. "Cancer does not have to equate with death," says Rev. Michael Gingerich, of the Cancer Recovery Foundation. "You can survive this and the fact is that we all someday will leave this earth and we don`t know when or why or how, but no matter how much time we have no matter how short it is or how long it is in this life it is important to live it with hope, to live it with joy and to live it well." If you would like a copy of the Cancer Recovery Contract visit www.cancerrecovery.org . . . . . . . . . (KFYR-TV News Stories, By Jen Dame, April 12, 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.sciencedaily.com/releases/20 ... 140502.htm ARTICLE: . . . . . . . . . The Good And Bad Side Of Anti-cancer Compounds ScienceDaily (Apr. 10, 2008) — Compounds known as "HDAC inhibitors" exhibit cancer-killing activities in cultured cells. While they are currently being tested as anti-cancer agents in clinical trials, just how they execute their effects is unclear. In a pair of recent papers, Vanderbilt-Ingram Cancer Center investigators provide a potential mechanism by which HDAC inhibitors specifically damage cancer cells and offer clues about possible adverse effects of these compounds -- findings with important implications for their clinical use as cancer therapies. Scott Hiebert, Ph.D., professor of Biochemistry and Medicine, and colleagues initially set out to study how chromosomal translocations -- which happen when chromosomes break and rejoin, creating new genes at the breakpoints -- cause acute leukemias. He previously had found that a chromosomal translocation common in acute myeloid leukemias led to the formation of a new protein, a mutant transcription factor, that actively turned genes off. Enzymes known as histone deacetylases (HDACs) helped the mutant protein turn genes off by stabilizing the tightly coiled structure of DNA in chromosomes, making it inaccessible to proteins that transcribe DNA. "We thought that if we could inhibit these HDACs, we could turn the genes back on and cure leukemia," Hiebert explained. While there are at least 17 different HDACs, Hiebert's work suggested that one in particular, called HDAC3, might be the critical HDAC in triggering acute leukemia. To investigate the effects of inhibiting HDAC3, Hiebert and colleagues genetically engineered mice lacking the protein. However, the mice died before birth. Even when grown in cell culture, mouse cells lacking HDAC3 died. "The question is: why are they dying? And what we found was kind of surprising," he said. In the April 11 issue of Molecular Cell, Hiebert and colleagues report that these cells die because they can't repair the DNA damage that occurs naturally when the cells copy their DNA during cell division. HDAC3 inhibition only killed cells that were in the process of DNA replication. However, cells cultured in a medium that stalled cell division -- a situation similar to the mature cells in most adult tissues -- survived. This provided an important clue as to why HDAC inhibitors specifically kill tumor cells -- which divide rapidly and prolifically -- and spare healthy cells. "If we take cells out of the cycle, making them quiescent, like most of your tissue cells are, they aren't affected by (HDAC inhibitors) or by the (genetic) inactivation of HDAC3. Whereas cells that are actively cycling or dividing, like the tumor cell, are susceptible," said Hiebert. "We think that these HDAC inhibitors are actually having a therapeutic benefit against cancer by causing DNA damage...and we're not repairing that damage. That eventually leads the cell to die," he explained. Although previous studies suggest that HDAC inhibitors have some tumor-killing ability on their own, Hiebert's recent findings especially support using HDAC inhibitors as adjuncts to chemotherapy or radiation treatment, both of which induce DNA damage. Giving an HDAC inhibitor beforehand may prevent tumor cells from being able to repair the DNA damage that will be inflicted by the radiation or chemotherapy treatments. "We're excited about that because that's where the real benefit of these drugs will eventually come in," he says. HDAC inhibition isn't without side effects, however. And another recent paper from Hiebert's lab, published in the EMBO Journal in March, provides some insight into how HDAC inhibition might cause liver damage. In that study, Hiebert's group turned off HDAC3 in the liver only. These mice, which did survive to adulthood, developed extensive liver damage with grossly enlarged and fatty livers. The mice also had major metabolic abnormalities, reflected in elevated cholesterol and triglyceride levels. Fortunately, the HDAC inhibitors currently under investigation are short-lived in the body, which may limit any potential adverse effects. "I think the short half-life in people is actually going to be a benefit for these compounds, because they are transient therapies," he noted. Hiebert's lab is following these mice to determine the long-term effects of HDAC inhibition. And, because the available HDAC inhibitors are relatively broad-spectrum, inhibiting several of the 17 HDACs, he is looking to develop HDAC inhibitors that more selectively target HDAC3. The Food and Drug Administration recently approved an HDAC inhibitor called SAHA (suberoylanilide hydroxamic acid) for treating a form of T-cell lymphoma -- which means that the drug will likely be given off-label for other types of tumors. While this marks a major step forward in the therapeutic use of HDAC inhibitors, Hiebert notes, "we think they can be used better. And that's why we're excited by these results." Graduate student Srividya Bhaskara, Ph.D., was first author on the Molecular Cell paper. Postdoctoral fellow Sarah Knutson was first author on the EMBO Journal paper. Both studies were funded by the TJ Martell Foundation. . . . . . . . . . (Science Daily, Source: Vanderbilt University Medical Center, via Eureka Alert, April 10, 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.nytimes.com/aponline/us/AP-D ... ref=slogin ARTICLE: . . . . . . . . . April 11, 2008 Drug Companies to Reveal Grant Practices By THE ASSOCIATED PRESS Filed at 1:38 p.m. ET WASHINGTON (AP) -- For years, the nation's largest drug and medical device manufacturers have courted doctors with consulting fees, free trips to exotic locales and sponsoring the educational conferences that physicians attend. Those financial ties in most cases need not be disclosed and can lead to arrangements that some say improperly influence medical care. Now, under the threat of regulation from Congress, the two industries are promising to be more forthcoming about their spending. A dozen of the nation's leading drug and device makers have told Sen. Charles Grassley, R-Iowa, that they have plans or are working on plans to publicly disclose grants to outside groups. The details will be provided on each company's Web sites. Watchdog groups say the companies are trying to derail legislation that would require public disclosure of their giving. ''If they were doing this out of the goodness of their heart, they would have done so decades ago,'' said Dr. Peter Lurie of the consumer group Public Citizen. Of particular interest to Grassley, top Republican on the Senate Finance Committee, is the money companies spend on continuing medical education. Physicians attend such conferences to fulfill their license requirements and to keep up to date with the latest treatment trends. Professional associations and companies frequently ask drug and device makers to help pay for the conferences. Recently, Grassley asked 15 companies whether they planned to follow the lead of Eli Lilly & Co., which now discloses its grants to such programs. ''If your company does not yet have any efforts or plans in place, please explain why not,'' Grassley wrote. The responses are in. They are wide-ranging but mostly what the senator wanted to hear. Indeed, many of the companies said they would go beyond disclosing grants for medical education. Some companies said they would also disclose payments to patient advocacy groups such as the American Heart Association or the American Diabetes Association. Boston Scientificsaid it was developing a system that even discloses certain payments to physicians. Medtronic Inc. said it will post payments for professional meetings and patient groups on its Web site beginning May 1. AstraZeneca PLC said it would do the same on Aug. 1, providing the amount spent and the purpose of the financing. AstraZeneca gets 4,000 to 5,000 grant applications each year and funds about a third of them. Merck and Co. was vague about its plans, but committed to the concept. ''We are currently in the process of developing an action plan,'' the company wrote to Grassley. Amgen Corp. and Abbott Laboratories said they had formed working groups to determine how to compile and display their grants. Schering-Plough Corp., however, told the senator what he didn't want to hear: ''We do not publish or have plans at the moment to publish a list of charitable contributions or educational grants that medical organizations have received from us.'' Grassley said, overall, he was happy with the responses. ''The way these companies are making information about financial relationships open to scrutiny is the right thing to do,'' he said. Two other companies said they already were disclosing third-party payments. The two, Zimmer Inc. and Stryker Orthopedics Inc., avoided criminal prosecution over financial inducements paid to surgeons to use their products, prosecutors announced last year. The companies agreed to new corporate compliance procedures and federal monitoring. Zimmer also had to pay the government $169.5 million. The hip-and-knee industry was the subject of a recent Senate Aging Committee hearing titled ''Surgeons for Sale.'' Companies routinely paid doctors $5,000 every three months for providing information on market trends and operating-room activity. However, the reports typically offered only cursory descriptions and often were duplicated from one quarter to the next. Also, companies sponsored consultant meetings at resort locations. The meetings lasted just a few hours each day. The physicians who presented information at the meetings spoke for as little as 10 minutes. ''Although the remainder of the day was available for recreational activities paid for by the company, the consultants were compensated $5,000 for a full day of work,'' said Gregory E. Demske, an assistant inspector general. Eli Lilly began listing its grants last year. It gave $18.9 million in the second quarter of 2007, according to the Prescription Project, a Boston-based group that promotes policies to reduce conflicts of interest. ''They support those organizations which they believe will have a positive impact on their drug sales,'' said David Rothman of Columbia University and associate director of the Prescription Project. ''It's self-evident but important.'' If all of the companies follow through with their commitments to Grassley, there also would be widespread disclosure of how much money they give patient advocacy groups. The groups rely on industry for much of their financing. For example, the American Heart Association said donations from the pharmaceutical and device industry make up about 6 percent of its annual income, and totaled $48.3 million in the organization's latest fiscal year. ''Donations from corporations, including the pharmaceutical and device industry, allow us to further enhance our programs and outreach, and to bring objective science and the highest quality of public education and information to more people,''said Maggie Francis, the association's communications manager. Grassley and Sen. Herb Kohl, D-Wis., have introduced legislation that would require drug and device makers to disclose anything of value given to physicians, such as payments, gifts or travel. The disclosure of medical education grants is an extension of that concept. Last year, the staff for the Senate Finance Committee issued a report that said the drug industry may be using the ''medical education industry to deliver favorable messages about off-label uses that the drug companies cannot legally deliver on their own.'' The committee report noted that Warner-Lambert, now owned by Pfizer Inc., paid $430 million to settle claims that medical conferences it sponsored were used to illegally promote off-label uses of the anti-seizure drug Neurontin. Serono-Laboratories paid $704 million to settle a similar claim concerning the AIDS drug Serostim. In a few states, such as Vermont and Minnesota, drug companies must disclose certain payments to physicians. Baxter International Inc. told Grassley that it could support legislation setting a national disclosure standard, but it's critical the standard pre-empt state laws. ''Overlapping and conflicting state requirements have created, and would continue to create, duplication, uncertainty, and burden in complying with them,'' a Baxter official wrote. . . . . . . . . . (The NYTimes, AP, April 11, 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.medicalnewstoday.com/articles/103597.php ARTICLE: . . . . . . . . . Researchers and executives from Biomoda, Inc. (OTC Bulletin Board: BMOD) (http://www.biomoda.com), a development stage medical diagnostics company, will present a paper entitled "New Non-Invasive Technology for the Early Detection of Cancer at the Cellular Level" at the 83rd Annual Multidisciplinary Meeting of the American Association for the Advancement of Science (AAAS) Southwestern and Rocky Mountain (SWARM) Division, Thursday, April 10, in Albuquerque. The paper will focus on Biomoda's non-invasive and cost-efficient screening technology for early detection of lung cancer. The technology, which was developed at Los Alamos National Laboratory, is based on a patented porphyrin molecule that preferentially binds to cancerous or aberrant cells extracted from the body as sputum, blood or urine. Cancerous or aberrant cells that bind porphyrin glow red under ultraviolet light; non-cancerous cells do not fluoresce. Current diagnostic methods for lung cancer -- the leading cause of cancer-related deaths in the United States -- often detect the disease only at more advanced stages. "This conference is an excellent venue for Biomoda to foster communication and share our research among other scientists and engineers," said John Cousins, Biomoda President. "We are excited about the opportunity to increase public understanding of our latest advances in in-vitro diagnostics for non-invasive testing for cancer at the cellular level." Biomoda is seeking international partners interested in collaborating in the development and use of its non-invasive early-stage cancer detection technology. Biomoda and the New Mexico Institute of Mining and Technology (New Mexico Tech) recently announced their partnership with the New Mexico Department of Veterans Services (DVS) to conduct a $350,000 clinical study using Biomoda's proprietary testing technology for detection of early lung cancer in the state's veterans. Biomoda will conduct the first year of the clinical program, while New Mexico Tech and DVS will oversee the study and provide treatment to those veterans who test positive for lung cancer. The New Mexico state legislature recently allocated an additional $1.3 million in funding through the Interim Tobacco Settlement Committee to the clinical screening program. Biomoda presenters at the SWARM conference include: Cousins; Leo S. Gomez, Ph.D., Director of Research; Constance J. Dorian, Director of Technical Operations; and Stephen M. Gomez, Ph.D., Senior Research Specialist. . . . . . . . . . (Medcial News Today, Lung Cancer, April 11, 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://news.bbc.co.uk/2/hi/health/7341336.stm ARTICLE: . . . . . . . . . A drug which may protect the body against damage from radiation has been developed by US scientists. It is hoped it could make radiotherapy safer for people with cancer and could also be used in the event of a "dirty bomb" or nuclear disaster. Known as CBLB502, and so far tested in animals, it switches on a biological mechanism that helps healthy cells survive blasts of radiation. The findings published in Science are set to be tested in clinical trials. Radiation kills cells by causing damage which encourages cell suicide, or apoptosis. But healthy cells may be killed alongside tumour cells in the process which is why radiologists need to target the tumour as specifically as possible. If the protective properties seen in this laboratory study can be reproduced in people with cancer, this could be an important step towards reducing side effects for people having radiotherapy Dr Joanna Owens, Cancer Research UK Researchers developed the drug after looking at how some resistant cancer cells are able to withstand radiotherapy. It works by inhibiting the protein that initiates the cell suicide programme. Studies in animals suggest CBLB502 protects healthy cells in the bone marrow and digestive tract against radiation but does not seem to protect tumour cells which remain vulnerable to treatment. Mice and monkeys injected with the drug between 45 minutes and 24 hours before being subjected to normally lethal radiation were more likely to survive or live longer than untreated animals, the researchers found. Side-effects One risk of preventing cell death is that defective cells may be allowed to survive which could then turn cancerous. However, the researchers found no sign of this happening in the laboratory tests on mice. Also, there were no apparent side effects. Protecting healthy cells against the effects of radiation may allow cancer patients to receive higher doses of radiotherapy, or longer courses of treatment. The drug may also be useful in protecting against fall out from a nuclear disaster, such as Chernobyl, or the effects of a terrorist "dirty bomb". Dr Andrei Gudkov from the Lerner Research Institute in Cleveland, Ohio, said they had set out to enable healthy cells to imitate the ability of tumour cells to avoid cell death. But they had to develop a way of making this effect temporary and reversible. "We demonstrated the drug is efficacious when injected before radiation and after radiation. "In summary, CBLB502 reduces radiation toxicity without diminishing the therapeutic anti-tumour effect of radiation and without promoting radiation-induced carcinogenicity." Dr Joanna Owens, science information officer at Cancer Research UK, said: "These are interesting results and we look forward to following the progress of CBLB502 through planned clinical trials. "If the protective properties seen in this laboratory study can be reproduced in people with cancer, this could be an important step towards reducing side effects for people having radiotherapy." . . . . . . . . . (BBC News, Health, April 10, 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.

Dear Bucky, You are so very smart to get help. So much of living with lung cancer is taken up in our minds and emotions. Seeking help is a first step in securing our peace of mind to be able to enjoy our lives. More and more people are realizing that, and know that taking care of the body is only one part of the equation that makes up the whole. May you receive that peace of mind, and enjoy those Lacrosse games. Sending you a big (((Hug))), Barbara

http://www.medicalnewstoday.com/articles/103672.php ARTICLE: . . . . . . . . . Kalos Therapeutics, a privately held biopharmaceutical company developing the Atrial Natriuretic Peptide (ANP) family for the treatment of human cancers, announced that David L. Vesely, M.D.,Ph.D., (University of South Florida) presented additional positive xenograft data today at the Experimental Biology 2008 Symposium on Heart Hormones. The data confirmed and expanded pre-clinical studies establishing the anti-cancer effect of this family of peptides naturally expressed in the human heart. Dr. Vesely had shown that the ANP family of peptides has very broad activity in animal models, inhibiting the growth of all of the cancers examined to date: human pancreatic, lung, and breast cancers. The additional studies reported at the Symposium were performed by TD2, an oncology drug development contract research organization affiliated with the Translational Genomics Research Institute (TGen, Scottsdale, AZ), and focused on the most active member of the ANP peptide family that is designated KT-220. These studies were designed to extend Dr. Vesely's previous findings by using a more challenging pancreatic tumor model system and including an additional, more aggressive type of pancreatic cancer. The results showed that KT-220 also has significant activity in these models. Kalos Therapeutics holds an exclusive, worldwide license to a 2005 patent resulting from the pioneering work of Dr. Vesely, at the University of South Florida's Cardiac Hormone Center. The patent covers the use of this family of cardiac hormones as cancer therapeutics. Dr. Vesely now serves on Kalos' Scientific Advisory Board. Dr. Norrie Russell, president and CEO of Kalos, said, "We are very encouraged by these study results, particularly in light of the National Cancer Institute analysis showing that an anti-cancer compound's breadth of activity in xenograft animal models is the best predictor of activity in human clinical studies. Based on these findings, and on the previous safe administration of KT-220 and other ANP family members to humans for another indication, we can confidently move forward with clinical development. Kalos is currently raising capital from institutional investors and qualified private individuals to initiate clinical trials of KT-220 in cancer." KT-220 and the other peptides of the ANP family exert their anti-cancer effects through a novel mechanism involving the inhibition of the Mitogen Activated Protein Kinase (MAPK) signaling pathway, a key mechanism in cancer cell proliferation. These peptide hormones selectively shut off the proliferative effects of this kinase pathway in cancer cells but not in normal cells. About the ANP Family of Peptides The ANP family of peptides consists of four peptides derived from the pro-ANP gene, and includes ANP itself. These peptides, which share certain structural features, act through cell surface receptors to produce their antiproliferative effects. These peptides occur at the highest concentration in the heart, and much lower levels throughout the body. High natural levels of ANP peptides in the heart may be responsible for the low incidence of metastatic as well as primary cardiac tumors. About Kalos Therapeutics Kalos Therapeutics is a biopharmaceutical company that in-licenses, develops and commercializes proprietary product candidates primarily for the treatment of cancer. The ANP family of peptides represents a portfolio from which many drugs can be developed addressing multiple indications within cancer and non-malignant hyperproliferative disorders. . . . . . . . . . (Medical News Today, Lung Cancer/Oncology, April 11, 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 Susan, I was sitting here this Friday morning, and catching up on some reading, and saw your introduction posting. Glad you jumped in with both feet, Susan. Wishing you much continued success, and a warm welcome from a "newbie" of sorts. Wishing you all the best, Barbara

Hello Shelly, A most warm welcome to you. I am sorry for the reason you found us, but you have come to a wonderful site for gaining support, and information. The people here are very responsive to newcomers, all those with lung cancer, and/or their loved ones. Shelly, you could not have said it better. The stigma attached to lung cancer, and not the other cancers, makes absolutely no sense. Just recently (in the past days/weeks) there have been results of scientific studies which pinpoint a genetic predisposition to developing lung cancer. You are also correct in the lack of lung cancer ads which explain all the information about stigma, blame, and recent study results. There is little mention, if any, of the majority of people being diagnosed being either former or never smokers. It's a disgrace! However, Shelly, there are many efforts to have walks for fundraising and awareness. I think you may find them listed here at the Index at this message board. Many, many people have participated in them. My heart goes out to you, Shelly. You are so very young. There are treatments, and there are others in the pipeline. I believe your oncologist is on the mark with his not planting the cause of your lung cancer completely at the doorstep of smoking. Please Shelly, come back and tell us more and give others the chance to welcome you and let you know that you are not alone. Sending you prayers, and good thoughts to you. All the best to you and your lovely family. Barbara

Yes, Dannnie, I agree with you that someday, surely, through sites such as this one, there will be an "awakening." Lung cancer research and funding is deserving of our attention and concern - rather than treated as a stigma by so many of the public. It does seem to be moving in that direction, especially when the majority of those diagnosed today are a combination of former or never smokers. Barbara

http://www.medicalnewstoday.com/articles/103355.php ARTICLE: . . . . . . . . . Small cell lung cancer (SCLC) patients treated with high-dose chemotherapy did not have better survival rates than those treated with standard doses, according to a randomized controlled trial published online April 8 in the Journal of the National Cancer Institute. SCLC accounts for nearly 13 percent of lung cancer cases in the United States. Although many patients with SCLC initially respond to chemotherapy, most suffer disease recurrence relatively quickly. Laboratory data suggest that increasing the dose of chemotherapy agents kills SCLC cells that were resistant to standard doses, and thus might improve patient survival. To test this possibility, Serge Leyvraz, M.D., of the University Hospital in Lausanne, Switzerland, and colleagues enrolled 140 patients with SCLC in a randomized trial that compared high-dose and standard-dose chemotherapy. Both groups were treated with the same chemotherapy agents, ifosfamide, carboplatin, and etoposide (ICE). The 3-year survival rates in the two arms were similar, with 18 percent of patients in the high-dose arm and 19 percent of patients in the standard-dose arm still alive. Additionally, a similar fraction of patients in both arms showed tumor shrinkage in response to therapy - 78 percent in the high-dose arm and 68 percent in the standard-dose arm, which was not a statistically significant difference. "The approach explored in the present trial succeeded in raising the peak dose, total dose, and dose intensity of ICE by threefold but has clearly been ineffective and highly toxic," the authors write. "As a result, this strategy should be abandoned." In an accompanying editorial, Paul A. Bunn Jr., M.D., agrees with that assessment and emphasizes that other avenues of therapy should now be explored. "The declining incidence of SCLC and the lack of progress seem to have dampened the enthusiasm of funding agencies and industry for exploring novel therapies. This is indeed unfortunate because SCLC remains a common cancer in both the developed and developing world," Bunn writes. . . . . . . . . . (Medical News Today, Lung Cancer, [adapted from original press release], Journal of the National Cancer Institute, April 9, 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.

Comment: There was also a warning issued by the FDA on this subject in my morning email. http://www.latimes.com/business/la-fiw- ... 7981.story Article: . . . . . . . . . Pfizer Inc. reported an increase of lung cancer among patients who used its discontinued inhaled insulin Exubera, another setback for developers of needle-free diabetes treatments. Shares of MannKind Corp., maker of a similar product that hasn't reached the market, fell 60% after Pfizer's disclosure. Nektar Therapeutics Inc., which developed Exubera with Pfizer, fell 25% after the cancer findings led it to cancel its search for a new partner. Exubera was the first inhaled insulin, approved in January 2006, and Pfizer gave up selling the product in October because its cost and unwieldy design made it unpopular with patients. Eli Lilly & Co., Novo Nordisk and Alkermes Inc. also abandoned experimental inhaled insulin this year, all but ending the industry's investment of more than $4 billion and a dozen years. "Concern over cancer will not be limited to Exubera solely," William Tanner, an analyst with Leerink Swann & Co. in New York, wrote in a research report today. "We no longer think there will be a major market for inhaled insulin" because of the cancer risk and because other forms of insulin have become more convenient, he said. Pfizer said today it updated Exubera's prescribing information to include a cancer warning after a review of clinical trial data found there were six cases of lung cancer among 4,740 patients using the drug, compared with one of 4,292 who did not take the drug. All cases were in former cigarette smokers. The lung cancer cases were twice the number as when Pfizer won regulatory approval for Exubera in January 2006, though too few cases to prove a link, Pfizer said. Pfizer said it will make the device available for an unspecified period while patients switch to other forms of insulin. There were 2,438 prescriptions written for Exubera in February, according to data research firm Wolters Kluwers. When Pfizer scrapped Exubera last year, it returned the rights to the drug's developer, Nektar Therapeutics. In a separate statement today, Nektar, of San Carlos, Calif., said it ended negotiations with potential partners for the product. Nektar fell $1.80, or 25%, to $5.39. MannKind, of Valencia, Calif., fell $2.35, or 60%, to $2.35. MannKind has lost 84% of its value in the past 12 months as bigger drugmakers quit inhaled insulin. The company said last month it plans to file an application late this year for U.S. clearance of its Technosphere insulin inhaler. The product is in the third and final round of human tests needed to support marketing approval. Three analysts, including Tanner, downgraded MannKind today. Nektar will now focus on other products, including treatments for colorectal cancer, cystic fibrosis and hospital acquired pneumonia, Chief Executive Howard Robin saidt. Exubera labeling already warned of a possible risk to the lungs from studies that showed it decreased lung function. Pfizer expected $1 billion in annual sales when the product went on sale in January 2006. The company wrote off $2.8 billion last year to abandon the drug. . . . . . . . . . (Los Angeles Times, Bloomberg News, April 9, 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.sciencedaily.com/releases/20 ... 132118.htm ARTICLE: . . . . . . . . . Double Binding Sites On Tumor Target May Provide Future Combination Therapy ScienceDaily (Apr. 8, 2008) — Researchers from the University of Pennsylvania School of Medicine and colleagues at Merck Serono Research in Germany have found that two drugs bind to receptor sites on some tumors in different places at the same time, suggesting the possibility of a new combination therapy for certain types of cancer. An increasing number of therapies targeting tumors that have proteins called epidermal growth factor receptors (EGFR) sitting on their surface are already being used in the clinic or are in late stages of development. For example, Herceptin is an established treatment for certain types of breast cancer and Erbitux and Vectibix are in use for other types of cancer. An additional drug called matuzumab is in phase II clinical trials. Three years ago, Kate Ferguson, PhD, Assistant Professor of Physiology, and colleagues determined the precise molecular details of how Erbitux, a colorectal and head and neck cancer drug, binds to its target on cancer cells. EGFR drugs halt cell proliferation by blocking EGFR's molecular doorway, keeping hormones from binding and signaling tumor growth. X-ray crystallography provided a snapshot of the interaction between Erbitux and the extracellular component of the cancer cell's receptors. As is characteristic of many epithelial cancers - such as cancers of the colon, head and neck, breast, ovary, lung, and pancreas - the surface of cancer cells possess abnormally high levels of EGFR. In a cancer cell, an extracellular hormone binds to the outer piece of EGFR, and causes the inside part to kick off a series of reactions that signal the cancerous cell to replicate and divide. In the present study, published in Cancer Cell, Ferguson and Merck colleagues found -- again using X-ray crystallography -- that matuzumab binds in a different place from Erbitux. Their binding does not overlap, and they can bind to EGFR at the same time. "These findings imply that a combination therapy using both types of EGFR drugs could be developed and tested," says Ferguson. "This has important implications for the clinical use of matuzumab and for developing new therapies that target EGFR." The research was governed by a Supported Research Agreement between Merck KGaA and the Trustees of the University of Pennsylvania and is financially supported in part by Merck KGaA, and the National Cancer Institute. Kate Ferguson is the Dennis and Marsha Dammerman Scholar of the Damon Runyon Cancer Research Foundation. . . . . . . . . . (Science Daily, Eureka Alert, Source: University of Pennsylvania School of Medicine, April 8, 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.independent.co.uk/life-style ... 06319.html ARTICLE: . . . . . . . . . Wednesday, 9 April 2008 Exaggerated claims are being made for new cancer treatments that are not justified by the evidence, scientists warned yesterday. Drugs hailed as breakthrough treatments for cancer, Britain's biggest cause of death, may be less effective and cause more harm than suspected, they said. A sharp increase in the number of trials being halted prematurely to deliver rapid results is undermining confidence in the drugs. Public demand for access to new treatments, allied to the pharmaceutical companies' eagerness to bank profits, creates pressure on researchers to terminate trials as soon as a drug reveals a benefit. But that can be before the full results are in. A review of 25 trials of cancer drugs that had been stopped early during the past decade because they had started to show a benefit to patients, found more than half (14) had been halted in the past three years. Of those, 11 were used to support an application for a drug licence in Europe or in the US, researchers discovered. One of the research team, Giovanni Apolone, from the Mario Negri Institute for Pharmacological Research in Milan, said: "This suggests a commercial component in stopping trials prematurely. We are aware that trials stopped early because they are showing benefit may result in the identification of promising new treatments for patients. "However, findings obtained in this way require subsequent confirmation. Without such evidence, unsafe and ineffective drugs could be marketed and patients' health could well be jeopardised." The drugs tested in the trials that were stopped early include some of the biggest new discoveries in cancer therapy, touted as heralding a new golden age in treatment. They include Herceptin (trastuzumab) for breast cancer, Avastin (bevacizumab) for bowel and kidney cancer, Campto (irinotecan) for lung and bowel cancer, Sutent (sunitinib) for kidney and gastrointestinal cancer, Nexavar (sorafenib) for kidney cancer, and TaxolCarbo (carboplatin) for ovarian and lung cancer. Dr Apolone said it could take years for the long-term benefits or dangerous side-effects of a drug to become evident, but the average duration of the 25 trials stopped early was just 30 months. Five had enrolled less than 40 per cent of the planned number of patients. Only 4 per cent of the trials were halted because of serious adverse effects but Dr Apolone said the main worry was that early stopping exaggerated the beneficial effects. Writing in the online edition of Annals of Oncology, the researchers say: "If a trial is evaluating long-term efficacy of a treatment of conditions such as cancer, short-term benefits – no matter how significant statistically – may not justify early stopping. Data on disease recurrence and progression, drug resistance, metastasis, or adverse events, all factors that weigh heavily in the benefit/risk balance, could easily be missed." Stuart Pocock, professor of medical statistics at the London School of Hygiene and Tropical Medicine, who had no involvement in the study, said all trials should have independent monitoring committees of experts to advise on when they should be stopped early. Statistically, stopping trials that showed early evidence of benefit while allowing the rest to run their full course would skew the overall results and exaggerate the benefits, he said. "Overall, there is an underlying bias towards exaggeration [of the results]. We can pretty reliably claim there is exaggeration going on. This is not as sober an environment as it should be. It has an aura of hot-headedness about it." Professor David Kerr, editor of Annals of Oncology, said researchers faced a dilemma. "If we see an effective cancer drug, it is our duty to get it into the clinic as quickly as possible. But we must not run down the quality of the evidence to support that drug." Cancer drug trials stopped early Herceptin Breast cancer – two trials started 2001 and 2003 Avastin Bowel cancer – trial started 2005 Campto Lung cancer – trial started 1995 Sutent Gastrointestinal cancer – trial started 2003 Nexavar Kidney cancer – trial started 2003 TaxolCarbo Ovarian cancer – trial started 1994 . . . . . . . . . (Independent.co.UK, By Jeremy Laurance, Health Editor, April 9, 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.

Comment: Carole sent this interesting article to me this morning. Thank you, Carole. http://www.tennessean.com/apps/pbcs.dll ... /804090458 ARTICLE: . . . . . . . . . VU research could produce blood test to detect top killer By CLAUDIA PINTO Staff Writer In 1971, lung cancer was the leading cancer killer, with about only about 15 percent of its victims alive after five years. In 2008, that's still true. Lung cancer kills more people than breast cancer, prostate cancer, kidney cancer, colon cancer, liver cancer and skin cancer combined. A lack of funding over the years has hampered research, advocates say. One reason is that lung cancer is often associated with smoking, and victims are blamed for their disease, but ex-smokers and nonsmokers now make up more than half of all new lung cancer cases. "The idea that lung cancer patients don't deserve support is incredibly unfair since cigarettes are not only legal but highly addictive, and it's especially unfair to the nearly 20,000 people per year who take care of themselves, never smoke and get lung cancer anyway," said Dr. David Carbone, professor of medicine and cancer biology at Vanderbilt-Ingram Cancer Center. Finding a way to detect lung cancer early is critical to improving survival rates. Researchers at Vanderbilt are working on developing a blood test that would find the cancer before symptoms appear. When cancer cells develop in the body, they sometimes shed proteins that show up in the blood, urine or tissue. Vanderbilt researchers are working to identify proteins that are unique to lung cancer. Carbone said there is currently no good way of detecting lung cancer early. X-rays are ineffective and CT scans detect nodules in 70 percent of people. Without removing part of the lung there's no way to know whether those nodules are cancerous. If lung cancer is detected early, patients have a 70 percent survival rate at five years. So, though a blood test to identify lung cancer early is years away, its impact would be enormous. "There are tens of millions of ex-smokers for which there is no early detection," Carbone said. Misperceptions common Kristen White thought lung cancer was a disease for old chain smokers. White, 47, of Russellville, Ky., had been biking 10 miles several times a week when she was diagnosed with the disease. She said she smoked socially a few times a year. "I was thinking, why me? I didn't do that. Look at all these people who smoke like chimneys. They're healthy," she said. White learned that her perception is a common one. One of the first questions she's asked after she tells people she has lung cancer is, "How much did you smoke?" Carbone's patients have told him similar stories. "Nobody asks heart attack patients how much ice cream they ate," he said. "They don't tell colon cancer patients that they should have eaten more fiber." Kay Cofrancesco of the Lung Cancer Alliance, a Washington, D.C.-based support and advocacy group, said the stigma surrounding lung cancer ultimately hampers research funding. "The mentality is: 'You smoked. You deserve lung cancer,' " Cofrancesco said. "The stigma prevents people from speaking out, so you don't have the awareness piece." Carbone said about 40 percent of new lung cancer cases occur among people who quit smoking three or more years ago. And almost 15 percent of new cases are people who never smoked. "More people die of lung cancer who have never touched a cigarette in their life than die of ovarian cancer," he said. Cofrancesco said another common misconception is that the lungs will repair the damage done by smoking within 10 years. That's not true, according to Dr. Pierre Massion, an associate professor of medicine and cancer biology at Vanderbilt-Ingram Cancer Center. "The risk of cancer never decreases for a smoker to the point of someone who never smoked," Massion said. Still, Massion said there is tremendous benefit to quitting. Just how much quitting lessens the chance of developing lung cancer depends on factors such as how long and how much a person smoked, he said. Protein study 'promising' Because there is no good way to detect the disease early on, lung cancer patients usually aren't diagnosed until the cancer has spread to other parts of the body. Only 25 percent of patients are candidates for surgery. But studies at Vanderbilt could one day change those statistics. In their effort to create a blood test, researchers at Vanderbilt and the University of Pittsburgh compared the blood of about 300 people. About half had lung cancer and the other half were considered to be at high risk for lung cancer. Massion said the research has identified seven proteins that may be unique among patients with lung cancer. "It's very promising," Massion said. "We'll need to conduct further studies to verify whether the protein profile is helpful in the diagnosis of lung cancer." But doing lung cancer research has gotten tougher, Carbone said. Grant money from the National Cancer Institute will be slashed by $400,000 a year for the next five years. Vanderbilt's $2.7 million annual grant was trimmed to $2.5 million two years ago and $2.3 million last year. "It caused us to eliminate an entire research project," Carbone said. Doctor, patient are hopeful Lung cancer researchers across the country face similar struggles. For every lung cancer death, $1,829 is spent on research by the National Cancer Institute, the Department of Defense and the Centers for Disease Control and Prevention. That compares with $5,216 per death for colon cancer, $14,369 for prostate cancer and $23,474 for breast cancer, according to the Lung Cancer Alliance. Lung cancer has fewer survivors raising awareness, fewer nonprofit organizations raising money and few treatment breakthroughs that would buoy research funding, Carbone said. The downturn in the economy is making it even tougher, he added. Yet despite the difficulties, Carbone is hopeful about progress that researchers are making. "I suspect in the next five or 10 years we'll have a blood test" for early detection, he said. Despite the odds, Kristen White is also hopeful. Medicine is keeping her cancer from growing. She wants to survive to see her daughter, a high school senior, graduate from college. "I hope in years to come, lung cancer will get the recognition of other cancers, and a cure will be found." . . . . . . . . . (Tennessean.com, Source: Vanderbuilt University Research, By Claudia Pinto, Staff Writer, April 9, 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.

Carole, You are great. I read your postings to Bill. They are uplifting and make so much sense. We have found that being proactive is important. Unfortunately, not every Cancer Center is offering palliative in that sense. Thankfully, from the very start, Bill's oncologist was in that thought mode. A team effort needs to be in place. Thank you so much, Barbara

http://www.cumc.columbia.edu/news/press ... omics.html Excerpt from press release: . . . . . . . . . Columbia University Medical Center and Rosetta Genomics Announce Columbia University’s Submission of the First Cancer Diagnostic Test Based on Rosetta Genomics Proprietary MicroRNA Technology for Approval to the New York State Department of Health Clinical Laboratory Evaluation Program The laboratory-developed test is designed to differentiate squamous from non-squamous non-small cell lung cancer (NSCLC), classifying squamous cell carcinoma of the lung with sensitivity of 96 percent and specificity of 90 percent Accurate diagnosis is important for guiding treatment. Bevacizumab(1) therapy for non-squamous NSCLC, includes a warning about potential higher rates of severe or fatal hemorrhage in patients with squamous NSCLC histology. Once approved by the New York State Department of Health, the test will be available nationwide through Columbia University Medical Center’s Molecular Pathology Laboratory, which developed and validated the test. Rehovot, Israel; Jersey City, New Jersey, New York (April 3, 2008) – Rosetta Genomics, Ltd. (NASDQ: ROSG) and Columbia University Medical Center (CUMC) announced today that the first molecular test based on Rosetta Genomics’ proprietary microRNA technology, developed by CUMC, has been submitted for approval by the New York State Department of Health. The test is designed to differentiate squamous from non-squamous NSCLC and is the first to use this technology to successfully classify two distinct types of the most common form of lung cancer. Once approved by New York State Department of Health, the test will be made available nationwide through Columbia University Medical Center’s High Complexity Molecular Pathology Laboratory, a laboratory licensed to use nucleic acids for better diagnosis of various cancers, which is part of the Department of Pathology and Cell Biology at CUMC. “With advancements toward more targeted therapies for cancer, there is a growing need for better diagnostics,” said Amir Avniel, President and CEO of Rosetta Genomics. The test, performed on a sample of the patient’s tumor and validated by Columbia University Medical Center, classifies squamous cell carcinoma of the lung with specificity of 90 percent and sensitivity of 96 percent. This is the first test utilizing microRNAs’ unique sensitivity and specificity as biomarkers that may offer a standardized and objective method for cancer classification. The genetic classification can be especially important for selecting proper treatment as therapies have been shown to act differently depending on cancer type, such as the case between squamous (scalelike) and non-squamous non-small cell lung cancer (NSCLC). Approximately 185,000 people are diagnosed with either squamous or non-squamous NSCLC each year in the United States. “The importance of accurately differentiating squamous cell from non-squamous NSCLC has recently been an issue of great interest and is gaining importance as new targeted therapies for NSCLC enter the market or proceed to late stages of development,” said Dr. Dalia Cohen, chief scientific officer of Rosetta Genomics. “This is a great advancement in terms of physicians’ ability to better treat patients with targeted therapies, which are currently highly effective in some patients while being less effective and sometimes harmful for others.” “We are excited to have performed the validation of the first diagnostic test based on microRNAs, and believe this endeavor is an important next step in bringing better diagnostics to patients and physicians,” noted Dr. Mahesh Mansukhani, director of the Molecular Pathology Laboratory at Columbia University Medical Center, who has led the validation process and submission of the test to the New York State Department of Health for approval. “Using a single microRNA biomarker, the test demonstrates high sensitivity and specificity, for squamous differentiation. Once approved, we will be pleased to offer this test through our pathology laboratory nationwide to doctors and patients as an objective aid in the classification of NSCLC. “ Data presented in peer reviewed publications has shown that two blinded expert observers, when asked to give an independent histological classification of NSCLC agreed only 74.7 percent of the time. Furthermore, sensitivity for squamous cell carcinoma was only 70.9 percent (2). A second study (3) looking at classification of squamous cell carcinoma showed that 40 percent of samples diagnosed as squamous cell lung cancer at regional labs were later reclassified as other lung cancers at central labs. The ability of physicians to accurately differentiate squamous (scalelike) from non-squamous NSCLC is an important treatment guide. Bevacizumab (1), an angiogenesis inhibitor and an important new modality of therapy for non-squamous NSCLC, includes a black-box warning about substantially higher rates of severe or fatal hemorrhage among patients with squamous NSCLC histology compared with non-squamous NSCLC. Currently, an estimated 60,000 patients per year are potential candidates for targeted therapy with Avastin™, a market available angiogenesis inhibitor, in the United States. Rosetta Genomics expects two additional tests based on its microRNA technology to be validated and submitted for regulatory approval during the second half of 2008 by laboratories in the United States. One test is designed to differentiate mesothelioma, an asbestos-associated cancer that develops in the pleura, from adenocarcinomas that either arise in the lung or spread to the lung and pleura from other sites. Another test is designed to identify the origin of a metastasis in patients presenting with cancer of unknown primary (CUP) origin. About microRNAs MicroRNAs (miRNAs) are recently discovered, naturally occurring, small RNAs that act as master regulators and have the potential to form the basis for a new class of diagnostics and therapeutics. Since many diseases are caused by the abnormal activity of proteins, the ability to selectively regulate protein activity through microRNAs could provide the means to treat a wide range of human diseases. In addition, microRNAs have been shown to have different expression in various pathological conditions. As a result, these differences may provide for a novel diagnostic strategy for many diseases. . . . . . . . . . (CUMC, Columbia University Medical Center, Press Release, April 8, 2008 [Contians Forward-looking Statements]) 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.stamfordadvocate.com/ci_8846783 ARTICLE: . . . . . . . . . Cancer gene therapy seminar set Staff Reports Stamford Advocate Article Launched:04/08/2008 01:00:00 AM EDT sharedstory The Alliance for Cancer Gene Therapy will host "The Promise of Cancer Gene Therapy for the Treatment of Lung Cancer," an April 16 seminar to explore advancements in treating lung cancer using gene therapy. Jack Roth, a member of the ACGT scientific advisory council, professor of molecular and cellular oncology and director of the W.M. Keck Cancer Center for Innovative Cancer Therapies at the University of Texas M.D. Anderson Cancer Center in Houston, will be the featured speaker. He will discuss lung cancer research, clinical trials and the prognosis of gene therapy as a potential cancer treatment. "For years we have used chemicals to treat the problem of cancer spreading from the local tumor (but) these chemicals are not very effective against cancer cells and highly toxic to normal cells," says Roth. "Gene therapy selectively targets abnormal biologic pathways in the cancer cell and may stimulate immune responses to cancer which will not harm normal cells. "Gene therapy for cancer is potentially more effective and much less toxic than current treatments." Edward Netter, chairman of the board of directors and co-founder with his wife, Barbara, of the Stamford-based ACGT, says Roth is considered a leading expert in the treatment of lung cancer. Roth has studied genetic phenomena in lung carcinogenesis, the process by which normal cells transform into cancer cells, and potential therapies that can target such phenomena. The ACGT was founded more than six years ago, Netter explains, to draw attention to gene therapy as an alternative protocol to chemotherapy and radiation, which can harm healthy cells and cause adverse side effects. "If you look at what's been going on with relation to cancer treatment, (medical professionals) are doing what they've always done," he says. "They are used to doing things the way they were taught." Since cancer is believed to be caused by a missing or defective gene, the ACGT's mission also includes funding research to develop drugs that attack only cancer cells. Connie Burnett-West, a lung cancer survivor who has been cancer-free for eight years since receiving gene therapy treatment, also will speak. * "The Promise of Cancer Gene Therapy for the Treatment of Lung Cancer" will be held April 16 at 7:15 p.m. at the Bruce Museum, 1 Museum Drive, Greenwich. Admission is free; reservations are required. Call 358-8000, ext. 349; or e-mail fyoung@acgtfoundation.org. - Camilla A. Herrera . . . . . . . . . (Stamford Advocate, April 8, 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 There, Ernie, THAT had to have been FUN. Clicking onto the slide show gave a much closer look at what must have been an exhilarating flight. The photos are great. Keeping positive, Barbara

Dear Carole, That is exactly what I have been thinking with regard to being "chronic." Of course, it usually takes some time before "semantics" is given a rest. Does it matter? It probably doesn't. Yes, we can be in palliative care toward whatever, and we can be in palliative care to elongate our survival. I have been so involved with this over these three plus years, that only those with the disease, or with someone special who has it, can fully understand the nuances of what palliative care can mean and internalizing that meaning for themselves. A couple of years ago, I read somewhere (lots of reading) that there were those who had received palliative care and had not only survived, but had been CURED). I believe, if I recall correctly, that the study was done in Australia. Does that happen often? It probably doesn't, but hey, let's go for it - if need be. Luv, Barbara