MsC1210

Dear Paulette I am so very sorry about all of this. I can understand what you are saying and I wish so very much that there was a way to make this all go away. Please know that you and Peter and your family are in my thoughts and prayers. I wish so very much I could do more. Hugs Chris

Hi Aaron and welcome I am so sorry to hear about your diagnosis but really glad you found this site. It sounds like you have a decent treatment plan in place and here's hoping that it continues to work! Please feel free to ask any and all questions you have and know that someone will be along with answers and/or advice soon. This site is the best place to find support and help and HOPE. Keep us posted and let us know how else we can help. My best to you, Chris

Plant-Derived Molecules, Genetic Manipulation Point To Future Chemoprevention Methods 17 Nov 2006 Scientists are using genetic studies and natural chemicals, such as plant-derived triterpenoids, to further our knowledge on how genetic and early molecular interactions can lead to cancer, and how those early interactions can be manipulated to stave off a variety of cancers. The latest studies with new and promising chemopreventive agents were presented at the American Association for Cancer Research's Frontiers in Cancer Prevention Research meeting on 13-Nov-2006. Trterpenoids and the rexinoid LG100268 prevent lung tumors induced by vinyl carbamate in strain A/J mice New synthetic drugs called triterpenoids which owe their origins to plant molecules have demonstrated their effectiveness in slowing the growth of lung cancer tumors, a research team from Dartmouth University has found. Following up on previous work showing strong links between inflammation and the development of cancer, Karen Liby, Ph.D., a postdoctoral fellow, and her colleagues found that the triterpenoid CDDO-MA, currently undergoing trails for leukemia and solid tumors (sponsored by Reata Pharmaceuticals), significantly reduced the number and sizes of tumors in mice. In addition, a chemically related drug developed by Ligand Pharmaceuticals called LG100268 was effective at preventing tumor growth. "Lung cancer is the leading cause of cancer deaths in the United States," said Liby. "Since the mortality from this disease is significant, and prognoses are poor once a patient has been diagnosed, prevention may provide the only avenues to combat this particular cancer. We think this study shows a promising role for triterpenoids and the drug LG100268 in stopping lung tumor growth." The scientists knew that the compounds had anti-inflammatory properties and that LG100268 in particular could stop certain types of breast cancer in animal models. The compounds inhibited inflammation in a number of ways: halting nitric oxide production, blocking cyclooxygenase and nitric oxide expression, curbing proliferation and inducing apoptosis in human lung cancer cells. They tested CDDO-MA and LG100268 on mice for 20 weeks. CDDO-MA and 268 reduced the number of lung tumors to 9.1 in the group fed CDDO and to 7.4 in the 268-fed group, compared to 15.5 in the control group. These tumors were smaller, too: 43 percent of tumors in CDDO-fed mice and 28 percent of tumors in the 268-fed group were less than 0.5 mm in diameter, compared to only four percent in the control groups. CDDO-ME and CDDO-EA, other synthetic forms of CDDO, also reduced tumors. After 15 weeks on a diet of the CDDO-ME triterpenoid, tumors numbered only 7.4, compared to 15.9 in the control mice. For mice on CDDO-EA, tumors were reduced to 7.8. No tumors in these groups were larger than 1 mm in diameter, while 20 percent of tumors in the control mice averaged more than this size. In fact, between 63 and 70 percent of tumors were less than 0.5 mm in diameter. The research suggests the potential for these compounds in preventing lung cancer, and points to the need for clinical trials to test their effectiveness in humans. The triterpenoid, CDDO-methyl ester, and the rexinoid, LG100268, synergize in the prevention of mammary tumors in a mouse model of estrogen receptor-negative breast cancer Triterpenoids and the rexinoid experimental drug LG100268 were also effective in combination against breast cancer development more than either compound individually, the Dartmouth research team found. Liby and her colleagues found that the synthetic triterpenoid CDDO-ME and the drug LG100268 eliminated tumors in mice that were fed the compounds. The work bolsters the potential for these drugs as a chemopreventive agent for an increasing range of cancers. "We previously reported that the rexinoid LG100268 and another potential drug, Afzoxifene, which modulates the estrogen receptor, synergize in the prevention and treatment of certain mammary tumors in mice," said Liby. "This study takes our work further, establishing a relationship between CDDO-ME triterpenoids, which are also effective anti-inflammation and anti-cancer compounds, and LG100268." The triterpenoid CDDO-ME had already been proven effective in inhibiting proliferation and inducing apoptosis (programmed cellular death, a process that's often disrupted in cancer) in breast cancer cells, and blocked the growth of breast cancer cells in mice. CDDO and its synthetic variant CDDO-ME are undergoing clinical trials for leukemia and solid tumors. Beginning at 10 weeks of age, mice that were genetically altered to become susceptible to breast cancer were fed either a control diet, a dose of CDDO-ME, LG 100268, or a combination of the two. After 40 weeks, all the control mice developed tumors. However, only 12 percent of mice on the CDDO-ME diet and 29 percent of the mice fed with LG100268 developed tumors. Most significantly, no tumors were found in the group fed a combination of both drugs. "The drugs that were fed in this experiment were apparently well tolerated, and the mice gained weight throughout the experiment," Liby said. "These studies indicate that CDDO-ME and LG100268, even as individual drugs, can delay tumor development in living organisms. But the combination of the triterpenoid and rexinoid compounds was particularly powerful. This synergy could hold the key to prevention of breast cancer and should be considered for future clinical trials." Genetic reduction of circulating insulin-like growth factor (IGF)-1 inhibits azoxymethane-induced colon tumorigenesis in mice Mice with a genetic alteration that reduced amounts of a key growth hormone had fewer carcinogen-induced tumors than mice with normal levels of the hormone, a research group from the National Cancer Institute (NCI), University of Texas-Austin and Mount Sinai School of Medicine found. The research suggests that reducing levels of the growth hormone IGF-1 could prove to be a promising method for preventing colon cancer from developing. It is also the first known study to successfully develop a way to examine depleted IGF-1 function in living animals. Susan Olivo-Marston, Ph.D., a postdoctoral fellow at the NCI, and her colleagues found that mice that lacked a gene that ultimately resulted in drastically reduced IGF-1 in the livers of mice had nearly half the number of tumors seen in mice with normal IGF-1 levels. Specifically, they found that mice with normal IGF-1 levels had an average of 13 colon tumors, but the IGF-deficient mice had only 7.2 tumors on average. In addition, the colon tumors in IGF-deficient mice were less likely to be found in the proximal colon; 25 percent of tumors were in the proximal colon of deficient mice, compared to 60 percent in the control mouse colons. Since IGF-1--in addition to its role in controlling the maximal, final growth of a young adult animal--also inhibits programmed cell death and stimulates colon epithelial cells, the scientists tested IGF-deficient mice for these cancer-causing characteristics. In fact, deficient mice had a decrease in proliferation in colon cells and an increase in apoptosis. The researchers were presented with a significant challenge, in that directly knocking out expression of IGF-1 in mice resulted in severe developmental abnormalities and very low survival rates. Therefore, the researchers found an existing type of mouse that lacked a gene called igf1 in the liver. These mice are IGF-1 deficient, but develop normally and have a 75 percent reduction in circulating levels of IGF-1. "High levels of IGF-1 have been associated with significant increases in colon cancer risk" said Olivo-Marston. "Since IGF-1 inhibits apoptosis and stimulates colon epithelium proliferation, we hypothesized that reducing, if not eliminating, its function could prove an effective deterrent against colon cancer growth. This small pilot study will need more follow-ups to verify our findings that reductions in IGF-1 may prevent colon tumor formation." Olivo-Marston's colleagues include Drs. Curt Harris and Jackie Lavigne at NCI, and Stephen Hursting at the University of Texas. ### The mission of the American Association for Cancer Research is to prevent and cure cancer. Founded in 1907, AACR is the world's oldest and largest professional organization dedicated to advancing cancer research. The membership includes more than 24,000 basic, translational, and clinical researchers; health care professionals; and cancer survivors and advocates in the United States and more than 70 other countries. AACR marshals the full spectrum of expertise from the cancer community to accelerate progress in the prevention, diagnosis and treatment of cancer through high-quality scientific and educational programs. It funds innovative, meritorious research grants. The AACR Annual Meeting attracts over 17,000 participants who share the latest discoveries and developments in the field. Special Conferences throughout the year present novel data across a wide variety of topics in cancer research, diagnosis and treatment. AACR publishes five major peer-reviewed journals: Cancer Research; Clinical Cancer Research; Molecular Cancer Therapeutics; Molecular Cancer Research; and Cancer Epidemiology, Biomarkers & Prevention. Its most recent publication, CR, is a magazine for cancer survivors, patient advocates, their families, physicians, and scientists. It provides a forum for sharing essential, evidence-based information and perspectives on progress in cancer research, survivorship and advocacy. Contact: Warren Froelich American Association for Cancer Research Article URL: http://www.medicalnewstoday.com/medical ... wsid=56636

Hello Farrah and welcome I am sorry to hear about your Dad but glad you found this site. Please let us know how we can be of help to you and your family. My best to you Chris

Prayers for you both. Chris

Hi Gerald and welcome I am sorry you have need of a site like this, but glad you have joined us. This is a very scary and overwhelming time in your life and so many of us here can relate to that. We are here to answer questions, offer advice, support and most importantly, HOPE. As Katie pointed out, this is not an easy fight, but there are survivors! Let us know how we can help you out and please read through the survivors and good news forums. You will find so much encouragement there. A good piece of advice for you which you will see mentioned throughout this site. Get a small notebook or an organizer to keep track of Dr appointments, tests and test results, and very important, write down any and ALL questions and/or concerns you have so you will not forget to ask about them. Keep us posted. We care. My best to you, Chris

I hope and pray every day that "the answer" will be found. Sooner rather than later. I hate this disease. Prayers and hugs to all Chris

I guess I understood what Aurora was getting at with the vent only forum idea. It is wonderful to have the carepages site for venting/sharing etc. I think though, a lot of people feel so comfortable with the LCSC site that the idea of beginning over, so to speak is daunting. Just my opinion and thanks Katie for all that you do here. Chris

RTA 402 Shown To Prevent Development Of Lung Cancer 16 Nov 2006 Reata Pharmaceuticals, Inc. today announced the presentation of preclinical data showing that RTA 402 prevented the development of lung cancer in an established mouse model of the disease. This data, produced in the laboratory of Dr. Michael Sxxx from the Dartmouth Medical School, was discussed in an oral presentation at the AACR Frontiers in Cancer Prevention Meeting being held in Boston, MA. In an oral presentation and poster, Dr. Karen Liby showed that RTA 402 (also known as "CDDOMe") protected mice from the development of invasive lung tumors following exposure to vinyl carbamate. This chemical reliably causes mice to develop a large number of tumors in their lungs. Furthermore, these tumors tend to be highly invasive and aggressive, which represents a fast- growing and deadly form of lung cancer. Mice that were administered RTA 402 after they had been exposed to vinyl carbamate were found to have 99% lower tumor burden than animals that did not receive the drug. RTA 402-treated animals developed one-fifth the number of tumors found in animals that did not receive RTA 402, and these tumors were much smaller and less invasive than in unprotected animals. In animals that did not receive RTA 402, almost all of the tumors were found to be of the invasive, deadly type, while in animals receiving RTA 402 fewer than half of tumors were considered invasive. Overall, RTA 402 exhibited a highly significant effect in protecting against lung cancer in this model. Previously, researchers at Dartmouth and Johns Hopkins demonstrated that a structural analogue of RTA 402 (RTA 403 or "CDDO-Im") prevented the formation of liver cancer induced by a potent carcinogen known as aflatoxin. This research was published as the cover article in the prestigious journal Cancer Research in February, 2006. This new study supports these earlier findings and indicates that this new class of drugs, known as the synthetic triterpenoids, holds great promise in the area of cancer prevention. Additionally, the data indicate that these drugs may prove useful in preventing the recurrence and metastasis of tumors that respond to initial therapies. About RTA 402 and Reata's Synthetic Triterpenoid Program RTA 402 and a number of related drugs with the same mechanism of action were licensed by Reata from Dartmouth College and The University of Texas M. D. Anderson Cancer Center. Two drugs from this series, RTA 402 and RTA 401, are currently in Phase 1 clinical trial for cancer indications. Trials in non- cancer indications are planned for early 2007. These drugs are first-in-class anti-cancer and anti-inflammatory agents with a unique mechanism of action. They selectively modulate the function of proteins that monitor and respond to changes in intracellular levels of oxidative stress. Consequently, they inhibit inflammatory processes that are essential for tumor growth, progression, and resistance to treatment. In normal cells, these drugs induce important antioxidant and anti-inflammatory responses, protecting the cells from toxic injury, inflammation, and carcinogenic transformation. Intensive preclinical studies have shown that Reata's triterpenoids selectively kill cancer cells while protecting normal tissue from radiation damage and chemotherapy-induced toxicity. Based on this unique combination of effects, these drugs have shown exceptional and broadbased activity in animal models of cancer, mucositis, autoimmune disease (rheumatoid arthritis, inflammatory bowel disease), respiratory disease, and transplantation. Available data from clinical studies suggest they are very well tolerated in humans and have significant anti- inflammatory and anticancer effects. About Reata Reata Pharmaceuticals, Inc. is a biopharmaceutical company focused on developing novel treatments for cancer, inflammation, and neurodegenerative diseases. Founded in 2002, Reata is developing five distinct classes of cancer drugs licensed from leading academic institutions. The company has three drugs in Phase 1 clinical development: RTA 744 for primary brain cancers; RTA 402 for solid tumors and lymphoid malignancies; and RTA 401 for leukemias and solid tumors. Reata is matching its clinical and preclinical drug development programs with a best-of-class drug discovery platform to identify small molecule chaperones that can induce proper folding of p53, SOD, and Tau, misfolded proteins that are involved in cancer and neurodegenerative disease. Reata Pharmaceuticals, Inc. http://www.reatadiscovery.com Article URL: http://www.medicalnewstoday.com/medical ... wsid=56772

Patients Respond Well To First Study To Test Higher Doses Of An Anti-Cancer Drug 14 Nov 2006 Researchers in the UK and the United States have found that a drug composed of an antibody carrying a highly toxic anti-cancer agent is well tolerated by patients at much higher doses than have been used before. The drug, BB-10901 (huN901-DM1), is being tested in a phase I clinical trial in patients who have relapsed or failed to respond to previous treatment for a range of cancers, such as small cell lung cancer (SCLC), other tumours in the lungs of neuroendocrine origin and non-pulmonary small cell carcinomas. Although the trial is not designed to test the efficacy of the drug, researchers report promising clinical responses in patients, including one patient who has remained in remission for more than a year. Dr Paul Lorigan reported to the EORTC-NCI-AACR [1] Symposium on Molecular Targets and Cancer Therapeutics in Prague today (Friday): "The results are important in that, in contrast to a prior regimen investigated in a phase I trial in the United States, significantly higher dose intensity is achieved with the current schedule. This has implications for the design of future trials with this agent, especially as the amount of the drug given is likely to be important in determining clinical response and outcome. In addition, the presence of a durable, complete response as well as other hints of clinical activity are very encouraging. "The tolerability of this agent compares very favourably with that of standard chemotherapy. The lack of clinically significant bone marrow toxicity by BB-10901 raises the possibility that such an agent could be used either alone or in combination with standard chemotherapy in future clinical trials." Dr Lorigan, a senior lecturer in medical oncology at the Christie Hospital, Manchester, UK, worked with colleagues in the UK and USA to investigate different dose levels, any adverse effects and how the drug was cleared from the body (pharmacokinetics). The drug, also known as huN901-DM1, is an immunoconjugate - a hybrid molecule specifically designed to deliver a potent cell-killing agent to cancer cells - and is created by attaching a cytotoxic drug DM1 to a monoclonal antibody, huN901. It binds to cells that have the molecule CD56 on their cell surfaces and the DM1 then can kill the cells. Several tumours are CD56 positive, including SCLC, neuroendocrine tumours, Wilms' tumours, and multiple myeloma. The researchers gave the drug by intravenous infusions for three consecutive days every three weeks. The researchers initially enrolled four patients at each dose level (4, 8, 16, 24, 36, 48, 60, 75 milligrams per squared metre of body surface area (mg/m2)). When a patient experienced a dose-limiting toxicity the cohort was enlarged to six patients at that dose. So far, 40 patients have been treated. Adverse effects were seen in six patients and included constipation, fatigue, leg pain, headache, inflamed pancreas, hypotension and myocardial infarction. Dr Lorigan said: "In general, the study drug was well tolerated, particularly when compared to standard chemotherapy. There was no clinically significant myelosuppression, most probably because the immunoconjugate is targeted at the tumour rather than the normal cells. Also, there was no clinical evidence of serious allergic or infusion reactions. The one side effect we have seen at higher doses is headache. This seems to be reduced if we increase the infusion time, and it may respond to other medication given with the study drug - we are investigating this further." One patient with metastatic, recurrent Merkel cell carcinoma (a rare, aggressive cancer that develops on, or just beneath, the skin and in hair follicles) had a durable, complete response and remains in clinical remission more than a year after treatment. "This patient had numerous prior relapses and had failed standard chemotherapy," said Dr Lorigan. Eight patients had stable disease lasting between six and 21 weeks. "It is difficult to draw any reliable conclusions from an early phase study such as this, but we are encouraged to see early signs of activity. While some tumours treated were indolent, others such as extensive SCLC were very aggressive. The presence of stable disease in a patient with SCLC over six cycles of therapy is very encouraging," he continued. Pharmacokinetics showed that drug was able to tackle tumour cells expressing CD56 more effectively at the higher doses. The researchers have not reached the maximum tolerated dose yet and are continuing to enrol new patients. "We are considering amending the protocol and adding three patients at 75 mg/m2/day, with pre-medication prior to infusions of BB-10901. While we have not seen dose-limiting toxicity at this level with the slower infusion (without pre-medication), we have seen headache in two patients, which is a moderate adverse effect. We anticipate that pre-medication will ameliorate or prevent this symptom. If well tolerated, we would then increase the dose to 94 mg/m2/day," said Dr Lorigan. He concluded: "Treatment options for these patients are limited and we are encouraged by the early results with this novel agent. We are grateful to the patients, their families, the investigators, clinical staff, and our colleagues at ImmunoGen (the sponsor of the clinical study) for their participation and continued support of this trial." ### Abstract no: 649 1. EORTC [European Organisation for Research and Treatment of Cancer, NCI [National Cancer Institute], AACR [American Association for Cancer Research]. Contact: Emma Mason European Organisation for Research and Treatment of Cancer Article URL: http://www.medicalnewstoday.com/medical ... wsid=56379

Paulette I am sorry about this latest development. Please know that you and Peter are and will continue to be in my thoughts and prayers. Chris

Hmm well that answers that.

Ann CONGRATULATIONS! She is beautiful! Chris

Aurora Great suggestion really, at least in my opinion. Katie? I'd be more than happy to moderate if this is something you feel worthy.. Chris

Hi Bobby I would think if the scans showed anything the doctor would have brought it up to your sister. I am here with you praying that no news is good news!! Sending hugs and positive thoughts to you and your sister, Chris

Hello Puglover and welcome I am sorry about all this sadness you have. Please know that we are here for you and will listen and offer advice whenever we can. I agree with the others regarding a 2nd or more opinion. And if the conventional treatments are not the right ones, there are many, many clincal trials out there that your Mom may qualify for. Please keep us posted. My thoughts and prayers are with you Chris

Joanie So glad to hear you are doing well!! Prayers for this trend to continue for you (and Brian) now. Chris

Congrats Ann and family! Chris

Maryanne So glad to read that Joel is doing better. Praying that he continues to do well now. Love and hugs Chris (AKA Your Female Friend lol )

Sharon, What a sweet post. Thank you for sharing this. Chris

Hi Chris Wow, what an amazing twist of fate. I am so glad that things are working out so well for you. As for someone looking out for you? I think you know who that is. Congratulations on the new position and keep in touch! Hugs and prayers, Chris

New Treatment Finds Success, Long Survival In Treating Tiniest Lung Tumors, 13 Nov 2006 Patients with metastatic cancer tumors in their lungs are much more likely to live disease-free if they have an experimental treatment involving shaped-beam radiosurgery rather that conventional treatment, according to a University of Rochester Medical Center study. The research, presented at the American Society of Therapeutic Radiology and Oncology conference in Philadelphia, offers a new option for the tens of thousands of patients annually who must cope with cancer that has spread to their lungs. Usually when the disease advances to that stage, the average survival time is 12 months and treatments are limited. In this study, some patients who were treated more than three years ago still have not had the disease spread. Shaped-beam, radiosurgery technology was originally designed for destroying brain tumors. Rochester oncologists are expanding its use to other parts of the body, studying whether it can be used to destroy other soft-tissue tumors that were previously considered untreatable. This includes tumors in the liver, adrenal glands and spine. Last year Paul Okunieff, M.D., and colleague Alan Katz, M.D., reported using the technology to achieve an 88 percent control rate for metastatic tumors in the liver, a result that was considered highly unlikely as recently as five years ago. The current study was funded in part by BrainLab, the maker of the Novalis radiosurgery system. In the study of 50 patients, 91 percent of the lung tumors treated between February 2001 and December 2005 never progressed, and about 25 percent of patients appear to be disease-free after three years of follow-up. Doctors hope that shaped-beam radiosurgery and chemotherapy might form a "synergistic combination that allows the drugs to destroy the microscopic cells that imaging studies can't see while the radiation therapy controls the tumors we can see," said Okunieff, chair of Radiation Oncology at the Medical Center's James P. Wilmot Cancer Center. Perhaps most importantly, this high-dose, focused radiation targets the tumor with very limited damage to healthy tissue that surrounds the lesion, and patients experience minimal side effects even when a large number of tumors are treated, Okunieff said. "We're getting better and better at finding smaller and smaller tumors that we can irradiate easily, and people are living longer," Okunieff said. Advances in CT imaging technology are allowing doctors to detect lung cancers earlier, generally improving a person's chance for survival. The new imaging techniques combined with other technologies like Novalis are making it possible for physicians to offer treatments that a few years ago were considered impossible. "We are now in the process of determining the circumstances in which these new technologies can benefit patients. We seem to have hit on some important ones,' Okunieff said. Okunieff's current study focused on patients with multiple lung lesions ranging in size from 3 millimeters to 7.7 centimeters between February 2001 and December 2005. Doctors treated 31 people with fewer than five tumors curatively and 19 others with more than five lesions palliatively to slow the disease. These patients had undergone multiple previous therapies for their metastatic disease prior to radiosurgery. Three years after follow-up, of the 125 lesions treated, 36 lesions (29 percent) disappeared completely, 32 lesions (26 percent) had shrunk, and 49 (39 percent) were stable after treatment. Only eight of the 125 lesions (6 percent) grew larger after the radiosurgery. "If we can kill the spots that we can see, and they are the most life-threatening, we can help people live longer," Okunieff said. "And when you deliver a one-two punch with chemotherapy to destroy the cancer cells we can't yet see, we dare to consider the potential of controlling metastatic disease comprehensively." ### Contact: Leslie White University of Rochester Medical Center Article URL: http://www.medicalnewstoday.com/medical ... wsid=56232

Hi Gwen So good to see your post. I have been thinking of you and wondering how things are going. Know that you and your family remain in my thoughts and prayers. As for the school? GO GET 'EM!!! And let us know how things go... Will be thinking of you.... Hugs and prayers Chris

Hello Stephanie and welcome I am glad you found this site. Once you have the test results and find out for certain what the mass is in Dad's lung be sure and let us know. It is hard not to worry especially in a case like this but try to remain positive. We are here for you and in the event that the tests do show the mass to be cancer, you will find so much information, answers to questions, support and HOPE here. Please keep us posted and know that you and your family are in my thoughts and prayers Chris

Hello Jackie and welcome I am sorry about your Mom's diagnosis. Please remember that statistics are nothing more than numbers and your Mom is an individual. Nobody can tell you how long she has. As Ry pointed out there are many members here on this site with other serious health issues who are fighting this and surviving. This site is incredible. Please ask any and all questions you have as there is always someone around who can and will offer you answers, advice etc. Read through the survivors stories and the good news stories. There is so much hope here as well as support. Let us know what you need and know we will be here to help you along the way, My best to you and your family Chris