In our state of the art drug screening lab we are examining a library of cannabinoids and their effect on several types of cancers, aiming to develop a proprietary treatment for different cancer types.
The research is comprised of a set of essays that have been designed to produce a comprehensive data set that can be used as basis for future anti-cancer clinical studies. Our preliminary results suggest that different THC / CBD ratios show differential effects on different cancer types.
Cannabics SR 5mg for Cancer Anorexia Cachexia Syndrome – CACS
Our clinical study was led by Professor Gil Bar-Sela, the Deputy Director of the Division of Oncology at Rambam Health Care Campus, Head of the Palliative and Supportive Oncology Unit, and Head of the service for Melanoma and Sarcoma Patients. The main endpoints of the treatment of patients with advanced cancer and CACS are weight gain and quality of life (QoL). The study is fully registered with the US NIH under “Cannabics Capsules as Treatment to Improve Cancer Related CACS in Advanced Cancer Patients”, Identifier NCT02359123, and may be found at https://clinicaltrials.gov/ct2/show/NCT02359123
According to Grand View Research, Inc., the global cancer diagnostics market size was valued at USD 124.0 billion in 2016 and is expected to grow at an annual rate of over 7%. This market is expected to reach USD 232.7 billion by 2025 according to Orbis Research.
The growth in cancer cases, growing demand for effective diagnostic tools that develop from rising awareness, government support and technological developments are driving the demand for this increase worldwide.
Cancer is one of the leading causes of deaths worldwide which leads to efforts to develop accurate diagnostic tools and effective treatment solutions. Early monitoring and pre-detection are being focused on as this leads to improved success rate in treatment. This leads to public awareness and healthcare support programs that promote routine check-ups which enable diagnosing the disease before first symptoms may appear.
Cannabis has long been suggested to stimulate appetite, decrease nausea and vomiting, and improve quality of life in cancer patients. Studies on the efficacy of cannabis for improving CACS and S-NIS have had mixed results. After trials showing improvement in weight gain among AIDS patients, cannabinoids were tested on cancer patients as well. In a controlled, random study comparing dronabinol to a placebo among cancer patients, dronabinol was associated with increased appetite in 38% vs 8% for placebo, and decreased nausea in 20% vs 7%, using acceptable measurement scales. Of the dronabinol patients, 22% gained ≥2 kg, compared with 10.5% of placebo recipients, but this datum did not reach significance, perhaps due to the advanced stage of cancer and the high mortality in both placebo and experimental group.
Another randomized study compared dronabinol to megestrol acetate or both treatments together. The research included 469 advanced cancer patients who had been suffering from a substantial appetite loss. A greater percentage of megestrol acetate-treated patients reported appetite improvement compared with dronabinol-treated patients, 75% vs 49% (p=0.0001). Combination treatment resulted in no significant differences compared with megestrol acetate alone. Another study, which included 243 patients, compared the administration of a combination of tetrahydrocannabinol and cannabinol to tetrahydrocannabinol alone, compared to placebo. It should be noted that cannabinoid dosages in the study were low, even in comparison to other studies. No significant differences between the groups were seen regarding improvement in appetite or weight-gain. In these two studies, no substantial side effects of cannabis products were found compared to the other arms. This may be related to the dosages of the drugs given.
A more recent study demonstrated improved chemosensory perception, appetite, sleep, and macronutrient preference in advanced cancer patients. However, the study included less than 50 patients. This research showed improvement in taste and smell perception in patients receiving chemotherapy, as well as appetite and caloric intake in the arm that received dronabinol compared to placebo.
Natural products have served as vital resources for cancer therapy (e.g.,Vinca alkaloids, paclitaxel, etc., which are used as conventional chemotherapeutic agents) and are also sources for novel drugs. Natural products from plants therefore represent an excellent resource for targeted therapies, as phytochemicals and herbal mixtures act multi-specifically, i.e. they attack multiple targets at the same time. Furthermore, the problem of drug resistance may be approached by integrating phytochemicals and phyto-therapy into academic western medicine through derivation and integration of data and as adjunct to conventional treatments. The integration of phytochemicals and phyto-therapy into cancer medicine represents a valuable asset to chemically synthesized chemicals and therapeutic antibodies. Cannabinoids are excellent candidates for this approach. Cannabinoids are a class of over 60 compounds derived from the plant cannabis sativa, as well as the synthetic or endogenous versions of these compounds. Cannabinoids show specific cytotoxicity against tumor cells, while protecting healthy tissue from apoptosis. These effects are exerted through cannabinoid receptors CB1 and CB2 in mammals and through non-receptor signaling pathways. Recent studies suggest that cannabinoids contribute to maintaining balance in cell proliferation and that targeting the endo-cannabinoid system can affect growth of several different types of cancer, including gliomas, breast, colon, prostate, and hepatocellular carcinoma.
Cannabis kills tumor cells
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Paweł Śledziński , Joanna Zeyland, Ryszard Słomski& Agnieszka Nowak. Cancer Medicine 2018; 7(3):765–775.
3. Preclinical and Clinical Assessment of Cannabinoids as Anti-Cancer Agents
Daniel A. Ladin, Eman Soliman, LaToya Griffin and Rukiyah Van Dross
Front. Pharmacol., 07 October 2016.
4. The stress-regulated protein p8 mediates cannabinoid-induced apoptosis of tumor cells.
5. The CB2 cannabinoid receptor signals apoptosis via ceramide-dependent activation of the mitochondrial intrinsic pathway.
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López-Rodríguez ML, Viso A, Ortega-Gutiérrez S, Díaz-Laviada I.
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7. Cannabinoids induce cancer cell proliferation via tumor necrosis factor alpha-converting enzyme (TACE/ADAM17)-mediated transactivation of the epidermal growth factor receptor.
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9. Anti-tumoral action of cannabinoids: involvement of sustained ceramide accumulation and extracellular signal-regulated kinase activation.
Uterine, testicular, and pancreatic cancers
10. Involvement of the CB2 cannabinoid receptor in cell growth inhibition and G0/G1 cell cycle arrest via the cannabinoid agonist WIN 55,212-2 in renal cell carcinoma.
11. GPR55 signaling promotes proliferation of pancreatic cancer cells and tumor growth in mice, and its inhibition increases effects of gemcitabine. Oncogen.2018.
R. Ferro, A. Adamska, R. Lattanzio, I. Mavrommati, C. E. Edling, S. A. Arifin, C. A. Fyffe, G. Sala, L. Sacchetto, G. Chiorino, V. De Laurenzi, M. Piantelli, O. J. Sansom, T. Maffucci, M. Falasca. Oncogene, 2018; DOI: 10.1038/s41388-018-0390-1.
12. Cannabis-derived substances in cancer therapy–an emerging anti-inflammatory role for the cannabinoids.
13. Cannabinoids induce apoptosis of pancreatic tumor cells via endoplasmic reticulum stress-related genes.
14. The expression level of CB1 and CB2 receptors determines their efficacy at inducing apoptosis in astrocytomas.
15. Opposite changes in cannabinoid CB1 and CB2 receptor expression in human gliomas.
16. Predominant CB2 receptor expression in endothelial cells of glioblastoma in humans
Schley M, Ständer S, Kerner J, Vajkoczy P, Schüpfer G, Dusch M, Schmelz M, Konrad C.Brain Res Bull. 2009 Jun 30;79(5):333-7. doi: 10.1016/j.brainresbull.2009.01.011. Epub 2009 Feb 6.
17. Cannabis use and cancer of the head and neck: Case-control study
Sarah Aldington,a Matire Harwood,a Brian Cox,b Mark Weatherall,c Lutz Beckert,a Anna Hansell,d Alison Pritchard,aGeoffrey Robinson, Richard Beasley,a,e,⁎ and Cannabis and Respiratory Disease Research Group. Otolaryngol Head Neck Surg. 2008 Mar; 138(3): 374–380.
18. Delta 9-tetrahydrocannabinol inhibits cell cycle progression by downregulation of E2F1 in human glioblastoma multiforme cells.
19. Cannabinoids and gliomas.
20. Cannabinoid receptors in human astroglial tumors.
21. Cannabidiol inhibits human glioma cell migration through a cannabinoid receptor-independent mechanism.
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22. Cannabidiol inhibits human glioma cell migration through a cannabinoid receptor‐independent mechanism
23. Hypothesis: cannabinoid therapy for the treatment of gliomas?
24. Appraising the “entourage effect”: Antitumor action of a pure cannabinoid versus a botanical drug preparation in preclinical models of breast cancer.
25. Phyto-, endo- and synthetic cannabinoids: promising chemotherapeutic agents in the treatment of breast and prostate carcinomas.
26. Cannabinoids may be therapeutic in breast cancer.
27. Cannabidiol as a novel inhibitor of Id-1 gene expression in aggressive breast cancer cells
28. Enhancing the Therapeutic Efficacy of Cancer Treatment with Cannabinoids.
29. Cannabinoid receptor-2 agonist inhibits macrophage induced EMT in non-small cell lung cancerby downregulation of EGFR pathway.
30. Cannabinoids increase lung cancer cell lysis by lymphokine-activated killer cells via upregulation of ICAM-1.
31. Cannabidiol inhibits lung cancer cell invasion and metastasis via intercellular adhesion molecule-1.
32. Cannabinoid receptors, CB1 and CB2, as novel targets for inhibition of non-small cell lung cancer growth and metastasis.
33. Anti-Proliferative Properties and Proapoptotic Function of New CB2 Selective Cannabinoid Receptor Agonist in Jurkat Leukemia Cells.
34. Anticancer effects of phytocannabinoids used with chemotherapy in leukemia cells can be improved by altering the sequence of their administration.2017. International Journal of Oncology.
35. Delta9-tetrahydrocannabinol-induced apoptosis in Jurkat leukemia T cells is regulated by translocation of Bad to mitochondria.
36. Gamma-irradiation enhances apoptosis induced by cannabidiol, a non-psychotropic cannabinoid, in cultured HL-60 myeloblastic leukemia cells.
37. Targeting CB2 cannabinoid receptors as a novel therapy to treat malignant lymphoblastic disease.
38. Inhibition of skin tumor growth and angiogenesis in vivo by activation of cannabinoid receptors.
39. The endocannabinoid system of the skin in health and disease: novel perspectives and therapeutic opportunities.
40. Anandamide-induced endoplasmic reticulum stress and apoptosis are mediated by oxidative stress in non-melanoma skin cancer: Receptor-independent endocannabinoid signaling.
41. The role of cannabinoids in dermatology.
42. Cannabinoid receptors as novel targets for the treatment of melanoma.
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liver and colon cancer
43. Anti-tumoral action of cannabinoids on hepatocellular carcinoma: role of AMPK-dependent activation of autophagy.
44. Estrogenic induction of cannabinoid CB1 receptor in human colon cancer cell lines.
45. Cannabinoid receptor activation induces apoptosis through tumor necrosis factor alpha-mediated ceramide de novo synthesis in colon cancer cells.
Cianchi F, Papucci L, Schiavone N, Lulli M, Magnelli L, Vinci MC, Messerini L, Manera C, Ronconi E, Romagnani P, Donnini M, Perigli G, Trallori G, Tanganelli E, Capaccioli S, Masini E. Clin Cancer Res. 2008 Dec 1;14(23):7691-700.