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***EDDIEKIRK*** · 07-31-2012, 11:25 AM

Cannabis cured my Cancer

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Causes, incidence, and risk factors

Prostate cancer is the most common cause of death from cancer in men over age 75. Prostate cancer is rarely found in men younger than 40.

People who are at higher risk include:

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African-American men, who are also likely to develop cancer at every age
Men who are older than 60
Men who have a father or brother with prostate cancer

Other people at risk include:

Men who have been around agent orange
Men who use too much alcohol
Farmers
Men who eat a diet high in fat, especially animal fat
Tire plant workers
Painters
Men who have been around cadmium

Prostate cancer is less common in people who do not eat meat (vegetarians).

A common problem in almost all men as they grow older is an enlarged prostate. This is called benign prostatic hyperplasia, or BPH. It does not raise your risk of prostate cancer. However, it can increase your PSA blood test results.

Symptoms

The PSA blood test is often done to screen men for prostate cancer. Because of PSA testing, most prostate cancers are now found before they cause any symptoms.

The symptoms listed below can occur with prostate cancer, usually at a late stage. These symptoms can also be caused by other prostate problems:

Delayed or slowed start of urinary stream
Dribbling or leakage of urine, most often after urinating
Slow urinary stream
Straining when urinating, or not being able to empty out all of the urine
Blood in the urine or semen
Bone pain or tenderness, most often in the lower back and pelvic bones (only when the cancer has spread)

Signs and tests

A biopsy is needed to tell if you have prostate cancer. A sample of tissue is removed from the prostate and sent to a lab.

Your doctor may recommend a prostate biopsy if:

You have high PSA level
A rectal exam shows a large prostate or a hard, uneven surface

The results are reported using what is called a Gleason grade and a Gleason score.

The Gleason grade tells you how fast the cancer might spread. It grades tumors on a scale of 1 - 5. You may have different grades of cancer in one biopsy sample. The two main grades are added together. This gives you the Gleason score. The higher your Gleason score, the more likely the cancer is to have spread past the prostate:

Scores 2 - 5: Low-grade prostate cancer
Scores 6 - 7: Intermediate- (or in the middle-) grade cancer. Most prostate cancers fall into this group.
Scores 8 - 10: High-grade cancer

The following tests may be done to determine whether the cancer has spread:

The PSA blood test will also be used to monitor your cancer after treatment. Often, PSA levels will begin to rise before there are any symptoms. An abnormal digital rectal exam may be the only sign of prostate cancer (even if the PSA is normal).

Treatment

Treatment depends on many things, including your Gleason score and your overall health. Your doctor will discuss your treatment options.

For early-stage prostate cancer, this may include:

Surgery (radical prostatectomy)
Radiation therapy, including brachytherapy and proton therapy

If you are older, your doctor may recommend simply monitoring the cancer with PSA tests and biopsies.

If the prostate cancer has spread, treatment may include:

Hormone therapy (medicines to reduce testosterone levels)
Surgery
Chemotherapy

Surgery, radiation therapy, and hormone therapy can affect your sexual desire or performance. Problems with urine control are common after surgery and radiation therapy. Discuss your concerns with your health care provider.

After treatment for prostate cancer, you will be closely watched to make sure the cancer does not spread. This involves routine doctor check-ups, including PSA blood tests (usually every 3 months to 1 year).

See also:

Prostate cancer - stages
Prostate radiation - discharge

Support Groups

You can ease the stress of illness by joining a support group whose members share common experiences and problems. See: Support group - prostate cancer

Expectations (prognosis)

How well you do depends on whether the cancer has spread outside the prostate gland and how abnormal the cancer cells are (the Gleason score) when you are diagnosed.

Many patients can be cured if their prostate cancer has not spread. Some patients whose cancer has not spread very much outside the prostate gland can also be cured.

Hormone treatment can improve survival, even in patients who cannot be cured.

Complications

The complications of prostate cancer are mostly due to different treatments.

Calling your health care provider

Discuss the advantages and disadvantages to PSA screening with your health care provider.

Prevention

You may lower your risk of prostate cancer by eating a diet that is:

High in omega-3 fatty acids
Low-fat
Similar to the traditional Japanese diet
Vegetarian

Finasteride (Proscar, generic) and dutasteride (Avodart) are drugs used to treat prostate enlargement (benign prostatic hyperplasia, or BPH). If you do not have prostate cancer and your PSA score is 3.0 or lower, ask your health care provider about the pros and cons of taking these drugs to prevent prostate cancer.

References

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[*]Theoret MR, Ning YM, Zhang JJ, et al. The risks and benefits of 5a-reductase inhibitors for prostate-cancer prevention. N Engl J Med. 2011 Jun 15.

[*]Antonarakis ES, Eisenberger MA. Expanding treatment options for metastatic prostate cancer. N Engl J Med. 2011 May 26;364:2055-2058.

[*]Andriole GL, Crawford ED, Grubb RI 3rd, Buys SS, Chia D, Church TR, et al. Mortality results from a randomized prostate-cancer screening trial. N Engl J Med. 2009;360:1310-1319.

[*]Babaian RJ, Donnelly B, Bahn D, Baust JG, Dineen M, Ellis D, et al. Best practice statement on cryosurgery for the treatment of localized prostate cancer. J Urol. 2008;180:1993-2004.

[*]Schrader FH, Hugosson J, Roobol MJ, Tammela TL, Ciatto S, Nelen V, et al. Screening and prostate-cancer mortality in a randomized European study. N Engl J Med. 2009;360:1320-1328.

[*]Walsh PC. Chemoprevention of prostate cancer. N Engl J Med. 2010 Apr 1;362(13):1237-8.

[*]Wilt TJ, MacDonald R, et al. Systematic review: comparative effectiveness and harms of treatments for clinically localized prostate cancer. Ann Intern Med. 2008;148(6):435-448.

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Review Date: 9/19/2011.

Reviewed by: Louis S. Liou, MD, PhD, Chief of Urology, Cambridge Health Alliance, Visiting Assistant Professor of Surgery, Harvard Medical School. Also reviewed by David Zieve, MD, MHA,

Arachidonoylglycerol

A Novel Inhibitor of Androgen-Independent Prostate Cancer Cell Invasion

Kasem Nithipatikom1, Michael P. Endsley1, Marilyn A. Isbell1, John R. Falck3, Yoshiki Iwamoto2, Cecilia J. Hillard1 and William B. Campbell1

Departments of 1 Pharmacology and Toxicology and 2 Urology, Medical College of Wisconsin, Milwaukee, Wisconsin; and 3 Departments of Biochemistry and Pharmacology, University of Texas Southwestern Medical Center, Dallas, Texas

Endocannabinoids have been implicated in cancer. Increasing endogenous 2-arachidonoylglycerol (2-AG) by blocking its metabolism inhibits invasion of androgen-independent prostate cancer (PC-3 and DU-145) cells. Noladin ether (a stable 2-AG analog) and exogenous CB1 receptor agonists possess similar effects. Conversely, reducing endogenous 2-AG by inhibiting its synthesis or blocking its binding to CB1 receptors with antagonists increases the cell invasion. 2-AG and noladin ether decrease protein kinase A activity in these cells, indicating coupling of the CB1 receptor to downstream effectors. The results suggest that cellular 2-AG, acting through the CB1 receptor, is an endogenous inhibitor of invasive prostate cancer cells.

source: http://cancerres.aac...ract/64/24/8826

Activation of Signal Transducer and Activator of Transcription 5 in Human Prostate Cancer Is Associated with High Histological Grade

Hongzhen Li1, Tommi J. Ahonen4, Kalle Alanen5, Jianwu Xie1, Matthew J. LeBaron1, Thomas G. Pretlow7, Erica L. Ealley1, Ying Zhang2, Martti Nurmi6, Baljit Singh3,1, Paula M. Martikainen8 and Marja T. Nevalainen1

Departments of 1 Oncology, 2 Biostatistics Unit, and 3 Pathology, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington DC; Departments of 4 Anatomy and Cell Biology and 5 Pathology, Institute of Biomedicine, University of Turku, Turku, Finland; 6 Department of Surgery, University Hospital of Turku, Turku, Finland; 7 Department of Pathology, Case Western Reserve Medical Center, Cleveland, Ohio; and 8 Deptartment of Pathology, Tampere University Hospital, Tampere, Finland

We have recently identified signal transducer and activator of transcription 5 (Stat5) as a critical survival factor for prostate cancer cells. We now report that activation of Stat5 is associated with high histological grade of human prostate cancer. Specifically, immunohistochemical analysis demonstrated a strong positive correlation with activation of Stat5 and high Gleason score in 114 human prostate cancers. To investigate the mechanisms underlying constitutive activation of Stat5 in prostate cancer, a dominant-negative mutant of Janus kinase 2 (Jak2) was delivered by adenovirus to CWR22Rv cells. Dominant-negative-Jak2 effectively blocked the activation of Stat5 whereas wild-type Jak2 enhanced activation, indicating that Jak2 is the main kinase that phosphorylates Stat5 in human prostate cancer cells. A ligand-induced mechanism for activation of Stat5 in prostate cancer was suggested by the ability of prolactin (Prl) to stimulate activation of both Jak2 and Stat5 in CWR22Rv human prostate cancer cells and in CWR22Rv xenograft tumors. In addition, Prl restored constitutive activation of Stat5 in five of six human prostate cancer specimens in ex vivo long-term organ cultures. Finally, Prl protein was locally expressed in the epithelium of 54% of 80 human prostate cancer specimens with positive correlation with high Gleason scores and activation of Stat5. In conclusion, our data indicate that increased activation of Stat5 was associated with more biologically aggressive behavior of prostate cancer. The results further suggest that Jak2 is the principal Stat5 tyrosine kinase in human prostate cancer, possibly activated by autocrine/paracrine Prl.

source: http://cancerres.aac...ract/64/14/4774

Suppression of Nerve Growth Factor Trk Receptors and Prolactin Receptors by Endocannabinoids Leads to Inhibition of Human Breast and Prostate Cancer Cell Proliferation1

Dominique Melck, Luciano De Petrocellis, Pierangelo Orlando, Tiziana Bisogno, Chiara Laezza, Maurizio Bifulco and Vincenzo Di Marzo

Istituto per la Chimica di Molecole di Interesse Biologico (D.M., T.B., V.D.M.), Istituto di Cibernetica (L.D.P.), and Istituto di Biochimica delle Proteine ed Enzimologia (P.O.), Consiglio Nazionale delle Ricerche, 80072 Arco Felice (NA); and Centro di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale delle Ricerche, and Dipartimento di Biologia e Patologia Cellulare e Molecolare, Universit di Napoli Federico II (C.L., M.B.), 80131 Naples, Italy

Address all correspondence and requests for reprints to: Dr. Vincenzo Di Marzo, Istituto per la Chimica di Molecole di Interesse Biologico, Consiglio Nazionale delle Ricerche, 80072 Arco Felice (NA), Italy. E-mail: vdm@trinc.icmib.na.cnr.it.

Anandamide and 2-arachidonoylglycerol (2-AG), two endogenous ligands of the CB1 and CB2 cannabinoid receptor subtypes, inhibit the proliferation of PRL-responsive human breast cancer cells (HBCCs) through down-regulation of the long form of the PRL receptor (PRLr). Here we report that 1) anandamide and 2-AG inhibit the nerve growth factor (NGF)-induced proliferation of HBCCs through suppression of the levels of NGF Trk receptors; 2) inhibition of PRLr levels results in inhibition of the proliferation of other PRL-responsive cells, the prostate cancer DU-145 cell line; and 3) CB1-like cannabinoid receptors are expressed in HBCCs and DU-145 cells and mediate the inhibition of cell proliferation and Trk/PRLr exp<b></b>ression. -NGF-induced HBCC proliferation was potently inhibited (IC50 = 50600 nM) by the synthetic cannabinoid HU-210, 2-AG, anandamide, and its metabolically stable analogs, but not by the anandamide congener, palmitoylethanolamide, or the selective agonist of CB2 cannabinoid receptors, BML-190. The effect of anandamide was blocked by the CB1 receptor antagonist, SR141716A, but not by the CB2 receptor antagonist, SR144528. Anandamide and HU-210 exerted a strong inhibition of the levels of NGF Trk receptors as detected by Western immunoblotting; this effect was reversed by SR141716A. When induced by exogenous PRL, the proliferation of prostate DU-145 cells was potently inhibited (IC50 = 100300 nM) by anandamide, 2-AG, and HU-210. Anandamide also down-regulated the levels of PRLr in DU-145 cells. SR141716A attenuated these two effects of anandamide. HBCCs and DU-145 cells were shown to contain 1) transcripts for CB1 and, to a lesser extent, CB2 cannabinoid receptors, 2) specific binding sites for [3H]SR141716A that could be displaced by anandamide, and 3) a CB1 receptor-immunoreactive protein. These findings suggest that endogenous cannabinoids and CB1 receptor agonists are potential negative effectors of PRL- and NGF-induced biological responses, at least in some cancer cells.

source: http://endo.endojour...tract/141/1/118

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.aacrjournals.org/cgi/cont...ract/66/13/6748

***EDDIEKIRK*** · 07-31-2012, 12:54 PM

Cannabis Chemicals May Help Fight Prostate Cancer

London -- Chemicals in cannabis have been found to stop prostate cancer cells from growing in the laboratory, suggesting that cannabis-based medicines could one day help fight the disease, scientists said Wednesday.

After working initially with human cancer cell lines, Ines Diaz-Laviada and colleagues from the University of Alcala in Madrid also tested one compound on mice and discovered it produced a significant reduction in tumor growth.

Their research, published in the British Journal of Cancer, underlines the growing interest in the medical use of active chemicals called cannabinoids, which are found in marijuana.

Experts, however, stressed that the research was still exploratory and many more years of testing would be needed to work out how to apply the findings to the treatment of cancer in humans.

"This is interesting research which opens a new avenue to explore potential drug targets but it is at a very early stage," said Lesley Walker, director of cancer information at Cancer Research UK, which owns the journal.

"It absolutely isn't the case that men might be able to fight prostate cancer by smoking cannabis," she added.

The cannabinoids tested by the Spanish team are thought to work against prostate cancer because they block a receptor, or molecular doorway, on the surface of tumour cells. This stops them from dividing.

In effect, the cancer cell receptors can recognize and "talk to" chemicals found in cannabis, said Diaz-Laviada.

"These chemicals can stop the division and growth of prostate cancer cells and could become a target for new research into potential drugs to treat prostate cancer," she said.

Her team's work with two cannabinoids -- called methanandamide and JWH-015 -- is the first demonstration that such cannabis chemicals prevent cancer cells from multiplying.

Some drug companies are already exploring the possibilities of cannabinoids in cancer, including British-based cannabis medicine specialist GW Pharmaceuticals.

It is collaborating with Japan's Otsuka on early-stage research into using cannabis extracts to tackle prostate cancer -- the most commonly diagnosed cancer in men -- as well as breast and brain cancer.

GW has already developed an under-the-tongue spray called Sativex for the relief of some of the symptoms of multiple sclerosis, which it plans to market in Europe with Bayer and Almirall.

Other attempts to exploit the cannibinoid system have met with mixed success. Sanofi-Aventis was forced to withdraw its weight-loss drug Acomplia from the market last year because of links to mental disorders.

Briefing: Cannabis compounds fight prostate cancer

* 12:28 19 August 2009 by Laura McGuinness

Compounds similar to those found in cannabis have been shown to stop prostate cancer cells from multiplying. Two cannabinoid compounds, JWH-015 and MET, stopped prostate tumour growth in human prostate cells in Petri dishes and also in mice with the disease. They halted the cell-division cycle and killed the cancer cells, and had the greatest effect on aggressive prostate cancer cell types, which do not respond to hormone treatments.

Some 192,000 men in the US alone are diagnosed with prostate cancer each year, and researchers Ins Daz-Laviada Marturet at the University of Alcal, Spain, and her colleagues say the results could offer hope to those affected. But before you go looking for a dealer, New Scientist answers a few questions.

Does this mean that smoking dope can protect against prostate cancer?

No. The findings do not imply that smoking cannabis can prevent or treat prostate cancer. Even aside from the harm to health that is associated with dope smoking, the cannabinoid compounds that this study tested are synthetic chemicals not found in cannabis plants, so no conclusions about the actual stuff can be drawn.

So if I shouldn't smoke cannabis to fight cancer, how can I use cannabinoids?

The chemicals that have been tested could eventually be used to develop prostate cancer treatments. These treatments would not be the same as cannabis they would simply contain cannabis-like chemicals as the active ingredients.

Would cannabis-derived drugs make patients feel stoned?

No. No drug developed from these compounds would affect the mind as cannabis use does. There are two types of receptor in the prostate to which cannabinoid compounds can attach. Both types are found in the brain but only one is associated with the psychotropic effects of using cannabis. Daz-Laviada Marturet's research looked specifically at cannabinoid compounds that attach to the CB2 receptor the one not associated with psychotropic effects.

Haven't cannabis chemicals already been found to protect against cancer?

There is a long list of cancers for which cannabinoids are thought to have a therapeutic benefit. This list includes leukaemia, lung and colon cancer.

So when will we see cannabis-derived anti-cancer drugs on the market?

Prostate cancer treatments based on these cannabis chemicals are still a long way from clinical trial. The chemicals tested have been shown to be effective both in cell cultures and in mice, but a lot more needs to be found out about these chemicals before anti-cancer drugs can be developed.

The Prostate Cancer Charity advises a healthy diet and lifestyle and recommends that as the symptoms of prostate cancer and other prostate problems can be similar, it is important to get a proper diagnosis because other treatments are already available.

source: http://www.newscient...ate-cancer.html

***EDDIEKIRK*** · 07-31-2012, 12:56 PM

Inhibition of human tumour prostate PC-3 cell growth by cannabinoids R(+)-Methanandamide and JWH-015: Involvement of CB2

We have previously shown that cannabinoids induce growth inhibition and apoptosis in prostate cancer PC-3 cells, which express high levels of cannabinoid receptor types 1 and 2 (CB1 and CB2). In this study, we investigated the role of CB2 receptor in the anti-proliferative action of cannabinoids and the signal transduction triggered by receptor ligation.

Methods:

The human prostate cancer cell lines, namely PC-3, DU-145 and LNCaP, were used for this study. Cell proliferation was measured using MTT proliferation assay, [3H]-thymidine incorporation assay and cell-cycle study by flow cytometry. Ceramide quantification was performed using the DAG kinase method. The CB2 receptor was silenced with specific small interfering RNA, and was blocked pharmacologically with SR 144528. In vivo studies were conducted by the induction of prostate xenograft tumours in nude mice.

Results:

We found that the anandamide analogue, R(+)-Methanandamide (MET), as well as JWH-015, a synthetic CB2 agonist, exerted anti-proliferative effects in PC-3 cells. R(+)-Methanandamide- and JWH-015-induced cell death was rescued by treatment with the CB2 receptor antagonist, SR 144528. Downregulation of CB2 exp<b></b>ression reversed the effects of JWH-015, confirming the involvement of CB2 in the pro-apoptotic effect of cannabinoids. Further analysing the mechanism of JWH-015-induced cell growth inhibition, we found that JWH-015 triggered a de novo synthesis of ceramide, which was involved in cannabinoid-induced cell death, insofar as blocking ceramide synthesis with Fumonisin B1 reduced cell death. Signalling pathways activated by JWH-015 included JNK (c-Jun N-terminal kinase) activation and Akt inhibition. In vivo treatment with JWH-015 caused a significant reduction in tumour growth in mice.

Conclusions:

This study defines the involvement of CB2-mediated signalling in the in vivo and in vitro growth inhibition of prostate cancer cells and suggests that CB2 agonists have potential therapeutic interest and deserve to be explored in the management of prostate cancer.

source: http://www.nature.co...s/6605248a.html

mednurse · 07-31-2012, 07:37 PM

Not sure if you've seen the video "What if Cannabis cured cancer" by Len Richmond with forward by Dr Andrew Weil. They've known cannabis cures cancer since the 70's and still the norm is radiation and chemo....what a croc

***EDDIEKIRK*** · 07-31-2012, 07:53 PM

Quote:Not sure if you've seen the video "What if Cannabis cured cancer" by Len Richmond with forward by Dr Andrew Weil. They've known cannabis cures cancer since the 70's and still the norm is radiation and chemo....what a croc

Thanks for reminding us, Yes i have seen it and have it posted somewhere on the site, I have brought here for those who have not seen it.

http://www.youtube.com/watch?v=Hy66MUZP538

***EDDIEKIRK*** · 11-29-2012, 06:11 PM

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