Medicinsk cannabis undersøges for effekten på kræft

Adskillige andre forskere har efterspurgt yderligere udforskning af cannabis-baserede terapier mod hjernekræft.[1] Selvom det er enkeltstående tilfælde, er det alligevel interessant, at en separat case rapport publiceret i 2011 i tidsskriftet International Society for Pediatric Neurosurgery, dokumenterede en spontan regression af hjernetumorer hos 2 børn, som fik cannabis.[2]

Andre separate præ-kliniske studier af cannabinoidernes evne til at hæmme glioma celler viser, at cannabinoider og endocannabinoider også kan hæmme delingen af forskellige andre kræftcelle linier, herunder bl.a. brystkræft,[3]prostatakræft,[4]kolorektal kræft,[5]mavekræft,[6] hudkræft,[7] leukæmi,[8]neuroblastoma,[9] lungekræft,[10] livmoderkræft,[11]kræft i skjoldbruskkirtlen,[12] bugspytkirtelkræft,[13]livmoderhalskræft,[14] hoved-halskræft,[15] galdegangskræft,[16] og lymfomer[17]

I nogle tilfælde forbedredes den kræfthæmmende aktivitet, når cannabinoiderne blev givet sammen med hinanden snarere end hver for sig.[18]

En rapport publiceret i Case Reports in Oncology  i 2013 fortalte om en succesfuld behandling med cannabis ekstrakt til en 14 år gammel patient med en aggressiv form for akut lymfocytisk leukæmi.[19] Populationsstudier viser ligeledes lovende resultater af brugen af cannabis og forekomsten af forskellige typer kræft, herunder lungekræft,[20] hoved-halskræft[21] og blærekræft.[22]

Som en konsekvens heraf anerkender nogle eksperter, at der eksisterer “solid videnskabelig evidens, som støtter, at cannabinoider udøver en bemærkelsesværdig kræfthæmmende aktivitet i præ-kliniske kræftforsøg,”[23] og mener, at cannabinoider måske en dag vil ”repræsentere en ny klasse af kræfthæmmende medicin, som svækker kræftvækst, hæmmer angiogenese og spredning af metastaser.[24]


[1] Parolaro and Massi. 2008. Cannabinoids as a potential new drug therapy for the treatment of gliomas. Expert Reviews of Neurotherapeutics 8: 37-49
Galanti et al. 2007. Delta9-Tetrahydrocannabinol inhibits cell cycle progression by downregulation of E2F1 in human glioblastoma multiforme cells. Acta Oncologica 12: 1-9.
Calatozzolo et al. 2007. Expression of cannabinoid receptors and neurotrophins in human gliomas. Neurological Sciences 28: 304-310.
[2] Foroughi et al. 2011. Spontaneous regression of septum pellucidum/forniceal pilocytic astrocytomas — possible role of cannabis inhalation. Child’s Nervous System 27: 671-679.
[3] Cafferal et al. 2006. Delta-9-Tetrahydrocannabinol inhibits cell cycle progression in human breast cancer cells through Cdc2 regulation. Cancer Research 66: 6615-6621.
Di Marzo et al. 2006. Anti-tumor activity of plant cannabinoids with emphasis on the effect of cannabidiol on human breast carcinoma. Journal of Pharmacology and Experimental Therapeutics Fast Forward 318: 1375-1387.
De Petrocellis et al. 1998. The endogenous cannabinoid anandamide inhibits human breast cancer cell proliferation. Proceedings of the National Academy of Sciences of the United States of America 95: 8375-8380.
McAllister et al. 2007. Cannabidiol as a novel inhibitor of Id-1 gene expression in aggressive breast cancer cells. Molecular Cancer Therapeutics 6: 2921-2927.
Cafferal et al. 2010. Cannabinoids reduce ErbB2-driven breast cancer progression through Akt inhibition. Molecular Cancer 9: 196.
[4] Sarfaraz et al. 2005. Cannabinoid receptors as a novel target for the treatment of prostate cancer. Cancer Research 65: 1635-1641.
Mimeault et al. 2003. Anti-proliferative and apoptotic effects of anandamide in human prostatic cancer cell lines. Prostate 56: 1-12.
Ruiz et al. 1999. Delta-9-tetrahydrocannabinol induces apoptosis in human prostate PC-3 cells via a receptor-independent mechanism. FEBS Letters 458: 400-404.
Ramos and Bianco. 2012. The role of cannabinoids in prostate cancer: Basic science perspective and potential clinical applications. Journal of Urology 28: 9-14.
DePetrocellis et al. 2013. Non-THC cannabinoids inhibit prostate carcinoma growth in vitro and in vivo: pro-apoptotic effects and underlying mechanisms. British Journal of Pharmacology 168: 79-102.
[5] Pastos et al. 2005. The endogenous cannabinoid, anandamide, induces cell death in colorectal carcinoma cells: a possible role for cyclooxygenase-2. Gut 54: 1741-1750.
Aviello et al. 2012. Chemopreventive effect of the non-psychotropic phytocannabinoid cannabidiol on experimental colon cancer. Journal of Molecular Medicine [E-pub ahead of print]
[6] Di Marzo et al. 2006. Anti-tumor activity of plant cannabinoids with emphasis on the effect of cannabidiol on human breast carcinoma. Journal of Pharmacology and Experimental Therapeutics Fast Forward 318: 1375-1387
[7] Casanova et al. Inhibition of skin tumor growth and angiogenesis in vivo by activation of cannabinoid receptors. 2003. Journal of Clinical Investigation 111: 43-50
[8] Powles et al. 2005. Cannabis-induced cytotoxicity in leukemic cell lines. Blood 105: 1214-1221
Jia et al 2006. Delta-9-tetrahydrocannabinol-induced apoptosis in Jurkat leukemic T cells in regulated by translocation of Bad to mitochondria. Molecular Cancer Research 4: 549-562.
Liu et al. 2008. Enhancing the in vitro cytotoxic activity of Ä9-tetrahydrocannabinol in leukemic cells through a combinatorial approach. Leukemia and Lymphoma 49: 1800-1809.
Scott et al. 2013. Enhancing the activity of cannabidiol and other cannabinoids in vitro through modifications to drug combinations and treatment schedules 33: 4373-4380.
Kampa-Schittenhelm et al. 2016. Dronabinol has preferential antileukemic activity in acute lymphoblastic and myeloid leukemia with lymphoid differentiation patterns. BMC Cancer. Open access at: http://bmccancer.biomedcentral.com/articles/10.1186/s12885-015-2029-8.
[9] Manuel Guzman. 2003. Cannabinoids: potential anticancer agents (PDF). Nature Reviews Cancer 3: 745-755.
Marcu et al. 2010. Cannabidiol enhances the inhibitory effects of delta9-tetrahydrocannabinol on human glioblastoma cell proliferation and survival. Molecular Cancer Therapeutics 9: 180-189.
[10] Guzman et al. 2003. Inhibition of tumor angiogenesis by cannabinoids. The FASEB Journal 17: 529-531
Preet et al. 2008. Delta9-Tetrahydrocannabinol inhibits epithelial growth factor-induced lung cancer cell migration in vitro as well as its growth and metastasis in vivo. Oncogene 10: 339-346.
[11] Manuel Guzman. 2003. Cannabinoids: potential anticancer agents (PDF). Nature Reviews Cancer 3: 745-755.
[12] Baek et al. 1998. Antitumor activity of cannabigerol against human oral epitheloid carcinoma cells. Archives of Pharmacal Research: 21: 353-356.
[13] Carracedo et al. 2006. Cannabinoids induce apoptosis of pancreatic tumor cells via endoplasmic reticulum stress-related genes. Cancer Research 66: 6748-6755.
Michalski et al. 2008. Cannabinoids in pancreatic cancer: correlation with survival and pain. International Journal of Cancer 122: 742-750.
[14] Ramer and Hinz. 2008. Inhibition of cancer cell invasion by cannabinoids via increased cell expression of tissue inhibitor of matrix metalloproteinases-1. Journal of the National Cancer Institute 100: 59-69.
Sindiswa and Motadi. 2016. Cannabidiol rather than cannabis sativa extracts inhibit cell growth and induce apoptosis in cervical cancer cells. BMC Complimentary and Alternative Medicine 16: 336.
[15] Whyte et al. 2010. Cannabinoids inhibit cellular respiration of human oral cancer cells. Pharmacology 85: 328-335.
[16] Leelawat et al. 2010. The dual effects of delta(9)-tetrahydrocannabinol on cholangiocarcinoma cells: anti-invasion activity at low concentration and apoptosis induction at high concentration. Cancer Investigation 28: 357-363.
[17] Gustafsson et al. 2006. Cannabinoid receptor-mediated apoptosis induced by R(+)-methanandamide and Win55,212 is associated with ceramide accumulation and p38 activation in mantle cell lymphoma. Molecular Pharmacology 70: 1612-1620.
Gustafsson et al. 2008. Expression of cannabinoid receptors type 1 and type 2 in non-Hodgkin lymphoma: Growth inhibition by receptor activation. International Journal of Cancer 123: 1025-1033.
[18] Torres et al. 2011. A combined preclinical therapy of cannabinoids and Temozolomide against glioma. Molecular Cannabis Therapeutics 10: 90.
Scott et al. 2013. Enhancing the activity of cannabidiol and other cannabinoids in vitro through modifications to drug combinations and treatment schedules 33: 4373-4380.
[19] Singh and Bali. 2013. Cannabis extract treatment for terminal acute lymphoblastic leukemia. Case Reports in Oncology 6: 585-592.
[20] Washington Post. May 26, 2006. “Study finds no cancer-marijuana connection.”
[21] Liang et al. 2009. A population-based case-control study of marijuana use and head and neck squamous cell carcinoma. Cancer Prevention Research 2: 759-768.
[22] Thomas et al. 2015. Association between cannabis use and the risk of bladder cancer: Results from the California Men’s Health Study. Urology 85: 388-393.
[23] Velasco et al. 2015. The use of cannabinoids as anticancer agents. Progress in Neuro-Psychopharmacology and Biological Chemistry. In print.
[24] Natalya Kogan. 2005. Cannabinoids and cancer. Mini-Reviews in Medicinal Chemistry 5: 941-952.
Sarafaraz et al. 2008. Cannabinoids for cancer treatment: progress and promise. Cancer Research 68: 339-342.
Ivanov VN1Wu J1, Hei TK: Regulation of human glioblastoma cell death by combined treatment of cannabidiol, γ-radiation and small molecule inhibitors of cell signaling pathways.
Oncotarget. 2017 May 27. doi: 10.18632/oncotarget.18240. [Epub ahead of print]
https://www.ncbi.nlm.nih.gov/pubmed/28599319