Bioidentical Hormones 101 
The Book, by Jeffrey Dach MD

Cannabis Acute Leukemia


ALL Acute Lymphoblastic Leukemia Remission with Cannabis OilCannabis Oil for Acute Leukemia,

Case Report

by Jeffrey Dach MD

The following case report appeared in the November 2013 Journal of Case Reports in Oncology.(1)  Left Image : Blast cells on blood smear in acute leukemia courtesy of Wikimedia commons.

Highly Aggressive Acute Blastic Leukemia in 14 year old Girl

In March 2006, P.K., a 14-year-old girl suffering from weakness and spontaneous bleeding was diagnosed with acute lymphoblastic leukemia (ALL), with more than 300,000 blast cells present on her peripheral blood smear.   Her form of leukemia was highly aggressive with a positive Philadelphia Chromosome (see Image below).  P.K.’s leukemia was treated at the Hospital for Sick Children, Toronto, Canada with bone marrow transplant, aggressive chemotherapy and radiation therapy.

Treatment Deemed Futile and a Failure

After 34 months, blast cells were again found in the blood and further treatment was deemed futile.  The doctors suspended all treatment and essentially gave up on her.  Her doctors noted in the chart: “the patient suffers from terminal malignant disease….She has been treated to the limits of available therapy… no further active intervention will be undertaken”. The patient, P.K., was offered palliative treatment and was sent home to die.  While at home, the leukemia blast cell counts continued to increase and frequent blood and platelet transfusions were required.

The Family Tries Hemp Oil

The family conducted their own research and found Dr. Guzman’s  2003 article on cannabis as anticancer agent.  Cannabis oil is safe, without any of the toxic effects of chemotherapy.

Finding Rick Simpson and Phoenix Tears

The family found an organization known as Phoenix Tears, and Rick Simpson, from whom they learned how to prepare their own cannabis extract given orally to their daughter, P.K.  With the introduction of this new cannabis oil treatment, the doctors observed a rapid dose-dependent reduction in leukemic blast cell count.  (See image below)

Cannabis Hemp Oil Remission in ALL Leukemia Blast Cells Left chart shows response to Hemp Oil Treatment.  Left vertical axis shows Leukemic Blast Cell count which starts at 374 (per thousand) Red Arrow.  Horizontal axis displays treatment dose on each day with reduction in Blast count (Green Arrows ) after administration of the Hemp Oil.  Image courtesy of  Karger and Dr Singh from Case Rep Oncol 2013;6:585-592 (1)

This case is important because it shows in graphic form (above chart) the potent anti-cancer effect of cannabis oil in acute leukemia. The authors state: “The results shown here cannot be attributed to the phenomenon of ‘spontaneous remission’ because a dose response curve was achieved. “(1)

Although the treatment was deemed a success, the patient ultimately succumbed to the toxic effects of chemotherapy which had suppressed her immune system leaving her susceptible to infection.  Sadly, the patient died of colon perforation and peritonitis on day 76.

A Case With A Better Outcome

A better outcome was reported by the family of Mykayla Comstock, treated successfully with Cannabis Oil for acute Leukemia. (see video below)

On July 14th, 2012, seven year old Mykayla was diagnosed with intermediate risk T-Cell acute lymphoblastic leukemia with leukemic infiltration of the brain and spinal fluid.  On July 23rd her   Leukemic Count on the blood smear was 31%.  By August 2, her Leukemic count had dropped to zero and has stayed there.  Doctors declared Mykayla to be in remission, and she continues to do well two years later.

Date   Leukemic Count

23-Jul 31%

24-Jul  Began Cannabis Oil

26-Jul 5%

30-Jul 3%

2-Aug 0%

6-Aug 0%

13-Aug 0%

20-Aug 0%

July 30th 2012 was the very last time they found lymphoblasts in Mykayla’s blood smear

Medical Research on Medicinal Cannabis and Leukemia

There has been abundant medical research on the effect of medicinal cannabis on leukemic cells. In-vitro, and in-vivo animal and human studies show medicinal cannabis is exceptionally efficacious in killing leukemic cells through signalling pathways which induce cell death (apoptosis). (2-12)  The research is summarized in references 2-12.

Dr. Christina Sanchez from Cannabis Planet on Vimeo.

Natural Medicine in Your Kitchen

Preparation of Cannabis Oil – as easy as a cup of coffee

Preparing the cannabis oil involves obtaining the proper medicinal cannabis strain plant material.  A reputable regulated grower is recommended.  For the highest level of quality it may be necessary to grow your own plant material from seed.

The cannabis strains (indica and sativa) may vary in THC (tetrahydrocannabidol) and CBD (cannabidiol) content.  Some strains tend to have a sedating effect, while others an energizing effect.

Once the plant material is obtained, the ground plant material is placed into a mixing bowel.  Food grade high-proof alcohol  such as Everclear 190 proof, is an excellent solvent which will dissolve the plant oils.  Once the alcohol is added to the plant material and mashed up to dissolve the oils, the mixture is then strained, and placed into a cooking container for evaporating off the solvent, usually with a rice cooker or double boiler.   Since the solvent is highly flammable, special precautions are used to avoid flames or sparks which may ignite the solvent.  Once solvent is evaporated off, the oil residue is left behind and can be drawn up into plastic syringes, and is ready for use.

A Note of Caution-
Medicinal Cannabis May be Illegal in Your State

As of this writing, 22 states or so have approved medicinal cannabis, and 2 states have approved recreational use.  However, some states still have laws on the books making possession of cannabis a criminal act.   At  the Federal level, the DEA continues to consider cannabis a schedule I drug of no medicinal value, and possession and use of cannabis remains a federal crime.  The Boston Globe reports the DEA has been harassing doctors involved with medical marijuana dispensaries by threatening revocation of their Controlled Substance Prescribing DEA license.

Link to video: How to Make a Small Batch of Rick Simpson Oil
Dr T. H. Hunt DNM

Links to videos on how to make Risk Simpson Oil.

Books on Medicinal Cannabis Growing etc:

Marijuana Grower’s Handbook: Your Complete Guide for Medical and Personal Marijuana Cultivation by Ed Rosenthal

Marijuana Horticulture: The Indoor/Outdoor Medical Grower’s Bible by Jorge Cervantes.

Articles with related Interest

This article is Part Six of a series:

Part One: Marijuana Cannabis Research Suppressed

Part Two: Alysa Erwin Cannabis Oil Remission from Malignant Astrocytoma

Part Three: Cannabis Oil Brain Tumor Remission

Part Four : Marijuana Refugees and Medicinal Cannabis for Seizures

Part Five: Medical Cannabis for Epilepsy Part Two

Jeffrey Dach MD
7450 Griffin Road Suite 190
Davie, Florida 33314
954-792-4663
http://www.jeffreydachmd.com/
http://www.drdach.com/
http://www.naturalmedicine101.com/
http://www.truemedmd.com/  http://www.bioidenticalhormones101.com

Links and references:

1) http://www.karger.com/Article/FullText/356446
Case Rep Oncol 2013;6:585-592
Fulltext PDF (934 Kb)  Published: November 2013

Cannabis Extract Treatment for Terminal Acute Lymphoblastic Leukemia with a Philadelphia Chromosome Mutation
Singh Y.a · Bali C.b  aBrampton, Ont. and bAjax, Ont., Canada

Acute lymphoblastic leukemia (ALL) is a cancer of the white blood cells and is typically well treated with combination chemotherapy, with a remission state after 5 years of 94% in children and 30-40% in adults. To establish how aggressive the disease is, further chromosome testing is required to determine whether the cancer is myeloblastic and involves neutrophils, eosinophils or basophils, or lymphoblastic involving B or T lymphocytes. This case study is on a 14-year-old patient diagnosed with a very aggressive form of ALL (positive for the Philadelphia chromosome mutation). A standard bone marrow transplant, aggressive chemotherapy and radiation therapy were revoked, with treatment being deemed a failure after 34 months. Without any other solutions provided by conventional approaches aside from palliation, the family administered cannabinoid extracts orally to the patient. Cannabinoid resin extract is used as an effective treatment for ALL with a positive Philadelphia chromosome mutation and indications of dose-dependent disease control. The clinical observation in this study revealed a rapid dose-dependent correlation.

full pdf available:

2) guzman_2003_cannabis_as_anticancer_agents
Nature Reviews Cancer 3, 745-755 (October 2003) | doi:10.1038/nrc1188

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3) http://bloodjournal.hematologylibrary.org/content/105/3/1214?variant=full-text&sso-checked=1
February 1, 2005; Blood: 105 (3)
Cannabis-induced cytotoxicity in leukemic cell lines: the role of the cannabinoid receptors and the MAPK pathway    Thomas Powles,    Robert te Poele,    Jonathan Shamash,     Tracy Chaplin,    David Propper,    Simon Joel,   Tim Oliver, and    Wai Man Liu     From the New Drug Study Group, St Bartholomew’s Hospital (SBH), London, United Kingdom; the Department of Medical Oncology, SBH, London, United Kingdom; the Centre for Cancer Therapeutics, Institute of Cancer Research, Surrey, United Kingdom; the Department of Medical Oncology, Charterhouse Square, London, United Kingdom; and the Barry Reed Oncology Laboratory, SBH, London, United Kingdom.

We have shown that THC is a potent inducer of apoptosis, even at 1 × IC50 (inhibitory concentration 50%) concentrations and as early as 6 hours after exposure to the drug. These effects were seen in leukemic cell lines (CEM, HEL-92, and HL60) as well as in peripheral blood mononuclear cells. Additionally, THC did not appear to act synergistically with cytotoxic agents such as cisplatin.

One of the most intriguing findings was that THC-induced cell death was preceded by significant changes in the expression of genes involved in the mitogen-activated protein kinase (MAPK) signal transduction pathways. Both apoptosis and gene expression changes were altered independent of p53 and the CB-Rs.

Accordingly, the expression changes in response to THC observed were an increase in MKP3 expression in all 3 samples and a decrease in MAP2K2 expression (Table 2). Both changes are consistent with decreased MAPK signaling.

Results indicated clear decreases in the expression of pERK as early as 3 hours of incubation with 1 × IC50 THC

Together, our results suggested that cytotoxicity was independent of the CB-R.   Together, these results suggested CB2-R to have a minor, if any, role in THC-induced cytotoxicity.

It is important to emphasize that THC was exceptionally efficacious, inducing cell kill as early as 6 hours, and although microarray analysis did not fully elucidate the precise mechanism of cell death, it reinforced the importance of the MAPK pathway in this process.

Our data suggest the involvement of the MAPK pathway in mediating the cellular effects of THC, possibly through inactivation of ERK2. Together, these data intimate a mechanism of action that may involve modulation of signal transduction pathways, possibly through receptor tyrosine kinases and/or G-protein–coupled receptors.

4) http://molpharm.aspetjournals.org/content/70/3/897.full
Cannabidiol-Induced Apoptosis in Human Leukemia Cells: A Novel Role of Cannabidiol in the Regulation of p22phox and Nox4 Expression  in Molecular Pharmacology September 2006 vol. 70 no. 3 897-908   Robert J. McKallip,    Wentao Jia,    Jerome Schlomer,    James W. Warren,    Prakash S. Nagarkatti and    Mitzi Nagarkatti   Department of Pathology, Microbiology, and Immunology, the University of South Carolina School of Medicine, Columbia, South Carolina (R.J.M., J.W.W., P.S.N., M.N.); and Department of Microbiology and Immunology, Virginia Commonwealth University, Richmond, Virginia (W.J., J.S.)      Dr. Robert J. McKallip. Department of Pathology, Microbiology and Immunology. University of South Carolina School of Medicine, 6439 Garner’s Ferry Road, Columbia, SC 29209.

Together, the results from this study reveal that cannabidiol, acting through CB2 and regulation of Nox4 and p22phox expression, may be a novel and highly selective treatment for leukemia.

Examination of the mechanism of cannabidiol-induced apoptosis revealed that cannabidiol was acting through CB2. Furthermore, we demonstrated the involvement of the NAD(P)H oxidases p22phox and Nox4 and the subsequent generation of reactive oxygen species in CBD-induced apoptosis. Together, these studies suggest that cannabidiol, acting through CB2, may be a novel regulator of NAD(P)H oxidase expression and that CBD may prove to be a potent nonpsychoactive and specific treatment of leukemia.

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More on NOX4

5) http://www.ncbi.nlm.nih.gov/pubmed/23519121
Cell Death Dis. 2013 Mar 21;4:e552. doi: 10.1038/cddis.2013.68.
Nox4-dependent ROS modulation by amino endoperoxides to induce apoptosis in cancer cells.
Zhu P1, Tong BM, Wang R, Chen JP, Foo S, Chong HC, Wang XL, Ang GY, Chiba S, Tan NS.

Tumor metastasis is the main cause of death in cancer patients. Anoikis resistance is one critical malefactor of metastatic cancer cells to resist current clinical chemotherapeutic treatments. Although endoperoxide-containing compounds have long been suggested as anticancer drugs, few have been clinically employed due to their instability, complex synthesis procedure or low tumor cell selectivity. Herein, we describe a one-pot strategy to synthesize novel amino endoperoxides and their derivatives with good yields and stabilities. In vitro cell-based assays revealed that 4 out of the 14 amino endoperoxides selectively induce metastatic breast carcinoma cells but not normal breast cells to undergo apoptosis, in a dose-dependent manner. Mechanistic studies showed that the most potent amino endoperoxide, 4-Me, is selective for cancer cells expressing a high level of Nox4. The anticancer effects are further shown to be associated with reduced O2(-):H2O2 ratio and increased ·OH level in the cancerous cells. Animal study showed that 4-Me impairs orthotopic breast tumor growth as well as tumor cell metastasis to lymph nodes. Altogether, our study suggests that anticancer strategies that focus on redox-based apoptosis induction in tumors are clinically viable.

6) http://www.ncbi.nlm.nih.gov/pubmed/20523116
Cancer Biol Ther. 2010 Aug 1;10(3):223-31. Epub 2010 Aug 3.
NADPH oxidase 4 is an oncoprotein localized to mitochondria.
Graham KA1, Kulawiec M, Owens KM, Li X, Desouki MM, Chandra D, Singh KK.

Reactive oxygen species (ROS) are known to be involved in many physiological and pathological processes. Initially ROS-producing NADPH oxidase (NOX) proteins were thought to be present in phagocytes. However, recent studies have demonstrated that NOX proteins are expressed in many other cell types and tissues. NOX family members’ expression and function seems to vary from tissue to tissue. We determined the expression of the NOX family of proteins (NOX1-5) in normal breast tissue and breast tumors. Our study revealed that normal breast tissues express NOX1, 4 and 5 genes. Similar pattern of expression was revealed in a breast epithelial cell line. We found that NOX4 was overexpressed in the majority of breast cancer cell lines and primary breast tumors. NOX4 was also overexpressed in ovarian tumors. Overexpression of NOX4 in normal breast epithelial cells resulted in cellular senescence, resistance to apoptosis, and tumorigenic transformation.

Overexpression of NOX4 in already transformed breast tumor cells also showed increased tumorigenicity. Strong evidence suggests that regulation of these processes occurs through NOX4 generation of ROS in the mitochondria. We demonstrate that the NOX4 protein contains a 73 amino acid long mitochondrial localization signal at the N-terminus that is capable of transporting a passenger protein GFP into the mitochondria. Treatment of NOX4 overexpressing cells with catalase resulted in decreased tumorigenic characteristics. Together, this study provides evidence for an oncogenic function for NOX4 protein localized to mitochondria and suggests that NOX4 is a novel source of ROS produced in the mitochondria. This study also identifies a possible treatment of NOX4-induced breast cancer by antioxidant treatment.

full pdf available

7) NOX Protein in Diseases_AD-2014-Matsuda
Nakanishi, Atsuko, et al. “Link between PI3K/AKT/PTEN Pathway and NOX Protein in Diseases.”

full pdf available

8) The NOX Family of ROS-Generating NADPH Oxidases- Physiology and Pathophysiology
Bedard, Karen, and Karl-Heinz Krause. “The NOX family of ROS-generating NADPH oxidases: physiology and pathophysiology.” Physiological reviews 87.1 (2007): 245-313.

Cellular Death and Cellular Senescence

A large number of studies describe cell death in
response to NOX activation (Table 3). ROS can trigger
apoptosis either indirectly, through damage to DNA, lipids,
and proteins or more directly by ROS-mediated activation
of signaling molecules. Such proapoptotic signaling
of ROS may occur through activation of MAP kinases,
such SAPK/JNK, ERK1/2, and p38 (413). MAP kinase activation
occurs in many instances through ROS-dependent
inhibition of tyrosine phosphatase (437). At higher
ROS concentrations, hydrogen peroxide can inhibit
caspases and thereby lead to a switch from apoptosis to
necrosis (340, 341).
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activation of MAPK by activation of CB1 cannabinoid receptor

9) http://www.ncbi.nlm.nih.gov/pubmed/8526880   full pdf avail
Biochem J. 1995 Dec 1;312 ( Pt 2):637-41.
Activation of mitogen-activated protein kinases by stimulation of the central cannabinoid receptor CB1.
Bouaboula M1, Poinot-Chazel C, Bourrié B, Canat X, Calandra B, Rinaldi-Carmona M, Le Fur G, Casellas P.

The G-protein-coupled central cannabinoid receptor (CB1) has been shown to be functionally associated with several biological responses including inhibition of adenylate cyclase, modulation of ion channels and induction of the immediate-early gene Krox-24. Using stably transfected Chinese Hamster Ovary cells expressing human CB1 we show here that cannabinoid treatment induces both phosphorylation and activation of mitogen-activated protein (MAP) kinases, and that these effects are inhibited by SR 141716A, a selective CB1 antagonist. The two p42 and p44 kDa MAP kinases are activated in a time- and dose-dependent manner. The rank order of potency for the activation of MAP kinases with various cannabinoid agonists is CP-55940 > delta 9-tetrahydrocannabinol > WIN 55212.2, in agreement with the pharmacological profile of CB1. The activation of MAP kinases is blocked by pertussis toxin but not by treatment with hydrolysis-resistant cyclic AMP analogues. This suggests that the signal transduction pathway between CB1 and MAP kinases involves a pertussis-toxin-sensitive GTP-binding protein and is independent of cyclic AMP metabolism. This coupling of CB1 subtype and mitogenic signal pathway, also observed in the human astrocytoma cell line U373 MG, may explain the mechanism of action underlying cannabinoid-induced Krox-24 induction.

10) http://www.ncbi.nlm.nih.gov/pubmed/8647116
Eur J Biochem. 1996 May 1;237(3):704-11.
Signaling pathway associated with stimulation of CB2 peripheral cannabinoid receptor. Involvement of both mitogen-activated protein kinase and induction of Krox-24 expression.
Bouaboula M1, Poinot-Chazel C, Marchand J, Canat X, Bourrié B, Rinaldi-Carmona M, Calandra B, Le Fur G, Casellas P.  Author information    1Sanofi Recherche, Department of Immunopharmacology, Montpellier, France.

Taken together, these findings provide evidence for a functional role of the CB2 receptor in gene induction mediated by the MAP kinase network.

More on NOX4

11) http://www.ncbi.nlm.nih.gov/pubmed/23519121
Cell Death Dis. 2013 Mar 21;4:e552. doi: 10.1038/cddis.2013.68.
Nox4-dependent ROS modulation by amino endoperoxides to induce apoptosis in cancer cells.  Zhu P1, Tong BM, Wang R, Chen JP, Foo S, Chong HC, Wang XL, Ang GY, Chiba S, Tan NS.

Tumor metastasis is the main cause of death in cancer patients. Anoikis resistance is one critical malefactor of metastatic cancer cells to resist current clinical chemotherapeutic treatments. Although endoperoxide-containing compounds have long been suggested as anticancer drugs, few have been clinically employed due to their instability, complex synthesis procedure or low tumor cell selectivity. Herein, we describe a one-pot strategy to synthesize novel amino endoperoxides and their derivatives with good yields and stabilities. In vitro cell-based assays revealed that 4 out of the 14 amino endoperoxides selectively induce metastatic breast carcinoma cells but not normal breast cells to undergo apoptosis, in a dose-dependent manner. Mechanistic studies showed that the most potent amino endoperoxide, 4-Me, is selective for cancer cells expressing a high level of Nox4. The anticancer effects are further shown to be associated with reduced O2(-):H2O2 ratio and increased ·OH level in the cancerous cells. Animal study showed that 4-Me impairs orthotopic breast tumor growth as well as tumor cell metastasis to lymph nodes. Altogether, our study suggests that anticancer strategies that focus on redox-based apoptosis induction in tumors are clinically viable.
————————–

https://www.youtube.com/watch?v=0sGWxz0DMSI
How to Make a Small Batch of Rick Simpson Oil
DrT. H. Hunt DNM DrT. H. Hunt DNM

https://www.youtube.com/results?search_query=Rick+Simpson+Oil+
making rick simpson oil videos

summary of anticancer effects:

http://www.cancer.gov/cancertopics/pdq/cam/cannabis/healthprofessional/page4#Section_26

Cannabis and Cannabinoids (PDQ®) Antitumor Effects

This summary is reviewed regularly and updated as necessary by the PDQ Cancer Complementary and Alternative Medicine Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).

Header Image: http://commons.wikimedia.org/wiki/File:ALL-KM-2.jpg  Furfur – Own work .  ALL-KM-2.jpg 185 KB  bone marrow smear (large magnification) from a patient with acute lymphoblastic leukemia

More case reports:

http://www.dailymail.co.uk/news/article-2372317/Dad-defends-decision-7-year-old-daughter-leukemia-marijuana-pain.html
Mykayla   Brandon Krenzler of Portland, Oregon

http://www.cureyourowncancer.org/elias-coopers-story-treating-leukemia-with-cannabis-oil.html
Elias Cooper Story: Treating Leukemia With Cannabis Oil By: Lincoln Horsley 11/19/2013
http://www.sltrib.com/sltrib/news/57085069-78/brian-marijuana-cannabis-cancer.html.csp
Brian Scott  acute myeloid leukemia
Young Utahn opts for cannabis to treat cancer
By Kirsten Stewart The Salt Lake Tribune
Published November 11, 2013 8:12 pm

http://www.sltrib.com/sltrib/blogspreps/57395127-52/scott-leukemia-brian-football.html.csp
Former Hurricane star Brian Scott loses battle to leukemia
Published on Jan 14, 2014 11:25AM

http://www.cureyourowncancer.org/elias-coopers-story-treating-leukemia-with-cannabis-oil.html
Elias Cooper Story: Treating Leukemia With Cannabis Oil    By: Lincoln Horsley 11/19/2013

http://www.cnn.com/2014/01/15/health/cannabis-landon-riddle/
Sierra Riddle, in St. George, Utah

Landon Riddle’s Story:
http://youtu.be/zbNVe57vKEk

http://canadianawareness.org/2014/04/cannabis-oil-advocate-ronnie-smith-suddenly-dies-from-leukemia/
Cannabis Oil Advocate Ronnie Smith Suddenly Dies from Leukemia/  Posted on April 11, 2014 by Frankie Gotz in Health, World News //

http://www.ladybud.com/2014/04/29/cannabis-versus-acute-lymphoblastic-leukemia-go-team-logan/
Apr 29, 2014  Cannabis Versus Acute Lymphoblastic Leukemia: Go Team Logan!
Maggie Volpo / Medical, News & Editorial /
Kimberly Ewell’ son, Logan,B cell acute lymphoblastic leukemia

http://maddiegorman.wordpress.com/
Madeline Gorman Acute Lymphoblastic Leukemia (ALL)
=============================================

http://www.cannabiscancersociety.com/

http://www.unitedpatientsgroup.com/blog/2014/01/05/cannabis-extract-treatment-for-terminal-acute-lymphoblastic-leukemia-by-justin-kander/
Cannabis Extract Treatment for Terminal Acute Lymphoblastic Leukemia by Justin Kander

//www.slideshare.net/TheHempSolution/comprehensive-report-on-the-cannabis-extract-movement
June 2014  The Comprehensive Report on the Cannabis Extract Movement and the Use of Cannabis Extracts to Treat Diseases [Kindle Edition]
Justin Kander (Author), Nicholas Davey (Editor)

Justin Kander is the webmaster of PhoenixTears.ca
Justin Kander is the webmaster of PhoenixTears.ca and an advocate for the use of cannabis extract medicine to treat cancer. He previously interned with Students for Sensible Drug Policy, one of the nation’s leading drug policy reform organizations.

In 2013, Justin completed the Comprehensive Report on the Cannabis Extract Movement, a 100-page report that examines and analyzes the mounting evidence in support of cannabis extracts as medicine. He presented his findings at the International Drug Policy Reform Conference in Denver the same year.

full pdf available

http://www.ncbi.nlm.nih.gov/pubmed/21336992
Childs Nerv Syst. 2011 Apr;27(4):671-9. doi: 10.1007/s00381-011-1410-4. Epub 2011 Feb 20.
Spontaneous regression of septum pellucidum/forniceal pilocytic astrocytomas–possible role of Cannabis inhalation.
Foroughi M1, Hendson G, Sargent MA, Steinbok P.
Author information
Abstract INTRODUCTION: Spontaneous regression of pilocytic astrocytoma after incomplete resection is well recognized, especially for cerebellar and optic pathway tumors, and tumors associated with Neurofibromatosis type-1 (NF1). The purpose of this report is to document spontaneous regression of pilocytic astrocytomas of the septum pellucidum and to discuss the possible role of cannabis in promoting regression.
CASE REPORT: We report two children with septum pellucidum/forniceal pilocytic astrocytoma (PA) tumors in the absence of NF-1, who underwent craniotomy and subtotal excision, leaving behind a small residual in each case. During Magnetic Resonance Imaging (MRI) surveillance in the first three years, one case was dormant and the other showed slight increase in size, followed by clear regression of both residual tumors over the following 3-year period. Neither patient received any conventional adjuvant treatment. The tumors regressed over the same period of time that cannabis was consumed via inhalation, raising the possibility that the cannabis played a role in the tumor regression.
CONCLUSION: We advise caution against instituting adjuvant therapy or further aggressive surgery for small residual PAs, especially in eloquent locations, even if there appears to be slight progression, since regression may occur later. Further research may be appropriate to elucidate the increasingly recognized effect of cannabis/cannabinoids on gliomas.

http://www.ncbi.nlm.nih.gov/pubmed/24123005
Anticancer Res. 2013 Oct;33(10):4373-80.
Enhancing the activity of cannabidiol and other cannabinoids in vitro through modifications to drug combinations and treatment schedules.
Scott KA1, Shah S, Dalgleish AG, Liu WM.
Cannabinoids are the bioactive components of the Cannabis plant that display a diverse range of therapeutic qualities. We explored the activity of six cannabinoids, used both alone and in combination in leukaemic cells. Cannabinoids were cytostatic and caused a simultaneous arrest at all phases of the cell cycle. Re-culturing pre-treated cells in drug-free medium resulted in dramatic reductions in cell viability. Furthermore, combining cannabinoids was not antagonistic. We suggest that the activities of some cannabinoids are influenced by treatment schedules; therefore, it is important to carefully select the most appropriate strategy in order to maximise their efficacy.

 

Jeffrey Dach MD
7450 Griffin Road Suite 190
Davie, Florida 33314
954-792-4663
http://www.jeffreydach.com/
http://www.drdach.com/
http://www.naturalmedicine101.com/
http://www.truemedmd.com/  http://www.bioidenticalhormones101.com

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Thanks to Sayer Ji , Founder of GreenMedInfo,com for bringing this case to my attention.

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