Posts: 96,117 Threads: 1,652 Thanks Received: 0 in 0 posts Thanks Given: 0 Joined: Jul 2011 Reputation: 0 CANCER- PANCREATIC/ and use of Cannabis Molecule That Facilitates Cancer Spread In Both Cells And Their Surroundings Found ScienceDaily (Jan. 21, 2008) The discovery that a molecule drives local tumor growth, as well as its ability to flourish and spread, opens a new window for understanding and treating cancer by taking aim at both cancer cells and their surrounding environment. A Dartmouth Medical School team led by Dr. Murray Korc found that a member of a common molecular family plays a role in the progress of a particularly resilient and aggressive pancreatic cancer, and that its influence is not restricted to that cancer. The work builds on studies by Korc, professor and chair of medicine at DMS, and colleagues at University of California, Irvine on glypican molecules, which interact with many growth factors implicated in cancer. A receptor called glypican-1 (GPC1) is abnormally abundant in pancreatic ductal adenocarcinoma, the most common and deadliest form of pancreatic cancer, often diagnosed after it has spread or metastasized. Human pancreatic cells deprived of their own GPC1 had reduced growth in culture, as well as when they were transplanted into immunocompromised mice (known as athymic for the lack of a thymus gland) that don't reject human cancer cells, the researchers demonstrated. "Tumors grow more slowly and are smaller. Interestingly, they also have less angiogenesis (blood vessel growth) and less metastasis," said Korc, also a professor pharmacology and toxicology and member of the Norris Cotton Cancer Center. Since GPC1 is common in many tissues, the researchers wanted to determine its role in the host environment, or how it functions in a patient. Knocking out the gene for GPC1 in mice, they created an athymic mouse population that lacked GPC1; then they introduced cancer cells. Host mice devoid of GPC1 had smaller pancreatic tumors that were less angiogenic and less metastatic when exposed to tumor cell lines with normal levels of GPC1. The metastatic potential of mouse melanoma (skin cancer) cells injected into mice with no GPC1 was also greatly decreased, the researchers found. "We've shown that GPC1 in the cancer cells and in the hostthat is, the patientis important not only for tumor growth, but for tumor angiogenesis and metastasis, Korc said. "This raises the possibility for therapeutic manipulations that will target GPC1 in both cancer cells and in patients to slow tumor growth and to prevent metastasis." Zeroing in on mechanisms that allow metastasis to occur more efficiently -namely, presence of GPC1in either the cancer cells or the host, offers new options against cancer. The approach seems promising because, added Korc, "Host-cancer interactions are becoming significant as clinicians and cancer researchers realize that the environment around cancer cells is just as important as the cancer cells themselves." This research was reported in the January Journal of Clinical Investigation. Co-authors on the research are Takuma Aikawa, Chery A. Whipple, Jason Gunn, Alison Young, of DMS, and Martha E. Lopez and Arthur D. Lander of UC Irvine. Adapted from materials provided by Dartmouth Medical School. source: http://www.scienceda...80117180113.htm Pancreatic cancer has one of the highest morbidity rates due mainly to the fact that early detection is rare. The symptom profile of most patients is not very distinct. I would encourage folks who have ANY issues with digestion or elimination to get it thoroughly checked A.S.A.P. This is one you don't want to mess with. Regardless of the type of treatment, early detection is the key to survival. Experimental Therapeutics, Molecular Targets, and Chemical Biology Cannabinoids Induce Apoptosis of Pancreatic Tumor Cells via Endoplasmic Reticulum StressRelated Genes Arkaitz Carracedo1, Meritxell Gironella2, Mar Lorente1, Stephane Garcia2, Manuel Guzmn1, Guillermo Velasco1 and Juan L. Iovanna2 1 Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, Madrid, Spain and 2 U624 Institut National de la Sante et de la Recherche Medicale, Marseille, France Requests for reprints: Guillermo Velasco, Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, c/ Jos Antonio Novais s/n, 28040 Madrid, Spain. Phone: 34-91-394-4668; Fax: 34-91-394-4672; E-mail: gvd@bbm1.ucm.es. Pancreatic adenocarcinomas are among the most malignant forms of cancer and, therefore, it is of especial interest to set new strategies aimed at improving the prognostic of this deadly disease. The present study was undertaken to investigate the action of cannabinoids, a new family of potential antitumoral agents, in pancreatic cancer. We show that cannabinoid receptors are expressed in human pancreatic tumor cell lines and tumor biopsies at much higher levels than in normal pancreatic tissue. Studies conducted with MiaPaCa2 and Panc1 cell lines showed that cannabinoid administration (a) induced apoptosis, ( increased ceramide levels, and up-regulated mRNA levels of the stress protein p8. These effects were prevented by blockade of the CB2 cannabinoid receptor or by pharmacologic inhibition of ceramide synthesis de novo. Knockdown experiments using selective small interfering RNAs showed the involvement of p8 via its downstream endoplasmic reticulum stressrelated targets activating transcription factor 4 (ATF-4) and TRB3 in 9-tetrahydrocannabinolinduced apoptosis. Cannabinoids also reduced the growth of tumor cells in two animal models of pancreatic cancer. In addition, cannabinoid treatment inhibited the spreading of pancreatic tumor cells. Moreover, cannabinoid administration selectively increased apoptosis and TRB3 exp<b></b> ression in pancreatic tumor cells but not in normal tissue. In conclusion, results presented here show that cannabinoids lead to apoptosis of pancreatic tumor cells via a CB2 receptor and de novo synthesized ceramide-dependent up-regulation of p8 and the endoplasmic reticulum stressrelated genes ATF-4 and TRB3. These findings may contribute to set the basis for a new therapeutic approach for the treatment of pancreatic cancer. (Cancer Res 2006; 66(13): 6748-55) Source: http://cancerres.aac...ract/66/13/6748 Cannabinoids Halt Pancreatic Cancer, Breast Cancer Growth, Studies Say by Paul Armentano, NORML, Cancer Research July 1st, 2006 Madrid, Spain: Compounds in cannabis inhibit cancer cell growth in human breast cancer cell lines and in pancreatic tumor cell lines, according to a pair of preclinical trials published in the July issue of the journal of the American Association for Cancer Research. In one trial, investigators at Complutense University in Spain and the Institut National de la Sante et de la Recherche Medicale (INSERM) in France assessed the anti-cancer activity of cannabinoids in pancreatic cancer cell lines and in animals. Cannabinoid administration selectively increased apoptosis (programmed cell death) in pancreatic tumor cells while ignoring healthy cells, researchers found. In addition, "cannabinoid treatment inhibited the spreading of pancreatic tumor cells ... and reduced the growth of tumor cells" in animals. "These findings may contribute to ... a new therapeutic approach for the treatment of pancreatic cancer," authors concluded. In the second trial, investigators at Spain's Complutense University reported that THC administration "reduces human breast cancer cell proliferation [in vitro] by blocking the progression of the cell cycle and by inducing apoptosis." Authors concluded that their findings "may set the bases for a cannabinoid therapy for the management of breast cancer." Previous preclinical data published in May in the Journal of Pharmacological and Experimental Therapeutics reported that non-psychoactive cannabinoids, particularly cannabidiol (CBD), dramatically halt the spread of breast cancer cells and recommended their use in cancer therapy. Separate trials have also shown cannabinoids to reduce the size and halt the spread of glioma (brain tumor) cells in animals and humans in a dose dependent manner. Additional preclinical studies have demonstrated cannabinoids to inhibit cancer cell growth and selectively trigger malignant cell death in skin cancer cells, leukemic cells, lung cancer cells, and prostate carcinoma cells, among other cancerous cell lines. source: http://safeaccessnow...cle.php?id=3563 Molecule That Facilitates Cancer Spread In Both Cells And Their Surroundings Found ScienceDaily (Jan. 21, 2008) The discovery that a molecule drives local tumor growth, as well as its ability to flourish and spread, opens a new window for understanding and treating cancer by taking aim at both cancer cells and their surrounding environment. A Dartmouth Medical School team led by Dr. Murray Korc found that a member of a common molecular family plays a role in the progress of a particularly resilient and aggressive pancreatic cancer, and that its influence is not restricted to that cancer. The work builds on studies by Korc, professor and chair of medicine at DMS, and colleagues at University of California, Irvine on glypican molecules, which interact with many growth factors implicated in cancer. A receptor called glypican-1 (GPC1) is abnormally abundant in pancreatic ductal adenocarcinoma, the most common and deadliest form of pancreatic cancer, often diagnosed after it has spread or metastasized. Human pancreatic cells deprived of their own GPC1 had reduced growth in culture, as well as when they were transplanted into immunocompromised mice (known as athymic for the lack of a thymus gland) that don't reject human cancer cells, the researchers demonstrated. "Tumors grow more slowly and are smaller. Interestingly, they also have less angiogenesis (blood vessel growth) and less metastasis," said Korc, also a professor pharmacology and toxicology and member of the Norris Cotton Cancer Center. Since GPC1 is common in many tissues, the researchers wanted to determine its role in the host environment, or how it functions in a patient. Knocking out the gene for GPC1 in mice, they created an athymic mouse population that lacked GPC1; then they introduced cancer cells. Host mice devoid of GPC1 had smaller pancreatic tumors that were less angiogenic and less metastatic when exposed to tumor cell lines with normal levels of GPC1. The metastatic potential of mouse melanoma (skin cancer) cells injected into mice with no GPC1 was also greatly decreased, the researchers found. "We've shown that GPC1 in the cancer cells and in the hostthat is, the patientis important not only for tumor growth, but for tumor angiogenesis and metastasis, Korc said. "This raises the possibility for therapeutic manipulations that will target GPC1 in both cancer cells and in patients to slow tumor growth and to prevent metastasis." Zeroing in on mechanisms that allow metastasis to occur more efficiently -namely, presence of GPC1in either the cancer cells or the host, offers new options against cancer. The approach seems promising because, added Korc, "Host-cancer interactions are becoming significant as clinicians and cancer researchers realize that the environment around cancer cells is just as important as the cancer cells themselves." This research was reported in the January Journal of Clinical Investigation. Co-authors on the research are Takuma Aikawa, Chery A. Whipple, Jason Gunn, Alison Young, of DMS, and Martha E. Lopez and Arthur D. Lander of UC Irvine. Adapted from materials provided by Dartmouth Medical School. source: http://www.scienceda...80117180113.htm Q. I would like you to know about medical marijuana for cancer. In her late 30s, my wife was diagnosed with pancreatic cancer, stage 4a. It was a 6 cm tumor that had grown around the hepatic artery and portal vein. At first I thought marijuana was just for nausea caused by her chemo, but then I found a study in the journal Cancer Research (July 1, 2006). It showed that cannabinoids specifically fight pancreatic tumor cells. I changed her diet and started her on a regimen and she is now cancer free. The regimen is being studied at the University of Wisconsin. I hope others can benefit from medical marijuana. A. For years, marijuana research was suspected of being a way to rationalize people getting high. But as a recent article in Science News points out, scientists are now starting to take it seriously (June 19, 2010). The article you cite demonstrates that compounds from marijuana make pancreatic tumor cells commit suicide. Other cancer researchers have followed up with studies on its effectiveness against a range of tumors in test tubes, including breast, colon, glioblastoma brain tumors and lymphoma, a blood cancer. None are yet in clinical trials, but this will be an interesting field to watch. We are delighted your wife got such a good response for such a difficult-to-treat cancer. Posts: 96,117 Threads: 1,652 Thanks Received: 0 in 0 posts Thanks Given: 0 Joined: Jul 2011 Reputation: 0 Cannabinoids Induce Apoptosis of Pancreatic Tumor Cells via Endoplasmic Reticulum StressRelated Genes To learn more More information from your American Cancer Society The following information on complementary and alternative therapies may also be helpful to you. These materials may be found on our Web site ( www.cancer.org) or ordered from our toll-free number (1-800-ACS-2345). Complementary treatments and herbal medicines Complementary and Alternative Methods for Cancer Management Guidelines for Using Complementary and Alternative Therapies Dietary Supplements: How to Know What Is Safe Placebo Effect The ACS Operational Statement on Complementary and Alternative Methods of Cancer Management Finding out about new ways to treat and prevent cancer Learning About New Ways to Treat Cancer Learning About New Ways to Prevent Cancer References American College of Physicians. Supporting research into the therapeutic role of marijuana. (Position paper, 2008.) Accessed at http://www.acponline.org/advocacy/where_...ijuana.pdf on January 13, 2012. Bhattacharyya S, Crippa JA, Allen P, et al. Induction of psychosis by {delta}9-tetrahydrocannabinol reflects modulation of prefrontal and striatal function during attentional salience processing. Arch Gen Psychiatry. 2012 Jan;69(1):27-36. Barsky SH, Roth MD, Kleerup EC, Simmons M, Tashkin DP. Histopathologic and molecular alterations in bronchial epithelium in habitual smokers of marijuana, cocaine, and/or tobacco. J Natl Cancer Inst. 1998;90:1198-1205. Bolla KI, Eldreth DA, Matochik JA, Cadet JL. Neural substrates of faulty decision-making in abstinent marijuana users. Neuroimage. 2005;26:480-492. Burgdorf JR, Kilmer B, Pacula RL. Heterogeneity in the composition of marijuana seized in California. Drug Alcohol Depend. 2011 Aug 1;117(1):59-61. Cannabis-In-Cachexia-Study-Group, Strasser F, Luftner D, Possinger K, et al. Comparison of orally administered cannabis extract and delta-9-tetrahydrocannabinol in treating patients with cancer-related anorexia-cachexia syndrome: a multicenter, phase III, randomized, double-blind, placebo-controlled clinical trial from the Cannabis-In-Cachexia-Study-Group. J Clin Onc. 2006;24:3394-3400. Cottencin O, Karila L, Lambert M, et al. Cannabis arteritis: review of the literature. J Addict Med. 2010 Dec;4(4):191-196. Disdier P, Granel B, Serratrice J, et al. Cannabis arteritis revisited--ten new case reports. Angiology. 2001;52:1-5. DuPont RL. Examining the debate on the use of medical marijuana users. Proc Assoc Am Physicians. 1999;111:166-172. Fusar-Poli P, Crippa JA, Bhattacharyya S, et al. Distinct effects of {delta}9-tetrahydrocannabinol and cannabidiol on neural activation during emotional processing. Arch Gen Psychiatry. 2009 Jan;66(1):95-105. Gruenwald J. PDR for Herbal Medicines. 3rd ed. Montvale, NJ: Thomson PDR; 2004. Haney M, Rabkin J, Gunderson E, Foltin RW. Dronabinol and marijuana in HIV(+) marijuana smokers: acute effects on caloric intake and mood. Psychopharmacology. (Berl). 2005;181:170-178. Hashibe M, Morgenstern H, Cui Y, et al. Marijuana use and the risk of lung and upper aerodigestive tract cancers: results of a population-based case-control study. Cancer Epidemiol Biomarkers Prev. 2006;15:1829-1834 Johnson JR, Burnell-Nugent M, Lossignol D, et al. Multicenter, double-blind, randomized, placebo-controlled, parallel-group study of the efficacy, safety, and tolerability of THC:CBD extract and THC extract in patients with intractable cancer-related pain. J Pain Symptom Manage. 2010 Feb;39(2):167-179. Joy JE, Watson SJ Jr, Benson JA Jr. eds. Marijuana and Medicine: Assessing the Science Base. Washington, DC: National Academy Press; 1999. Kalb C. No green light yet: a long-awaited report supports medical marijuana. So now what? Newsweek. 1999;133:35. Karschner EL, Darwin WD, Goodwin RS, et al. Plasma cannabinoid pharmacokinetics following controlled oral delta9-tetrahydrocannabinol and oromucosal cannabis extract administration. Clin Chem. 2011 Jan;57(1):66-75. Karst M, Salim K, Burstein S, et al. Analgesic effect of the synthetic cannabinoid CT-3 on chronic neuropathic pain: a randomized controlled trial. JAMA. 2003;290:1757-1762. McAllister SD, Christian RT, Horowitz MP, Garcia A, Desprez PY. Cannabidiol as a novel inhibitor of Id-1 gene expression in aggressive breast cancer cells. Mol Cancer Ther. 2007;6:29212927. Mehra R, Moore BA, Crothers K, Tetrault J, Fiellin DA. The association between marijuana smoking and lung cancer: a systematic review. Arch Intern Med. 2006;166:1359-1367. Mittleman MA, Lewis RA, Maclure M, Sherwood JB, Muller JE. Triggering myocardial infarction by marijuana. Circulation. 2001;103:2805-2809. Nahas G, Latour C. The human toxicity of marijuana. Med J Aust. 1992;156:495-497. National Cancer Institute. Cannabis and cannabinoids (PDQ) Health Professional Version, updated 12/14/11. Accessed at www.cancer.gov/cancertopics/pdq/cam/cannabis/healthprofessional on January 12, 2012. Robson P. Therapeutic aspects of cannabis and cannabinoids. Br J Psychiatry. 2001 Feb;178:107-115. Rog DJ, Nurmikko TJ, Young CA. Oromucosal delta9-tetrahydrocannabinol/cannabidiol for neuropathic pain associated with multiple sclerosis: an uncontrolled, open-label, 2-year extension trial. Clin Ther. 2007 Sep;29(9):2068-2079. Ross SA, ElSohly MA, Sultana GN, et al. Flavonoid glycosides and cannabinoids from the pollen of Cannabis sativa L. Phytochem Anal. 2005 Jan-Feb;16(1):45-48. Smigel K. Cancer problems lead list for potential marijuana research studies. J Natl Cancer Inst. 1997;89:1255. Smith PF. New approaches in the management of spasticity in multiple sclerosis patients: role of cannabinoids. Ther Clin Risk Manag. 2010 Mar 3;6:59-63. Tramr MR, Carroll D, Campbell FA, et al. Cannabinoids for control of chemotherapy induced nausea and vomiting: quantitative systematic review. BMJ. 2001;323:16-21. Voth EA, Schwartz RH. Medicinal applications of delta-9-tetrahydrocannabinol and marijuana. Ann Intern Med. 1997;126:791-798. Woolridge E, Barton S, Samuel J, et al. Cannabis use in HIV for pain and other medical symptoms. J Pain Symptom Manage. 2005;29:358-367. Zuardi AW. History of cannabis as a medicine: a review. Rev Bras Psiquiatr. 2006 Jun;28(2):153-157. Available online at http://www.scielo.br/scielo.php?script=s...so&tlng=en. Accessed 1/12/12. Note: This information may not cover all possible claims, uses, actions, precautions, side effects or interactions. It is not intended as medical advice, and should not be relied upon as a substitute for consultation with your doctor, who is familiar with your medical situation. Posts: 96,117 Threads: 1,652 Thanks Received: 0 in 0 posts Thanks Given: 0 Joined: Jul 2011 Reputation: 0 Letter to the Editor <ol style="list-style-type: decimal">[*]Letter to the Editor GLI1 Modulates EMT in Pancreatic CancerLetter - <li>Shingo Inaguma,
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</li></ol> Cancer Res Published OnlineFirst July 3, 2012; doi:10.1158/0008-5472.CAN-12-0379 ...Editor GLI1 Modulates EMT in Pancreatic Cancer-Letter Shingo Inaguma Kenji Kasai...epithelial-mesenchymal transition in pancreatic cancer cells (1). This conclusion was mainly...E-cadherin expression in several pancreatic cancer cell lines. The transcriptional activity... [*] Letter to the Editor GLI1 Modulates EMT in Pancreatic CancerResponse - Simon Joost,
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Cancer Res July 1, 2012 72:3414-3423; Published OnlineFirst May 2, 2012; doi:10.1158/0008-5472.CAN-12-0299 ...Sci U S A 2007;104:973-8. 16. Li C , Heidt DG, Dalerba P, Burant CF, Zhang L, Adsay V, et al Identification of pancreatic cancer stem cells. Cancer Res 2007;67:1030-7. 17. Scheel C , Eaton EN, Li SH, Chaffer CL, Reinhardt F, Kah KJ, et al... Posts: 1,594 Threads: 216 Thanks Received: 0 in 0 posts Thanks Given: 0 Joined: Feb 2014 Reputation: 0 Oh My Word... What A blessing---> Thank You.
I promise to read it all... Just as soon as I can. I go south to Eugene to see my Pain Specialist
on April 30th... Plus, I get to finally meet Dearest Suzy. She's giving me some oil and some
balm she made for my painful fingers. Funny how all the medical terminology is coming back to me.
Must get with my Jess to talk things over again. She's an R.N. now and wants to work with the addicted.
If I forget... She'll run it down to me and it locks-Usually it's gone the next day. I am getting a more clear head
as I am titrating downward now. If not complete detox... At least less damage. Great piece of work my friend.
Much Peace Within Your Souls, Wellness,Happiness, And Love To You And Cheri Along With Your Caring Children.
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