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Hanf (Cannabis sativa L.)

Arzneipflanze des Jahres 2018

Das Endocannabinoidsystem

ist ein wichtiger Teil des zentralen und peripheren Nervensystems zuständig für Signalübertragung zwischen Hirn, Rückenmark, Vegetatives Nervensystem und Organen sowie Regulator der  optimalen physiologischer und kognitiver Prozesse wie: Immunsystem,[1] vegetative nervous system,[2] soziales Verhalten und Angst[3] Bewegung, Gedächtnis, Lernprozesse[4] kontrolle über das Neubildung  Überleben oder Tod von neuronalen und nicht-neuronalen Zellen[5] Appetit[6] Schmerz Entzündungen[7] Fett- Energiestoffwechsel[8], und vieles mehr.
Veränderung in Endocannabinoidsystem oder Cannabinoid Mangel führen zu schlecht funktionierenden Immunsystems und einer Vielzahl von Krankheitszuständen.

Hanf in Antike Heilkunst

Die Geschichte der Verwendung von Hanf ist seit mehr als 4.800 jahre für breite spektrum von krankheiten dokumentiert.

Chinesen verwendeten ihn für Betäubung während chirurgischer Eingriffe, Malaria, Rheuma, Darmverstopfung, weiblichen Fortpflanzungssystems Störungen, als Abführmittel,[9]

In India war eingesetzt als Analgetikum (Zahnschmerzen, Kopfschmerzen, und Neuralgie), bei Krämpfen (Tetanus, Tollwut, Kolik, Durchfall und Epilepsie), zum  Beruhigung (Manie, Hysterie und Angst), Schmerzlinderung Bei entzündlichen Erkrankungen wie z.b. Rheuma, als Antibiotikum, bei Asthma, Bronchitis und viele andere[10] [11] [12].

Ägypter heilten mit Hanf Glaukom [13], gynäkologischen Erkrankungen, schmerz[14], Fieber, Geburtshilfe[15], Parasiten[16] Tumoren, Wunden, Schwellungen, Abszessen Fieber[17] Augen, Krebs und Anorektale Krankheiten[18]

Im Westen hat Hanf erst im 19 Jahrhundert ein Boom als Arznei gelöst.
Hunderte von wissenschaftliche Artikel über Heilkraft von Hanf würden veröffentlicht.[19] Es würde eine breite Spektrum von Krankheiten behandelt. Bis 1930 sind mehr als 2000 Medikamente auf Hanfbasis geboten[20] Zahlreiche Medizinische Anwendungen von Hanf waren zusammengefasst in “Sajous's Analytic Cyclopedia of Practical Medicine (1924)”[21]
Nach globales verbot in “Genfer Opiumkonferenz 1925” und Dämonisierung Kampagne Cannabis ist als Arznei verschwunden.

Die Wiederentdeckung

Unter öffentlichem Druck aufgrund die Krankheiten, für dies die Schulmedizin ratlos ist haben Wissenschaftler in 70 igem Jahren das therapeutische wert von Cannabis unter die Lupe genommen. Mittlerweile sind über 100.000 Studien und Fachartikel über Cannabis und Cannabinoide veröffentlicht. In Deutschland ist Behandlung mit Medikamente auf Cannabis Basis für über 60 Krankheiten rezeptpflichtig erlaubt.[22]
Laut Studien Cannabinoide könnten aufgrund ihres natürlichen Ursprungs und ihres geringen Nebenwirkungsprofils und Schutzfunktion von pathologischen Zustände eine sichere, kostengünstige Therapie für breite Palette von Krankheitszuständen darstellen.

Cannabinoiden und Schmerz

Einnahme von Cannabinoiden beseitigt Endocannabinoid-Mangel als hauptursache für Migräne, Fibromyalgie[23], Reizdarmsyndrom[24] und anderen behandlungsresistenten kronische Schmerzen.[25]  Cannabinoide beeinflussen Nucleus ventro caudalis einem Teil des Zwischenhirns die für Schmerzsinn zuständig ist und sind bei verringerung des schmerzempfinden 10 Mal wirksamer als Morphin.[26] Das Endocannabinoidsystem beeinflusst Schmerzkontrolle und vermittelt zentrale stressinduzierte Analgesie (Schmerzunempfindlichkeit)[27] Cannabinoid Agonisten unterdrücken Chronische und neuropathische Schmerzen durch Aktivierung  CB 1 - und CB 2 -Rezeptoren im Rückenmark[28]. Cannabinoide reduzieren Hyperalgesie (gesteigerte Empfinden Schmerzreizes) durch Hemmung des Calcitonin-Gen-verwandten Peptids[29]. Cannabinoide hemmen Glutamatfreisetzung und verringern neuropathischer Schmerzen und sekundären sowie tertiären Hyperalgesie (gesteigerte Empfinden Schmerzreizes) bei Migräne und Fibromyalgie[30]. Cannabinoide stimulieren produktion von Beta-Endorphin ein körpereigenes Morphin mit analgetischer Wirkung[31]. Cannabinoide haben zwanzigfache entzündungshemmende Wirksamkeit von Aspirin und die doppelte Wirkung von Hydrocortison[32]. Cannabinoid-2-Rezeptor-Agonist mildert durch Knochenkrebs verursachte Schmerzen und Knochenschwund[33] [34]. Cannabinoiden mildern durch Krebs verursachte Schmerzüberempfindlichkeit und entzündlichen Muskelschmerzen[35]

Cannabinoiden und Krebs

Wichtigste Eigenschaft den Cannabinoiden bei der Krebsbehandlung ist Fähigkeit Tumorzellen gezielt abzutöten.[36] Studien legen nahe dass Cannabinoide wirken gegen: Lungenkarzinom[37], Hirntumoren[38] [39] [40] [41], Brustkrebs[42] [43] [44] , Bauchspeicheldrüsenkrebs[45] [46] [47], Lymphom [48] [49] [50], Schilddrüsenkrebs [51] [52], Hautkarzinom [53] [54], Uteruskarzinom [55], Prostatakarzinom [56] [57] [58], Dickdarmkrebs [59] [60] [61] und Knochenkrebs [62] [63]. Cannabinoide haben ähnliche oder bessere Wirksamkeit bei der Milderung durch Chemotherapie verursachter Übelkeit und Erbrechen als zugelassene Antiemetika Medikamenten.[64]

Cannabinoiden bei Verletzungen und chronische neurodegenerative Krankheiten

Cannabinoide sind wegen Reduzierung klassischer neurotoxischer Ereignisse, Entfernung pathologischer Ablagerungen durch verbesserte neurologische Leistung, verringerte Ödeme, Infarktgröße, Gliosen, Entzündungen,  Blut-Hirn-Schranke-Störungen, vielversprechend bei behandlung von Hirnverletzung [65], Schlaganfälle [66] [67] [68] und chronische neurodegenerative krankheiten wie: Alzheimer [69] [70] [71] [72],  Parkinson [73] [74], Amyotrophe Lateralsklerose [75] [76] [77] Multiplen Sklerose [78]

Cannabinoiden bei Psychose, Depression und Angst

Cannabinoiden schwächen: akuten Stress [79] [80], Panikattacken und phobische Ängste [81], depressionen [82] [83] [84], mit Stress verursachten schaden auf Hippocampus [85], Psychosen [86] Schizophrenie [87] [88]

Neuroprotektiven und neuro regenerativen eigenschaften von Cannabinoiden

Cannabinoiden fordern Neuroplastizität (Fähigkeit des Gehirns, auf Erfahrungen als Reaktion sich zu verändern und anpassen) [89], Reparatur, Nach Wachstum [90] [91] und behüten Nervenzellen vor dem Absterben [92] [93]. Auf diese Weise bilden sie schutz vor neurodegenerativer Erkrankungen wie posttraumatische Belastungsstörungen (PTBS), Stimmungsstörungen, Alzheimer, Huntington, Parkinson, und Schizophrenie [94].

Cannabinoiden und Epilepsie

Patienten mit arzneimitteln resistenter Epilepsie haben weniger Anfälle [95], Degeneration und den Neuronenverlust im Hippocampus [96] insbesondere bei Lennox-Gastaut und Dravet-Syndrom [97] [98] [99] [100] Patienten haben Wenige oder keine Anfälle, bessere Stimmung, Kommunikation, Motorik, Sprache, Verhalten, Wachsamkeit  und  Schlaf      [101] [102] Hanfextrakte mit grosse CBD und geringe THC anteil haben bessere Antiepileptische wirkung als zugelassene arznei wie Diphenylhydantoin und  Mysolin [103]

Cannabinoiden Hemmen Opiatabhängigkeit und Entzugserscheinungen

Cannabidiol hemmt Betäubungsmitteln sucht, Entzugserscheinungen, Heroinsucht [104] [105] [106] Kokainsucht [107] Morphiumsucht [108] [109] [110] und Tabbaksucht [111]

Quellen:

[1] Pandey R., Mousawy K., Nagarkatti M., Nagarkatti P. (August 2009). "Endocannabinoids and immune regulation" . Pharmacological Research. 60 (2): 85–92. doi : 10.1016 / j.phrs.2009.03.019
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[2] Elphick MR, Egertová M (March 2001). "The neurobiology and evolution of cannabinoid signalling". Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences. 356 (1407):
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[3] Häring M, Kaiser N, Monory K, Lutz B (2011). Burgess HA (ed.). "Circuit specific functions of cannabinoid CB1 receptor in the balance of investigatory drive and exploration". PLOS ONE. 6 (11): e26617. Bibcode:2011PLoSO...626617H. doi:10.1371/journal.pone.0026617.
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[4] Goodman J, Packard MG. The influence of cannabinoids on learning and memory processes of the dorsal striatum. Neurobiol Learn Mem. 2015;125:1-14. doi:10.1016/j.nlm.2015.06.008
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[5]Cannabinoids and cell fate Manuel Guzmán CristinaSánchez Ismae Galve-Roperh Pharmacology & Therapeutics Volume 95, Issue 2, August 2002, Pages 175-184
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[6] Jesudason D, Wittert G. Endocannabinoid system in food intake and metabolic regulation. Curr Opin Lipidol 2008;19:344–348.
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[7]Burstein SH, Zurier RB. Cannabinoids, endocannabinoids, and related analogs in inflammation. AAPS J 2009;11:109–119.
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[8] Ruminska A, Dobrzyn A. [The endocannabinoid system and its role in regulation of metabolism in peripheral tissues] Postepy Biochem. 2012;58(2):127–134.
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[9] Merlin MD. Archaeological evidence for the tradition of psychoactive plant use in the old world. Econ Bot 2003;57:295-323
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[10] Touwn M. The religious and medicinal uses of Cannabis in China, India and Tibet. J Psychoactive Drugs. 1981;13(1):23-34.
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[11] Mikuriya TH. Marijuana in medicine: past, present and future. Calif Med. 1969;110(1):34-40.
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[12] Ethan Budd Russo CReDO Science Cannabis in India: Ancient lore and modern medicine
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[13] “Papyrus Ramesseum III”.
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[14] “Papyrus Ebers”
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[15] “Berliner Papyrus”
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[16] “Papyrus Hearst”
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[17] Medical Book from Crocodilopolis  P. Vindob. D. 6257
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[18] Papyrus Chester Beatty IV
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[19] Grinspoon L. Marihuana reconsidered. Cambridge, MA: Harvard University Press; 1971.

[20][The Antique Cannabis Book]

[21] "Sajous's analytic cyclopedia of practical medicine" Charles E de M Sajous; Louis T de M Sajous Philadelphia, F.A. Davis Company, 1924

[22] Der Stand der medizinischen Versorgung mit Cannabis und Cannabinoiden in Deutschland Dr. Franjo Grotenhermen “akzept e.V. Bundesverband für akzeptierende Drogenarbeit und humane Drogenpolitik” D-12161 Berlin
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[23] Delta-9-THC based monotherapy in fibromyalgia patients on experimentally induced pain, axon reflex flare, and pain relief Schley M., Legler A., ??Skopp G., Schmelz M., Konrad C., Rukwied R. Curr Med Res Opin. 2006 Jul; 22 (7): 1269 & ndash; 76.
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[25] Russo EB. Clinical endocannabinoid deficiency (CECD): can this concept explain therapeutic benefits of cannabis in migraine, fibromyalgia, irritable bowel syndrome and other treatment-resistant conditions? Neuro Endocrinol Lett. 2004 Feb-Apr;25(1-2):31-9. PMID: 15159679.
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[26] Suppression of noxious stimulus-evoked activity in the ventral posterolateral nucleus of the thalamus by a cannabinoid agonist: correlation between electrophysiological and antinociceptive effects. Martin WJ, Hohmann AG, Walker JM J Neurosci. 1996 Oct 15; 16(20):6601-11.
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[28] Activation of cannabinoid CB1 and CB2 receptors suppresses neuropathic nociception evoked by the chemotherapeutic agent vincristine in rats. Rahn EJ, Makriyannis A, Hohmann AG Br J Pharmacol. 2007 Nov; 152(5):765-77.
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[29] Antihyperalgesic effects of spinal cannabinoids. Richardson JD, Aanonsen L, Hargreaves KM Eur J Pharmacol. 1998 Mar 19; 345(2):145-53.
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[30] Cannabinoid receptor agonists inhibit glutamatergic synaptic transmission in rat hippocampal cultures. Shen M, Piser TM, Seybold VS, Thayer SA J Neurosci. 1996 Jul 15; 16(14):4322-34.
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[31] Chronic administration of cannabinoids regulates proenkephalin mRNA levels in selected regions of the rat brain. Manzanares J, Corchero J, Romero J, Fernandez-Ruiz JJ, Ramos JA, Fuentes JA Brain Res Mol Brain Res. 1998 Mar 30; 55(1):126-32.
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[32] Review Cannabinoids: the separation of central from peripheral effects on a structural basis. Evans FJ Planta Med. 1991 Oct; 57(7):S60-7.
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[33] Jia Sun, Ya-Qun Zhou, Shu-Ping Chen, Xiao-mei Wang, Bing-Yang Xu, Dan-Yang Li, Yu-Ke Tian, Da-Wei Ye, The endocannabinoid system: Novel targets for treating cancer induced bone pain, Biomedicine & Pharmacotherapy, Volume 120, 2019, 109504,
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[34] AN Lozano-Ondoua , C. Wright , A. Vardanyan , T. King , TM Largent-Milnes , M. Nelson , JM Jimenez-Andrade , PW Mantyh , TW Vanderah A cannabinoid 2 receptor agonist attenuates bone cancer-induced pain and bone loss Life Sci. , 86 ( 17-18 ) ( 2010 ) , S.. 646 - 653
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[35] Lois J Kehl, Darryl T Hamamoto, Paul W Wacnik, Devin L Croft, Blake D Norsted, George L Wilcox, Donald A Simone, A cannabinoid agonist differentially attenuates deep tissue hyperalgesia in animal models of cancer and inflammatory muscle pain
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[36] Chakravarti B, Ravi J, Ganju RK. Cannabinoids as therapeutic agents in cancer: current status and future implications. Oncotarget. 2014;5(15):5852-5872. doi:10.18632/oncotarget.2233
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[37] Ravi J, Sneh A, Shilo K, Nasser MW, Ganju RK. FAAH inhibition enhances anandamide mediated anti-tumorigenic effects in non-small cell lung cancer by downregulating the EGF/EGFR pathway. Oncotarget. 2014;5(9):2475–2486.
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[38] Blazquez C, Casanova ML, Planas A, Gomez Del Pulgar T, Villanueva C, Fernandez-Acenero MJ, Aragones J, Huffman JW, Jorcano JL, Guzman M. Inhibition of tumor angiogenesis by cannabinoids. Faseb J. 2003;17(3):529–531.
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[39] Carracedo A, Lorente M, Egia A, Blazquez C, Garcia S, Giroux V, Malicet C, Villuendas R, Gironella M, Gonzalez-Feria L, Piris MA, Iovanna JL, Guzman M, Velasco G. The stress-regulated protein p8 mediates cannabinoid-induced apoptosis of tumor cells. Cancer Cell. 2006;9(4):301–312.
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[40] Blazquez C, Salazar M, Carracedo A, Lorente M, Egia A, Gonzalez-Feria L, Haro A, Velasco G, Guzman M. Cannabinoids inhibit glioma cell invasion by down-regulating matrix metalloproteinase-2 expression. Cancer Res. 2008;68(6):1945–1952.
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[41] Nabissi M, Morelli MB, Santoni M, Santoni G. Triggering of the TRPV2 channel by cannabidiol sensitizes glioblastoma cells to cytotoxic chemotherapeutic agents. Carcinogenesis. 2013;34(1):48–57.
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[42] Nasser MW, Qamri Z, Deol YS, Smith D, Shilo K, Zou X, Ganju RK. Crosstalk between chemokine receptor CXCR4 and cannabinoid receptor CB2 in modulating breast cancer growth and invasion. PLoS One. 2011;6(9):e23901.
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[43] Zlotnik A, Burkhardt AM, Homey B. Homeostatic chemokine receptors and organ-specific metastasis. Nat Rev Immunol. 2011;11(9):597–606.
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[44] Caffarel MM, Sarrio D, Palacios J, Guzman M, Sanchez C. Delta9-tetrahydrocannabinol inhibits cell cycle progression in human breast cancer cells through Cdc2 regulation. Cancer Res. 2006;66(13):6615–6621.
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[45]Michalski CW, Oti FE, Erkan M, Sauliunaite D, Bergmann F, Pacher P, Batkai S, Muller MW, Giese NA, Friess H, Kleeff J. Cannabinoids in pancreatic cancer: correlation with survival and pain. Int J Cancer. 2008;122(4):742–750.
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[46]Carracedo A, Gironella M, Lorente M, Garcia S, Guzman M, Velasco G, Iovanna JL. Cannabinoids induce apoptosis of pancreatic tumor cells via endoplasmic reticulum stress-related genes. Cancer Res. 2006;66(13):6748–6755.
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[47] Fogli S, Nieri P, Chicca A, Adinolfi B, Mariotti V, Iacopetti P, Breschi MC, Pellegrini S. Cannabinoid derivatives induce cell death in pancreatic MIA PaCa-2 cells via a receptor-independent mechanism. FEBS Lett. 2006;580(7):1733–1739.
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[50] Gustafsson K, Christensson B, Sander B, Flygare J. Cannabinoid receptor-mediated apoptosis induced by R(+)-methanandamide and Win55,212-2 is associated with ceramide accumulation and p38 activation in mantle cell lymphoma. Mol Pharmacol. 2006;70(5):1612–1620.
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[51] Shi Y, Zou M, Baitei EY, Alzahrani AS, Parhar RS, Al-Makhalafi Z, Al-Mohanna FA. Cannabinoid 2 receptor induction by IL-12 and its potential as a therapeutic target for the treatment of anaplastic thyroid carcinoma. Cancer Gene Ther. 2008;15(2):101–107.
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[54] Differential role of cannabinoids in the pathogenesis of skin cancer Nicole Glodde, Mira Jakobs, Tobias Bald, Thomas Tüting, Evelyn Gaffal, Laboratory of Experimental Dermatology, Dept. of Dermatology and Allergy, University of Bonn, 53105 Bonn, Germany Life Sciences Volume 138, 1 October 2015, Pages 35-40
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[55] Arachidonyl ethanolamide induces apoptosis of uterine cervix cancer cells via aberrantly expressed vanilloid receptor-1 Gynecologic Oncology Volume 93, Issue 1, April 2004, Pages 182-188 Emmanuel Contassot, Mirna Tenan, Valérie Schnüriger, Marie-Françoise Pelte, Pierre-Yves Dietrich
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[56] Melck D, De Petrocellis L, Orlando P, Bisogno T, Laezza C, Bifulco M, Di Marzo V. Suppression of nerve growth factor Trk receptors and prolactin receptors by endocannabinoids leads to inhibition of human breast and prostate cancer cell proliferation. Endocrinology. 2000;141(1):118–126.
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[60] Cannabinoid Receptor Activation Induces Apoptosis through Tumor Necrosis Factor a–Mediated Ceramide De novo Synthesis in Colon Cancer Cells DOI: 10.1158/1078-0432.CCR-08-0799 Published December 2008 Fabio Cianchi, Laura Papucci, Nicola Schiavone, Matteo Lulli, Lucia Magnelli, Maria Cristina Vinci, Luca Messerini, Clementina Manera, Elisa Ronconi, Paola Romagnani, Martino Donnini, Giuliano Perigli, Giacomo Trallori, Elisabetta Tanganelli, Sergio Capaccioli and Emanuela Masini
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[61] The endogenous cannabinoid, anandamide, induces COX-2-dependent cell death in apoptosis-resistant colon cancer cells  July 1, 2010  
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[62] Lozano-Ondoua AN, Wright C, Vardanyan A, King T, Largent-Milnes TM, Nelson M, Jimenez-Andrade JM, Mantyh PW, Vanderah TW. A cannabinoid 2 receptor agonist attenuates bone cancer-induced pain and bone loss. Life Sci. 2010;86(17-18):646–653.
[PMC]

[63] Ofek O, Karsak M, Leclerc N, Fogel M, Frenkel B, Wright K, Tam J, Attar-Namdar M, Kram V, Shohami E, Mechoulam R, Zimmer A, Bab I. Peripheral cannabinoid receptor, CB2, regulates bone mass. Proceedings of the National Academy of Sciences of the United States of America. 2006;103(3):696–701.
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[64] Melissa E. Badowski A review of oral cannabinoids and medical marijuana for the treatment of chemotherapy-induced nausea and vomiting: a focus on pharmacokinetic variability and pharmacodynamics Cancer Chemotherapy and Pharmacology volume 80, pages 441–449(2017)
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[75] Carter GT, Abood ME, Aggarwal SK, Dr. Weiss. Cannabis and amyotrophic lateral sclerosis: hypothetical and practical applications, and a call for clinical trialsAm J Hosp Palliat Care 2010; 27: 347 & ndash; 356.Return to ref 152 in article
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