TESTICULAR CANCER & Cannabis studies completed
Testicular cancer is cancer that develops in the testicles, a part of the male reproductive system.
The use of cannabinoids in treating the side effects of cancer chemotherapy is more widely-studied than many other potential therapeutic applications, and a number of clinical studies have taken place investigating the use of THC and synthetic cannabinoids as anti-emetic agents.
Antioxidants, such as retinol, are important for a healthy immune system. Studies have found that higher intake of retinol-rich foods, such as fish, milk, eggs, dark green leafy vegetables, and super foods such as shelled hemp seeds. Cannabis has been around for many years as a treatment for cancer.
Science & Research
Undated - Anecdotal - Chemotherapy for Testicular Cancer2009 - Study - Weak link found between smoking pot, testicular cancer
Chemotherapy for Testicular Cancer
I am a 27-year-old male who was diagnosed with testicular cancer 6 months ago. I have undergone several operations to rid my body of the cancer. During the second operation it was apparent that chemotherapy was necessary to significantly decrease my odds of recurrence.
Prior to my experience with this illness, I was your typical "Just say no" type when it came to using any recreational drugs.
Shortly after my first round of chemo, I found myself feeling sick to my stomach. I felt as though I had eaten just enough d-con rat killer not to kill me. I was miserable, and the $25 a pill anti-nausea medicine they prescribed was not working at all.
After trying several types of medication, I was losing weight to the tune of 8-10 lbs a week. At that point I was given a prescription for Marinol. I had an immediate turnaround with regard to food consumption and overall mental health. I do realize that this synthetic THC is a replica of one of several cannabinoids that contribute to the overall affect of the drug. I was happy to see that the FDA isolated synthetic THC to help me at this point in my life.
By my third round of chemo the Marinol began to wane in its effects, and with much reservation I obtained and smoked marihuana. I was smoking through a water-filtered device and receiving relief from the ever-worsening affects of the chemotherapy. It was the only thing that gave me relief.
I have been clear for the last two checkups and was happy to return to work and my daily routine without the need for marihuana. I am now an advocate for medicinal marihuana, having first-hand experience on the subject.
For the last 5 years I have been working with a law enforcement background. The events written in this brief story are meant to help others who are having trouble taking the plunge. It is no longer a question of ethics but of choice.
Published by Jan
Testicular cancer is cancer that starts in the testicles, the male reproductive glands located in the scrotum.
The exact cause of testicular cancer is unknown. There is no link between vasectomy and testicular cancer. Factors that may increase a man's risk for testicular cancer include:
• Abnormal testicle development
• History of testicular cancer
• History of undescended testicle
• Klinefelter syndrome
Testicular cancer is the most common form of cancer in men between the ages of 15 and 35. It can occur in older men, and rarely, in younger boys. White men are more likely than African-American and Asian-American men to develop this type of cancer. There are two main types of testicular cancer: seminomas and nonseminomas. These cancers grow from germ cells, the cells that make sperm. Although testicular cancer can be derived from any cell type found in the testicles, more than ninety five percent of testicular cancers are germ cell tumors. Most testicular germ cell tumors have too many chromosomes.
Seminoma: This is a slow-growing form of testicular cancer usually found in men in their thirties and forties. The cancer is usually just in the testes, but it can spread to the lymph nodes. Seminomas are very sensitive to radiation therapy.
Nonseminoma: This more common type of testicular cancer tends to grow more quickly than seminomas. Nonseminoma tumors are often made up of more than one type of cell, and are identified according to these different cell types:
• Choriocarcinoma (rare)
• Embryonal carcinoma
• Yolk sac tumor
SymptomsThere may be no symptoms. Symptoms that may occur can include:
• Discomfort or pain in the testicle, or a feeling of heaviness in the scrotum
• Pain in the back or lower abdomen
• Enlargement of a testicle or a change in the way it feels
• Excess development of breast tissue (gynecomastia), however, this can occur normally in adolescent boys who do not have testicular cancer
• Lump or swelling in either testicle
Signs and testsA physical examination typically reveals a firm lump (mass) in one of the testicles. When the health care provider holds a flashlight up to the scrotum, the light does not pass through the lump.
Other tests include:
• Abdominal and pelvic CT scan
• Blood tests for tumor markers: alpha fetoprotein (AFP), human chorionic gonadotrophin (beta HCG), and lactic dehydrogenase (LDH)
• Chest x-ray
• Ultrasound of the scrotum
An examination of the tissue is usually done after the entire testicle is surgically removed.
Treatment depends on the:
• Type of testicular tumor
• Stage of the tumor
Once cancer is found, the first step is to determine the type of cancer cell by examining it under a microscope. The cells can be seminoma, nonseminoma, or both. The next step is to determine how far the cancer has spread to other parts of the body. This is called "staging."
• Stage I cancer has not spread beyond the testicle.
• Stage II cancer has spread to lymph nodes in the abdomen.
• Stage III cancer has spread beyond the lymph nodes (it could be as far as the liver, lungs, or brain).
• Surgical treatment removes the testicle (orchiectomy) and may also remove nearby lymph nodes (lymphadenectomy). This is usually performed in the case of both seminoma and nonseminomas.
• Radiation therapy using high-dose x-rays or other high-energy rays may be used after surgery to prevent the tumor from returning. Radiation therapy is usually only used for treating seminomas.
• Chemotherapy uses drugs such as cisplatin, bleomycin, and etoposide to kill cancer cells. This treatment has greatly improved survival for patients with both seminomas and nonseminomas.
A man with one remaining testis can lead a normal life, because the remaining testis takes up the burden of testosterone production and will generally have adequate fertility. However, it is worth the (minor) expense of measuring hormone levels before removal of a testicle, and sperm banking may be appropriate for younger men who still plan to have children, since fertility may be lessened by removal of one testicle, and can be severely affected if extensive chemotherapy and/or radiotherapy is done.
Less than five percent of those who have testicular cancer will have it again in the remaining testis. A man who loses both testicles will normally have to take hormone supplements (in particular, testosterone, which is created in the testicles), and will be infertile, but can lead an otherwise normal life.
Before 1970, men with recurrent testicular cancer were destined to have rapid progression and death from disseminated disease. Currently, although 7000 to 8000 new cases of testicular cancer occur in the United States yearly, only 400 men are expected to die of the disease. Much of this improvement is due to advances in adjuvant therapy.
Due to the risk of subsequent metastasis, post-surgical adjuvant therapy may be offered to the patient following orchiectomy. The type of adjuvant therapy depends largely on the histology of the tumor and the stage of progression at the time of surgery. These two factors contribute to the risk of recurrence, including metastasis. Adjuvant treatments may involve chemotherapy, radiotherapy or careful surveillance by frequent CT scans and blood tests by oncologists.
The three basic types of treatment are surgery, radiation therapy, and chemotherapy.
Surgery is performed by urologists; radiation therapy is administered by radiation oncologists; and chemotherapy is the work of medical oncologists. In most patients with testicular cancer, the disease is cured readily with minimal long-term morbidity.
While it may be possible, in some cases, to remove testicular cancer tumors from a testis while leaving the testis functional, this is almost never done, as the affected testicle usually contains pre-cancerous cells spread throughout the entire testicle. Thus removing the tumor alone without additional treatment greatly increases the risk that another cancer will form in that testicle . Since only one testis is typically required to maintain fertility, hormone production, and other male functions, the afflicted testis is almost always removed completely in a procedure called inguinal orchiectomy. (The testicle is almost never removed through the scrotum; an incision is made beneath the belt line in the inguinal area.) In the UK, the procedure is known as a radical orchidectomy.
Retroperitoneal Lymph Node Dissection (RPLND)
In the case of nonseminomas that appear to be stage I, surgery may be done on the retroperitoneal/Paraaortic lymph nodes (in a separate operation) to accurately determine whether the cancer is in stage I or stage II and to reduce the risk that malignant testicular cancer cells that may havemetastasized to lymph nodes in the lower abdomen. This surgery is called Retroperitoneal Lymph Node Dissection (RPLND). However, this approach, while standard in many places, especially the United States, is out of favor due to costs and the high level of expertise required to perform the surgery. The urologist may take extra care in the case of males who have not fathered children, to preserve the nerves involved in ejaculation.
Many patients are instead choosing surveillance, where no further surgery is performed unless tests indicate that the cancer has returned. This approach maintains a high cure rate because of the growing accuracy of surveillance techniques.
Lymph node surgery may also be performed after chemotherapy to remove masses left behind, particularly in the cases of advanced initial cancer or large nonseminomas.
Radiation may be used to treat stage 2 seminoma cancers, or as adjuvant (preventative) therapy in the case of stage 1 seminomas, to minimize the likelihood that tiny, non-detectable tumors exist and will spread (in the inguinal and para-aortic lymph nodes). Radiation is never used as a primary therapy for nonseminoma.
As an adjuvant treatment, use of chemotherapy as an alternative to radiation therapy in the treatment of seminoma is increasing, because radiation therapy appears to have more significant long-term side effects (for example, internal scarring, increased risks of secondary malignancies, etc.). Two doses, or occasionally a single dose of carboplatin, typically delivered three weeks apart, is proving to be a successful adjuvant treatment, with recurrence rates in the same ranges as those of radiotherapy. However, very long term data on the efficacy of adjuvant carboplatin in this setting does not exist. Since seminoma can recur decades after the primary tumor is removed, patients receiving adjuvant chemotherapy should remain vigilant and not assume they are cured five years after treatment. The concept of carboplatin as a single-dose therapy was developed by Tim Oliver, Professor of Medical Oncology at Barts and The London School of Medicine and Dentistry.
Chemotherapy is the standard treatment for non-seminoma when the cancer has spread to other parts of the body (that is, stage 2B or 3). The standard chemotherapy protocol is three, or sometimes four, rounds of Bleomycin-Etoposide-Cisplatin (BEP). This treatment was developed by Dr.Lawrence Einhorn at Indiana University. An alternative, equally effective treatment involves the use of four cycles of Etoposide-Cisplatin (EP).
While treatment success depends on the stage, the average survival rate after five years is around ninety five percent , and stage 1 cancers cases (if monitored properly) have essentially a one hundred percent survival rate (which is why prompt action, when testicular cancer is a possibility, is extremely important).
In the New England Journal of Medicine, treatment of testicular cancer has been called one of the success stories of modern medicine, with sustained response to treatment in more than ninety percent of cases, regardless of stage. Because of advances in chemotherapy, cure rates now approach eighty five percent overall, with better than ninety five percent for localized disease and eighty percent for metastatic disease—the best response by any solid tumor.
Cannabinoids and Testicular Cancer
The use of cannabinoids in treating the side effects of cancer chemotherapy is more widely-studied than many other potential therapeutic applications, and a number of clinical studies have taken place investigating the use of THC and synthetic cannabinoids as anti-emetic agents. Two preparations have been licensed for use in clinical treatment either in the UK or elsewhere, including dronabinol (synthetic THC) and Nabilone (a novel synthetic cannabinoid).
Side effects of chemotherapy and wasting diseases: The powerful drugs used in cancer chemotherapy effectively kill reproducing cells, including both the malignant tumour cells and also, as a side effect, many cells continually reproducing such as hair follicle cells and those lining the gut, leading to severe nausea & vomiting. These side effects can be very severe and many patients find these difficult or impossible to tolerate, falling into a wasting syndrome through malnutrition brought on by a combination of reduced appetite and poor gastrointestinal efficiency, which can itself shorten life expectancy.
There is variation between the effects of different anti-cancer drugs. Cisplatin, one of the most effective chemotherapy agents, induces vomiting in over 99% of patients not taking an antiemetic, with around 10 vomiting episodes per dose, although methotrexate causes emesis in under 10% of patients .
The main beneficial effects reported from use of cannabinoids are a reduction in the incidence and severity of nausea and vomiting (emesis), and stimulation of appetite, together reducing the severity of cachexia - wasting syndrome - in patients receiving chemotherapy treatment.
Studies involving natural cannabis: Vinciguerra et al studied 56 cancer patients unresponsive to conventional antiemetic agents, who were asked to rate the effectiveness of marijuana compared to prior chemotherapy cycles. Smoked marijuana was rated as "moderately effective" or "highly effective" by 78% of patients. The authors concluded that marijuana had antiemetic efficacy, but no control group was used and the patient population varied with respect to prior marijuana use or THC therapy.
Cannabinoids and anti-tumor activity
Recent scientific developments-anti-tumour activity: Recent scientific advances in the study of cannabinoid receptors and endocannabinoids have produced exciting new leads in the search for anti-cancer treatments, with CB1 and CB2 agonists (like THC) associated with tumor regression, reduced proliferation and blood supply to tumors, and apoptosis (programmed cell-suicide) among cells of various cancer types.
Blazquez et al reported "Cannabinoids, the active components of marijuana and their derivatives, induce tumor regression in rodents... Inhibition of tumor angiogenesis may allow new strategies for the design of cannabinoid-based anti-tumoral therapies." Sanchez et al reported "growth of the rat glioma (one of the most malignant forms of cancer) is inhibited by psychoactive cannabinoids" and that "local administration of (a) selective CB(2) agonist... induced a considerable regression of malignant tumors".
Parolaro et al concluded "Modulation of the endocannabinoid system interferes with cancer cell proliferation either by inhibiting mitogenic autocrine/paracrine loops or by directly inducing apoptosis; however, the proapoptotic effect of anandamide is not shared by other endocannabinoids and suggests the involvement of non-cannabinoid receptors" Bifulco & Di Marzo reviewed studies of antitumor activity and concluded "Recently, evidence has accumulated indicating that stimulation of cannabinoid receptors by either THC or the endocannabinoids influence the intracellular events controlling the proliferation and apoptosis of numerous types of cancer cells, thereby leading to anti-tumor effects both in vitro and in vivo. This evidence is reviewed here and suggests that future anti-cancer therapy might be developed from our knowledge of how the endocannabinoid system controls the growth and metastasis of malignant cells."
There would appear to be growing evidence of direct anti-tumor activity of cannabinoids, specifically CB1 and CB2 agonists, in a range of cancer types including brain (gliomas), skin, pituitary, prostate and bowel. The antitumor activity has led in laboratory animals and in-vitro human tissues to regression of tumors, reductions in vascularisation (blood supply) and metastases (secondary tumors), as well as direct inducement of death (apoptosis) among cancer cells. Indeed, the complex interactions of endogenous cannabinoids and receptors is leading to greater scientific understanding of the mechanisms by which cancers develop.
In the very least, cannabinoids should be used as adjunct treatment for testicular cancer. Use whole plant extracts from Sativa x Indica hybrids.
^ Cancer Facts and Figures 2003. Atlanta, GA: American Cancer Society. 2003. Retrieved 2008-04-24.
^ Cancer Facts and Figures 2007. Atlanta, GA: American Cancer Society. 2007. Retrieved 2008-04-24.
^ CancerStats, 2007 UK incidence data, Cancer Research UK.
^ Hayes-Lattin, Brandon; Nichols, Craig R. (October 2009). "Testicular Cancer: A Prototypic Tumor of Young Adults". Seminars in oncology36 (5): 432–438. doi:10.1053/j.seminoncol.2009.07.006.PMC 2796329. PMID 19835738.
^ a b Feldman DR; Bosl GJ, Sheinfeld J, Motzer RJ (February 13, 2008). "Medical treatment of advanced testicular cancer". JAMA 299(6): 672–684. doi:10.1001/jama.299.6.672. PMID 18270356. Retrieved June 24, 2011.
^ Eble J.N., Sauter G., Epstein J.I., Sesterhenn I.A. (Eds.): World Health Organization Classification of Tumours. Pathology and Genetics of Tumours of the Urinary System and Male Genital Organs. IARC Press: Lyon 2004. ISBN 92 832 2412 4
^ Mills, S (ed.) 2009.Sternberg's Diagnostic Pathology. 5th Edition.ISBN 978-0-7817-7942-5
^ Screening for testicular cancer: a brief evidence update for the U.S. Preventive Services TaskForce. Rockville, MD: Agency for Healthcare Research and Quality; February 2004.http://www.ahrq.gov/clinic/3rduspstf/testicular/testiculup.htm
^ Testicular Cancer: Early Detection, Diagnosis, and Staging. July 2010.http://www.cancer.org/Cancer/TesticularCancer/DetailedGuide/testicular-cancer-detection
^ a b c d e Motzer, Robert J.; Bosl, George J. (2005). "82. Testicular Cancer". In Kasper, Dennis L.; Jameson, J. Larry. Harrison's Principles of Internal Medicine (16th ed.). McGraw-Hill. pp. 550–553.ISBN 0071391401.
^ a b c d e f g Shaw, Joel (February 15, 2008). "Diagnosis and Treatment of Testicular Cancer". American Family Physician(American Academy of Family Physicians) 77 (4): 469–474.ISSN 1532-0650. PMID 18326165. Retrieved August 5, 2010.
^ Atkin NB, Baker MC (December 1982). "Specific chromosome change, i(12p), in testicular tumours?". Lancet 2 (8311): 1349.PMID 6128640.
^ "Testicular Cancer Resource Center's Staging Page". Retrieved 2007-12-13.
^ "How is testicular cancer staged?". cancer.org. American Cancer Society. 01/19/2011. Retrieved 12 July 2011.
^ "Testicular Cancer Treatment (PDQ)". National Cancer Institute. 2009-01-15. Retrieved 2009-02-13.
^ "Chemotherapy - BEP and EP". Retrieved 2009-02-16.
^ Huang, William C. (June 5, 2008). "Book Review: Urological Oncology". The New England Journal of Medicine (Massachusetts Medical Society) 358 (23): 2527. doi:10.1056/NEJMbkrev59744.ISSN 1533-4406. Retrieved August 9, 2010.
^ Krege, S.; Beyer, J.; Souchon, R.; Albers, P.; Albrecht, W.; Algaba, F.;et al. (2008). "European consensus conference on diagnosis and treatment of germ cell cancer: a report of the second meeting of the European Germ Cell Cancer Consensus group (EGCCCG): part I".European Urology 53 (3): 478–496.doi:10.1016/j.eururo.2007.12.024.
^ Rustin, G. J.; Mead, G. M.; Stenning, S. P.; Vasey, P. A.; Aass, N.; Huddart, R. A.; et al. (2007). "Randomized trial of two or five computed tomography scans in the surveillance of patients with stage I nonseminomatous germ cell tumors of the testis: Medical Research Council Trial TE08; ISRCTN56475197—the National Cancer Research Institute Testis Cancer Clinical Studies Group". JCO 25(11): 1310–1315. doi:10.1200/JCO.2006.08.4889.
^ "Cancer of the testicle Causes - Health encyclopaedia - NHS Direct". Archived from the original on 2007-12-10. Retrieved 2007-12-13.
^ Leendert H. J. Looijenga; J. Wolter Oosterhuis (May 1999)."Pathogenesis of testicular germ cell tumours" (PDF). Rev. Reprod.4 (2): 90–100. doi:10.1530/ror.0.0040090. ISSN 1359-6004.PMID 10357096.
^ Holmes L; Escalante C, Garrison O, Foldi BX, Ogungbade GO, Essien EJ, Ward D (September 2008). "Testicular cancer incidence trends in the United States (1975−2004): Plateau or shifting racial paradigm?". Public Health 122 (9): 862–872.doi:10.1016/j.puhe.2007.10.010. PMC 2551560.PMID 18555499.
^ Forman, D; M C Pike, G Davey, S Dawson, K Baker, C E D Chilvers, R T D Oliver, C A C Coupland (28 May 1994). "Aetiology of testicular cancer: association with congenital abnormalities, age at puberty, infertility, and exercise". BMJ 308 (6941): 1393–9. PMC 2540340.PMID 7912596.
^ Swerdlow, AJ; Huttly SR, Smith PG. (January 1987). "Testicular cancer and antecedent diseases". Br. J.Cancer 55 (1): 97–103.doi:10.1038/bjc.1987.20. PMC 2001571. PMID 2880604.
^ Jones, T. C., R. D. Hunt, and N. W. King (1997). Veterinary pathology (6th ed.). Wiley-Blackwell. p. 1210. ISBN 0683044818, 9780683044812.
 Gralla RJ, Itri LM, Pisko SE, et al. 1981. Antiemetic efficacy of high dose metoclopramide: randomized trials with placebo and prochlorperazine in patients with chemotherapy induced nausea vomiting. New England Journal of Medicine 305:905-909.
 Davis CJ. 1995. Emesis research: A concise history of the critical concepts and experiments. In: Reynolds DJ' Andrews PL, Davis CJ, Editors. Serotonin and the scientific basis of anti-emetic therapy. Oxford: Oxford Clinical Communications. Pp.9-24.
 Hesketh PJ, Kris MG, Grunberg SM, Beck T. Hainsworth ID, Harker G. Aapro MS, Gandara D, Lindley CM. 1997. Proposal for classifying the acute emetogenicity of cancer chemotherapy. Journal of Clinical Oncology 15:103-109.
 British Medical Association. 1997. Therapeutic uses of cannabis. Amsterdam, The Netherlands: Harwood Academic Publishers.
 DeMulder PH, Seynaeve C, Vermorker JB, et al. 1990. Ondansetron compared with highdose metoclopramide in prophylaxis of acute and delayed cisplatin-induced nausea and vomiting: A multicenter, randomized, double-blind, crossover study. Annals of Internal Medicine 113:834-840.
 Jamshidi N, Taylor DA.  Anandamide administration into the ventromedial hypothalamus stimulates appetite in rats.Br J Pharmacol. 134(6):1151-4.
 Inui A.  Cancer anorexia-cachexia syndrome: current issues in research and management. CA Cancer J Clin. 52(2):72-91.
 Croxford JL.  Therapeutic potential of cannabinoids in CNS disease. CNS Drugs. 17(3):179-202.
 Walsh D, Nelson KA, Mahmoud FA.  Established and potential therapeutic applications of cannabinoids in oncology. Support Care Cancer. 11(3):137-43. Epub 2002 Aug 21.
 Grotenhermen F.  Pharmacokinetics and pharmacodynamics of cannabinoids. Clin Pharmacokinet. 42(4):327-60
 Parker LA, Mechoulam R, Schlievert C, Abbott L, Fudge ML, Burton P.  Effects of cannabinoids on lithium-induced conditioned rejection reactions in a rat model of nausea. Psychopharmacology (Berl). 166(2):156-62. Epub 2003 Jan 15.
 Zurcher G.  [Anorectic syndrome] [Article in German] Z Gastroenterol. 2002 Apr;40 Suppl 1:S71-S5.
 Russmann S, Winkler A, Lovblad KO, Stanga Z, Bassetti C  Lethal ischemic stroke after cisplatin-based chemotherapy for testicular carcinoma and cannabis inhalation. Eur Neurol. 2002;48(3):178-80.
 Drewe J.  [In Process Citation] [Article in German] Ther Umsch. 2003 Jun;60(6):313-6.
 Gardner B, Zhu LX, Sharma S, Tashkin DP, Dubinett SM  Methanandamide increases COX-2 expression and tumor growth in murine lung cancer. FASEB J. 17(14):2157-9. Epub 2003 Sep 04.
 Sallan SE, Zinberg NE, Frei E. 1975. Antiemetic effect of delta-9-THC in patients receiving cancer chemotherapy. New England Journal of Medicine 293 :795-797.
 Chang AK, Shiling DJ, Stillman RC, et al. 1979. Delta-9-tetrahydrocannabinol as an Antiemetic in patients receiving high-dose methotrexate: A prospective, randomized evaluation. Annals of Internal Medicine 91:819-824.
 Frytak S. Moertel CG, O'Fallon J. et al. 1979. Delta-9-tetrahydrocannabinol as an antiemetic in patients treated with cancer chemotherapy: a double comparison with prochloperazine and a placebo. Annals of Internal Medicine 91 :825-830.
 Orr LE, McKernan JF, Bloome B. 1980. Antiemetic effect of Tetrahydrocannabinol. Compared with placebo and prochlorperazine in chemotherapy-associated nausea and emesis. Archives of Internal Medicine 140:1431
 Lucas VS Jr & Laszlo J (1980) D9 THC for refractory vomiting induced by cancer chemotherapy JAMA 243 pp1241-1243
 Chang AK, Shiling DJ, Stillman RC, Goldberg NH, Seipp CA, Barofsky I, Rosenberg SA. (1981). A prospective evaluation of delta-9-tetrahydrocannabinol as an antiemetic in patients receiving adriamycin and cytoxan chemotherapy. Cancer 47:1746-51.
 Niedhart J, Gagen M, Wilson H & Young D (1981) Comparative trial of the antiemetic effects of THC and haloperidol. J Clin Pharmacol 21 p385
 Gralla RJ, Itri LM, Pisko SE, et al. (1981). Antiemetic efficacy of high dose metoclopramide: randomized trials with placebo and prochlorperazine in patients with chemotherapy induced nausea vomiting. New England Journal of Medicine 305:905-909.
 Ungerleider JT, Andrysiak TA, Fairbanks L, Goodnight J, Sarna G & Jamieson K. (1982). Cannabis and Cancer Chemotherapy, a comparison of oral D9 THC and prochlorperazine. Cancer 50 pp636-645.
 LaneM, Vogel CL, & Ferguson J (1991) Dronabinol and prochlorperazine in combination are better than either agent alone for treatement of chemotherapy-induced nausea and vomiting. Proc Am Soc Clin Oncologists 8 p236
 Nagy CM, Furnas BE, Einhorn LH, & Bond WH (1978) Nabilone: antiemetic crossover study in cancer chemotherapy patients. Proc Am Soc Cancer Research 19 p30
 Herman TS, Einhorn LH, Jones SE, Nagy CM, Chester AB, Dean JC, Furnas B, Williams ST, Leigh SA, Dorr RT & Moon TE (1979) Superiority of nabilone over prochlorperazine as an antiemetic in patients receiving cancer chemotherapy. NEJM 300 pp1295-1297
 Einhorn LH, Nagy C, Furnas B & Williams SD (1981) Nabilone: an effective antiemetic in patients receiving cancer chemotherapy. J Clin Pharmacol 21 pp645-695
 Wada JK, Bogdon DL, Gunnell JC, Hum GJ, Gota CH & Rieth TE (1982) Double-blind randomised crossover trial of nabilone vs placebo in cancer chemotherapy. Cancer Treatment Reviews 9 (supplement B) pp39-44
 Levitt M (1982) Nabilone vs placebo in treatment of chemotherapy induced nausea and vomiting in cancer patients. Cancer Treatment Reviews 9 (supplement B) pp49-53
 Johannson R, Kikku P & Groenroos M (1982) A double-blind controlled trial of nabilone vs prochlorperazine for refractory emesis induced by cancer chemotherapy. Cancer Treatment Reviews 9 (supplement B) pp25-33
 Ahmedzal S, Carlyle DL, Calder IT & Moran F (1983) Antiemetic efficacy and toxicity of nabilone, a synthetic cannabinoid, in lung cancer chemotherapy. Br J Cancer 48 pp67-663
 Niiranen A & Mattson K (1985) A crossover comparison of nabilone and prochlorperazine for emesis induced by cancer chemotherapy. Am J Clin Oncology 8 pp36-340
 Jones SE, Durant JR, Greco FA & Roberstone A (1982) A multi-institutional phase III study of nabilone vs placebo in chemotherapy-induced nausea and vomiting. Cancer Treatment Review 9 pp455-485
 Niederle N, Schutte J & Schmidt CG (1986) Crossover comparison of the antiemetic efficacy of nabilone and alizapride in patients with nonseminomatous testicular cancer receiving cisplatin therapy. Klinische Wochenschrift 64 pp 362-265
 Pomeroy M, Fennelly JJ, Towers M (19867) Prospective randomised double-blind trial of nabilone vs domperidone in the treatment of cytotoxic-induced emesis. Cancer Chemotherapy & Pharmacology 17 pp 285-288
 Dalzell AM, Bartlett H Lilleyman JS (1986) Nabilone: an alternative antiemetic for cancer chemotherapy Ach Diseases of Childhood. 89 pp1314-1319
 Chan HSL, Correia JA & MacLeod SM (1987) Nabilone versus prochlorperazine for control of cancer chemotherapy induced emesis in children - a double blind crossover trial. Pediatrics 79 pp946-952.
 Vinciguerra V, Moore T. Brennan E. 1988. Inhalation marijuana as an antiemetic for cancer chemotherapy. New York State Journal of Medicine 88:525-527.
 Levitt M, Faiman C, Hawks R. et al. 1984. Randomized double-blind comparison of delta-9- THC and marijuana as chemotherapy antiemetics. Proceedings of the American Society for Clinical Oncology 3:91.
 Lindgren JE, Ohlsson A, Agurell S. Hollister LE, Gillespie H. 1981. Clinical effects and plasma levels of delta 9-tetrahydrocannabinol (delta 9-THC) in heavy and light users of cannabis. Psychopharmacology (Berl) 74:208-12.
 Ohlsson A, Lindgren J-E, Wahlen A, Agurell S. Hollister L E, Gillespie HK. 1980. Plasma delta-9-tetrahydrocannabinol concentrations and clinical effects after oral and intravenous administration and smoking. Clinical Pharmacology and Therapeutics 28:409-416.
 Huestis MA, Henningfield JE, Cone EJ. 1992. Blood Cannabinoids. I. Absorption of THC and formation of 11-OH-THC and THCCOOH during and after smoking marijuana. Journal of Analytical Toxicology 16:276-282.
 Haney M, Ward AS, Comer SD, Foltin RW, Fischman MW. 1999. Abstinence symptoms following oral THC administration to humans. Psychopharmacology 141:385-394.
 British Medical Association. 1997. Therapeutic uses of cannabis. Amsterdam, The Netherlands: Harwood Academic Publishers.
 Janet E. Joy, Stanley J. Watson, Jr., and John A. Benson, Jr., Editors (1999) Marijuana and Medicine - Assessing the Science Base. Institute of Medicine/National Academy Press Washington, D.C
 House of Lords (1998) op cit paras 5.12, 8.9-8.11
 Blazquez C, Casanova ML, Planas A, Del Pulgar TG, Villanueva C, Fernandez-Acenero MJ, Aragones J, Huffman JW, Jorcano JL, Guzman M.  Inhibition of tumor angiogenesis by cannabinoids. FASEB J. 17(3):529-31. Epub 2003 Jan 02.
 Sanchez C, de Ceballos ML, del Pulgar TG, Rueda D, Corbacho C, Velasco G, Galve-Roperh I, Huffman JW, Ramon y Cajal S, Guzman M.  Inhibition of glioma growth in vivo by selective activation of the CB(2) cannabinoid receptor. Cancer Res.61(15):5784-9.
 Casanova ML, Blazquez C, Martinez-Palacio J, Villanueva C, Fernandez-Acenero MJ, Huffman JW, Jorcano JL, Guzman M.  Inhibition of skin tumor growth and angiogenesis in vivo by activation of cannabinoid receptors. J Clin Invest. 111(1):43-50
 Di Marzo V, Melck D, Orlando P, Bisogno T, Zagoory O, Bifulco M, Vogel Z, De Petrocellis L.  Palmitoylethanolamide inhibits the expression of fatty acid amide hydrolase and enhances the anti-proliferative effect of anandamide in human breast cancer cells.Biochem J. 358(Pt 1):249-55
 De Petrocellis L, Bisogno T, Ligresti A, Bifulco M, Melck D, Di Marzo V.  Effect on cancer cell proliferation of palmitoylethanolamide, a fatty acid amide interacting with both the cannabinoid and vanilloid signalling systems. Fundam Clin Pharmacol. 16(4):297-302.
 Fowler CJ, Jonsson KO, Andersson A, Juntunen J, Jarvinen T, Vandevoorde S, Lambert DM, Jerman JC, Smart D.  Inhibition of C6 glioma cell proliferation by anandamide, 1-arachidonoylglycerol, and by a water soluble phosphate ester of anandamide: variability in response and involvement of arachidonic acid. Biochem Pharmacol. 66(5):757-67.
 Portella G, Laezza C, Laccetti P, De Petrocellis L, Di Marzo V, Bifulco M  Inhibitory effects of cannabinoid CB1 receptor stimulation on tumor growth and metastatic spreading: actions on signals involved in angiogenesis and metastasis.FASEB J. 17(12):1771-3. Epub 2003 Jul 03.
 Mimeault M, Pommery N, Wattez N, Bailly C, Henichart JP.  Anti-proliferative and apoptotic effects of anandamide in human prostatic cancer cell lines: implication of epidermal growth factor receptor down-regulation and ceramide production. Prostate. 56(1):1-12.
 Recht LD, Salmonsen R, Rosetti R, Jang T, Pipia G, Kubiatowski T, Karim P, Ross AH, Zurier R, Litofsky NS, Burstein S.  Antitumor effects of ajulemic acid (CT3), a synthetic non-psychoactive cannabinoid. Biochem Pharmacol. 62(6):755-63.
 Ligresti A, Bisogno T, Matias I, De Petrocellis L, Cascio MG, Cosenza V, D'argenio G, Scaglione G, Bifulco M, Sorrentini I, Di Marzo V.  Possible endocannabinoid control of colorectal cancer growth. Gastroenterology. 125(3):677-87.
 Jacobsson SO, Wallin T, Fowler CJ.  Inhibition of rat C6 glioma cell proliferation by endogenous and synthetic cannabinoids. Relative involvement of cannabinoid and vanilloid receptors. J Pharmacol Exp Ther. 2001 Dec;299(3):951-9.
 Gomez del Pulgar T, Velasco G, Sanchez C, Haro A, Guzman M.  De novo-synthesized ceramide is involved in cannabinoid-induced apoptosis. Biochem J. 363(Pt 1):183-8.
 Gomez Del Pulgar T, De Ceballos ML, Guzman M, Velasco G.  Cannabinoids protect astrocytes from ceramide-induced apoptosis through the phosphatidylinositol 3-kinase/protein kinase B pathway. J Biol Chem. 277(39):36527-33. Epub 2002 Jul 19.
 Gonzalez S, Mauriello-Romanazzi G, Berrendero F, Ramos JA, Franzoni MF, Fernandez-Ruiz J.  Decreased cannabinoid CB1 receptor mRNA levels and immunoreactivity in pituitary hyperplasia induced by prolonged exposure to estrogens. Pituitary. 3(4):221-6.
 Pagotto U, Marsicano G, Fezza F, Theodoropoulou M, Grubler Y, Stalla J, Arzberger T, Milone A, Losa M, Di Marzo V, Lutz B, Stalla GK.  Normal human pituitary gland and pituitary adenomas express cannabinoid receptor type 1 and synthesize endogenous cannabinoids: first evidence for a direct role of cannabinoids on hormone modulation at the human pituitary level. J Clin Endocrinol Metab. 86(6):2687-96
 Rubovitch V, Gafni M, Sarne Y.  The cannabinoid agonist DALN positively modulates L-type voltage-dependent calcium-channels in N18TG2 neuroblastoma cells. Brain Res Mol Brain Res. 101(1-2):93-102.
 Bifulco M, Laezza C, Portella G, Vitale M, Orlando P, De Petrocellis L, Di Marzo V.  Control by the endogenous cannabinoid system of ras oncogene-dependent tumor growth. FASEB J. 15(14):2745-7. Epub 2001 Oct 29.
 Guzman M, Sanchez C, Galve-Roperh I.  Cannabinoids and cell fate. Pharmacol Ther. 95(2):175-84.
 Guzman M.  Cannabinoids: potential anticancer agents. Nat Rev Cancer. 3(10):745-55
 Parolaro D, Massi P, Rubino T, Monti E.  Endocannabinoids in the immune system and cancer. Prostaglandins Leukot Essent Fatty Acids. 66(2-3):319-32.
 Bifulco M, Di Marzo V. [The endocannabinoid system as a target for the development of new drugs for cancer therapy] [Article in Italian] Recenti Prog Med. 94(5):194-8.
 Abrahamov A, Abrahamov A, Mechoulam R.  An efficient new cannabinoid antiemetic in pediatric oncology. Life Sci. 56(23-24):2097-102
 Lockwood AH.  Marihuana and alcohol intolerance in Hodgkin's disease. N Engl J Med. 288(10):526.
 McKallip RJ, Lombard C, Fisher M, Martin BR, Ryu S, Grant S, Nagarkatti PS, Nagarkatti M.  Targeting CB2 cannabinoid receptors as a novel therapy to treat malignant lymphoblastic disease. Blood. 100(2):627-34.
 Islam TC, Asplund AC, Lindvall JM, Nygren L, Liden J, Kimby E, Christensson B, Smith CI, Sander B.  High level of cannabinoid receptor 1, absence of regulator of G protein signalling 13 and differential expression of Cyclin D1 in mantle cell lymphoma. Leukemia. 2003 Sep;17(9):1880-90.
 Joosten M, Valk PJ, Jorda MA, Vankan-Berkhoudt Y, Verbakel S, van den Broek M, Beijen A, Lowenberg B, Delwel R.  Leukemic predisposition of pSca-1/Cb2 transgenic mice. Exp Hematol. 30(2):142-9.
 Jorda MA, Verbakel SE, Valk PJ, Vankan-Berkhoudt YV, Maccarrone M, Finazzi-Agro A, Lowenberg B, Delwel R.  Hematopoietic cells expressing the peripheral cannabinoid receptor migrate in response to the endocannabinoid 2-arachidonoylglycerol. Blood. 99(8):2786-93.
 Levitt M, Faiman C, Hawks R. et al. 1984. Randomized double-blind comparison of delta-9- THC and marijuana as chemotherapy antiemetics. Proceedings of the American Society for Clinical Oncology 3:91.
 Herkenham M, Lynn AB, Johnson MR, Melvin LS, de Costa BR, Rice KC. (1991). Characterization and localization of cannabinoid receptors in rat brain: a quantitative in vitro autoradiographic study. Journal of Neuroscience 11 :563-583.
 Herkenham M, Lynn AB, Little MD, Johnson MR, Melvin LS, de Costa BR, Rice KC. (1990). Cannabinoid receptor localization in the brain. Proceedings of the National Academy of Sciences of the United States of America 87:1932- 1936.
 Miller AD. 1998. Nausea and vomiting: Underlying mechanisms and upcoming treatments Journal of the Japan Broncho-Esophagological Society 49:57-64.
 Treaster JB.  Survey finds support for marijuana use by cancer patients.NY Times (Print). 1991 May 1;:D22.
 Lissoni P, Cangemi P, Pirato D, Roselli MG, Rovelli F, Brivio F, Malugani F, Maestroni GJ, Conti A, Laudon M, Malysheva O, Giani L.  A review on cancer--psychospiritual status interactions. Neuroendocrinol Lett. 22(3):175-80.
The antiemetic efficacy of nabilone
|Title||Crossover comparison of the antiemetic efficacy of nabilone and alizapride in patients with nonseminomatous testicular cancer receiving cisplatin therapy.|
|Author(s)||Niederle N, Schutte J, Schmidt CG.|
|Journal, Volume, Issue||Klin Wochenschr. 1986 Apr 15;64(8):362-5.|
|Major outcome(s)||Nabilone superior to alizapride.|
Twenty nonseminomatous testicular cancer patients not pretreated with emetogenic chemotherapy were included in a crossover study of antiemetic therapy. Patients were randomly assigned to receive either nabilone (2 X 2 mg/day) or alizapride (3 X 150 mg/day) prior to beginning low-dose cisplatin chemotherapy. Patients on nabilone had significantly fewer episodes of emesis than those on alizapride (medians, 1.1 vs 2.9; p less than 0.01). Nabilone was superior to alizapride in giving complete relief from nausea (medians, 65% vs 30%; p less than 0.01), and was more effective in shortening the duration of nausea (medians, 1.3 h vs 5.1 h; p less than 0.01); however, it caused more adverse effects. It is concluded that nabilone has greater antiemetic activity than alizapride in young patients receiving low-dose cisplatin chemotherapy. Nabilone dosage should be reduced to decrease the incidence and degree of adverse reactions while leaving the definite antiemetic activity unchanged.
All Conditions Benefited by Medical Marijuana
|Dose(s)||2 X 2 mg/day|
|Participants||20 cancer patients|
|Type of publication||Medical journal|
|Address of author(s)|