Exodus 30:23 for the recipe.
A study published by the US National Library of Medicine, conducted by Harvard Medical School investigated
the role of cannabinoid receptors in lung cancer cells. They determined its effectiveness and suggested that
it should be used for treatment against lung cancer cells.—————-Cancer Prev Res (Phila). 2011 Jan;4(1):65-75. doi: 10.1158/1940-6207.CAPR-10-0181. Epub 2010 Nov 19.
Cannabinoid receptors, CB1 and CB2, as novel targets for inhibition of non-small cell lung cancer growth and metastasis.
Preet A1, Qamri Z, Nasser MW, Prasad A, Shilo K, Zou X, Groopman JE, Ganju RK.
Author information1Division of Experimental Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston,
————————-(AbstractNon-small cell lung cancer (NSCLC) is the leading cause of cancer deaths worldwide; however, only limited
therapeutic treatments are available. Hence, we investigated the role of cannabinoid receptors, CB1 and CB2,
as novel therapeutic targets against NSCLC. We observed expression of CB1 (24%) and CB2 (55%) in NSCLC patients.
Furthermore, we have shown that the treatment of NSCLC cell lines (A549 and SW-1573) with CB1/CB2- and CB2-specific
agonists Win55,212-2 and JWH-015, respectively, significantly attenuated random as well as growth factor-directed
in vitro chemotaxis and chemoinvasion in these cells.
In addition, pretreatment with CB1/CB2 selective antagonists, AM251 and AM630, prior to JWH-015 and Win55,212-2
treatments, attenuated the agonist-mediated inhibition of in vitro chemotaxis and chemoinvasion. In addition,
both CB1 and CB2 agonists Win55,212-2 and JWH-133, respectively, significantly inhibited in vivo tumor growth and
lung metastasis (~50%). These effects were receptor mediated, as pretreatment with CB1/CB2 antagonists abrogated
CB1/CB2 agonist-mediated effects on tumor growth and metastasis.
Upon further elucidation into the molecular mechanism, we observed that both CB1 and CB2 agonists inhibited
phosphorylation of AKT, a key signaling molecule controlling cell survival, migration, and apoptosis, and
reduced matrix metalloproteinase 9 expression and activity. These results suggest that CB1 and CB2 could be
used as novel therapeutic targets against NSCLC.©2010 AACR.)—————-A study published by the US National Library of Medicine by the Institute of Toxicology and Pharmacology,
from the Department of General Surgery in Germany determined that cannabinoids inhibit cancer cell invasion.
Effects were confirmed in primary tumour cells from a lung cancer patient. Overall, data indicated that
cannabinoids decrease cancer cell invasiveness.http://www.ncbi.nlm.nih.gov/pubmed/22198381?dopt=Abstract
FASEB J. 2012 Apr;26(4):1535-48. doi: 10.1096/fj.11-198184. Epub 2011 Dec 23.Cannabidiol inhibits lung cancer cell invasion and metastasis via intercellular adhesion molecule-1.Ramer R1, Bublitz K, Freimuth N, Merkord J, Rohde H, Haustein M, Borchert P, Schmuhl E, Linnebacher M, Hinz B.(AbstractCannabinoids inhibit cancer cell invasion via increasing tissue inhibitor of matrix metalloproteinases-1
(TIMP-1). This study investigates the role of intercellular adhesion molecule-1 (ICAM-1) within this action.
In the lung cancer cell lines A549, H358, and H460, cannabidiol (CBD; 0.001-3 µM) elicited concentration-dependent
ICAM-1 up-regulation compared to vehicle via cannabinoid receptors, transient receptor potential vanilloid 1, and
p42/44 mitogen-activated protein kinase.Up-regulation of ICAM-1 mRNA by CBD in A549 was 4-fold at 3 µM, with
significant effects already evident at 0.01 µM. ICAM-1 induction became significant after 2 h, whereas significant
TIMP-1 mRNA increases were observed only after 48 h.Inhibition of ICAM-1 by antibody or siRNA approaches reversed
the anti-invasive and TIMP-1-upregulating action of CBD and the likewise ICAM-1-inducing cannabinoids
?(9)-tetrahydrocannabinol and R(+)-methanandamide when compared to isotype or nonsilencing siRNA controls.
ICAM-1-dependent anti-invasive cannabinoid effects were confirmed in primary tumor cells from a lung cancer patient.
In athymic nude mice, CBD elicited a 2.6- and 3.0-fold increase of ICAM-1 and TIMP-1 protein in A549 xenografts, as
compared to vehicle-treated animals, and an antimetastatic effect that was fully reversed by a neutralizing antibody
against ICAM-1 [% metastatic lung nodules vs. isotype control (100%): 47.7% for CBD + isotype antibody and 106.6%
for CBD + ICAM-1 antibody]. Overall, our data indicate that cannabinoids induce ICAM-1, thereby conferring TIMP-1
induction and subsequent decreased cancer cell invasiveness.)———A study published in the journal Oncogene, by Harvard Medical Schools Experimental Medicine Department
determined that THC inhibits epithelial growth factor induced lung cancer cell migration and more.
They go on to state that THC should be explored as novel therapeutic molecules in controlling the growth
and metastasis of certain lung cancers.http://www.nature.com/onc/journal/v27/n3/abs/1210641a.html
(?9-Tetrahydrocannabinol (THC) is the primary cannabinoid of marijuana and has been shown to either
potentiate or inhibit tumor growth, depending on the type of cancer and its pathogenesis.
Little is known about the activity of cannabinoids like THC on epidermal growth factor receptor-overexpressing
lung cancers, which are often highly aggressive and resistant to chemotherapy. In this study, we characterized the effects of THC on the EGF-induced growth and metastasis of human non-small cell
lung cancer using the cell lines A549 and SW-1573 as in vitro models.
We found that these cells express the cannabinoid receptors CB1 and CB2, known targets for THC action, and that THC inhibited
EGF-induced growth, chemotaxis and chemoinvasion.
Moreover, signaling studies indicated that THC may
act by inhibiting the EGF-induced phosphorylation of ERK1/2, JNK1/2 and AKT.
THC also induced the phosphorylation of focal adhesion kinase at tyrosine 397. Additionally, in in vivo studies in severe combined immunodeficient mice, there was significant inhibition of the subcutaneous tumor growth and lung metastasis of A549 cells in THC-treated animals as compared to vehicle-treated controls.
Tumor samples from THC-treated animals revealed antiproliferative and antiangiogenic effects of THC.
Our study suggests that cannabinoids like THC should be explored as novel therapeutic molecules in controlling the growth and metastasis of certain lung cancers.)
?9-Tetrahydrocannabinol inhibits epithelial growth factor-induced lung cancer cell migration in vitro as
well as its growth and metastasis in vivo
A Preet1, R K Ganju1,2 and J E Groopman1,2
1Division of Experimental Medicine, Department of Medicine, Beth Israel Deaconess Medical Center,
Harvard Medical School, Boston, MA, USA
Correspondence: Drs JE Groopman or RK Ganju, Division of Experimental Medicine, Beth Israel Deaconess
Medical Center, Harvard Institutes of Medicine Building, 4 Blackfan Circle, Boston, MA 02115, USA. E-mail:
firstname.lastname@example.org or email@example.com
2JEG and RKG share the senior and corresponding authorship.
Received 21 January 2007; Revised 29 May 2007; Accepted 1 June 2007; Published online 9 July 2007.
its called propoganda and a deeply ingrained societal stigma carefully crafted against cannabis.
“Citicoline (also known as: Cytidine disphosphate-choline (CDO-Choline) & Cytidine 5′-diphosphocholine) is involved in making the chemical called phosphatidylcholine, phosphatidylcholine is a major component of all your major cell membranes.
Citicoline elevates your levels of Acetylcholine, Acetylcholine is a Neurotransmitter. When you take a functional (THC) dose and you are feeling good / euphoria while some can never take too much but for most people who take too much become unhappy.
Citicoline doesn’t work the same way as CBD or Pregnenolone how that inhibits the high by working through the CB1 receptor.
Both Citicoline and Cannabidiol work by directly inhibiting CB1 activity but which is getting you high, but is also killing a lot of Cancers based on studies.
Different Cancers require CB1 activation in order to kill them. Citicoline doesn’t work in that way at all, it works by making more Acetylcholine, what that implies is that THC is known to inhibit Acetylcholine what that all suggests is that the fear and paranoia of taking too much Cannabis comes because your turning down the Acetycholine levels in parts of your Brain the outcome of turning Acetycholine levels down is fear and paranoia.
Citicoline elevates the Acetycholine that was inhibited by the THC that gave you the fear and paranoia and you don’t hallucinate as much using Citicoline and we produce it ourselves.
Citicoline works effectively when given 3-5 times more than Cannabis, the in-experienced start them off with very low doses to feel the experience then introduce Citicoline depending on ones personal THC comfort level.”
Dr. Robert Melamede
+sarys73 SYDNEY: DOWN UNDER BUT ON TOP OF FACTS You (sarys73) mentioned that Citicoline didn’t work for you.
I’m assuming you didn’t take enough, as Dr. Melamede recommends (for people who don’t want the high) taking 3-5 times OR more of Citicoline compared to the amount of Cannabis PRIOR to Cannabis use.
Again everyone is different some may prefer a (slight) high feeling, in about 1-2 weeks the body becomes accustomed to THC.
the idea of this is disgusting. you might as well just take pharmaceuticals… why do people always want to come in with an outside thing and fuck cannabis up?
Brings a tear to my eye watching an ordinary woman who has her faith and good man beside her ,trusting Cannabis to show her a different picture.
My own mother got breast cancer and as I was too weak I let my brother and sister allow the State health service to kill our Mam and in thirteen short painful months and while I could have gotten bricks of green in a few phone calls, my christian school teacher sister would have called the Law to have me arrested ….fucked up crazy world .It is Simple Madness that this amazing plant is still illegal …why !
Cancer industry is too profitable..and U.N. Agenda 21 is the plan to depopulate