Linked Life Data

15749859

Source:http://linkedlifedata.com/resource/pubmed/id/15749859

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2005-3-7
pubmed:abstractText
In the current study, we tested the central hypothesis that exposure to Delta-9-tetrahydrocannabinol (Delta9-THC), the major psychoactive component in marijuana, can lead to enhanced growth of tumors that express low to undetectable levels of cannabinoid receptors by specifically suppressing the antitumor immune response. We demonstrated that the human breast cancer cell lines MCF-7 and MDA-MB-231 and the mouse mammary carcinoma 4T1 express low to undetectable levels of cannabinoid receptors, CB1 and CB2, and that these cells are resistant to Delta9-THC-induced cytotoxicity. Furthermore, exposure of mice to Delta9-THC led to significantly elevated 4T1 tumor growth and metastasis due to inhibition of the specific antitumor immune response in vivo. The suppression of the antitumor immune response was mediated primarily through CB2 as opposed to CB1. Furthermore, exposure to Delta9-THC led to increased production of IL-4 and IL-10, suggesting that Delta9-THC exposure may specifically suppress the cell-mediated Th1 response by enhancing Th2-associated cytokines. This possibility was further supported by microarray data demonstrating the up-regulation of a number of Th2-related genes and the down-regulation of a number of Th1-related genes following exposure to Delta9-THC. Finally, injection of anti-IL-4 and anti-IL-10 mAbs led to a partial reversal of the Delta9-THC-induced suppression of the immune response to 4T1. Such findings suggest that marijuana exposure either recreationally or medicinally may increase the susceptibility to and/or incidence of breast cancer as well as other cancers that do not express cannabinoid receptors and are resistant to Delta9-THC-induced apoptosis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
174
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3281-9
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:15749859-Animals, pubmed-meshheading:15749859-Antibodies, Monoclonal, pubmed-meshheading:15749859-Apoptosis, pubmed-meshheading:15749859-Base Sequence, pubmed-meshheading:15749859-Breast Neoplasms, pubmed-meshheading:15749859-Cell Line, Tumor, pubmed-meshheading:15749859-Cytokines, pubmed-meshheading:15749859-Female, pubmed-meshheading:15749859-Gene Expression, pubmed-meshheading:15749859-Humans, pubmed-meshheading:15749859-Immune Tolerance, pubmed-meshheading:15749859-Interleukin-10, pubmed-meshheading:15749859-Interleukin-4, pubmed-meshheading:15749859-Lung Neoplasms, pubmed-meshheading:15749859-Lymphocyte Activation, pubmed-meshheading:15749859-Mammary Neoplasms, Experimental, pubmed-meshheading:15749859-Marijuana Smoking, pubmed-meshheading:15749859-Mice, pubmed-meshheading:15749859-RNA, Neoplasm, pubmed-meshheading:15749859-Receptor, Cannabinoid, CB1, pubmed-meshheading:15749859-Receptor, Cannabinoid, CB2, pubmed-meshheading:15749859-Tetrahydrocannabinol, pubmed-meshheading:15749859-Th1 Cells, pubmed-meshheading:15749859-Th2 Cells
pubmed:year
2005
pubmed:articleTitle
Delta-9-tetrahydrocannabinol enhances breast cancer growth and metastasis by suppression of the antitumor immune response.
pubmed:affiliation
Department of Microbiology and Immunology, Medical College of Virginia Campus, Virginia Commonwealth University, Richmond, VA 23298, USA. rjmckall@hsc.vcu.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't