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how to use cbd oil for skin cancer

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The thing to remember about cannabis, particularly in the treatment of cancer, is that there is a big difference between CBD and THC. While cannabidiol is non-psychoactive, THC can produce a high along with unwanted effects like euphoria or sedation. CBD is legal in the United States [11] as long as it contains less than 0.3% tetrahydrocannabinol but you may need a prescription if you want to try medical cannabis, depending what state you live in.

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Yes, CBD oil is legal as long as it contains less than 0.3% tetrahydrocannabinol. If you want to try medical marijuana, you may need a prescription and/or a medical marijuana card, depending what state you live in.

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Cannabinoids do bind to receptors which are present in many cells and there is some evidence in highly controlled laboratory circumstances that cannabinoids may inhibit some cancers. Sadly, there is also evidence that it may actually accelerate growth in others. There have been no useful trials in living humans and animal trials are not conclusive. The link at the end of this article gives more information and is maintained by the Uk Cancer Society so may be seen as a trusted and valid reference.

If you think you may have a skin cancer, please make an appointment – our doctors are very good at skin diagnoses and can give you proper treatment advice from leaving harmless things alone through creams to surgical removal if required.

Addendum September 2016:

A search of the internet lists many sites where people claim to have had skin cancers cured by cannabis oil. This effect may occur for one of the following reasons:

The proposed mechanisms of action of cannabis oil are plausible but unfortunately that does not make it safe or effective.

Conflict of interest: The authors have declared that no conflict of interest exists.

Immunohistochemical analysis of cannabinoid receptor expression in mouse normal skin and skin tumors. (a) Immunolocalization of CB1 and CB2 receptors. (b) Controls without primary Ab (only with secondary biotinylated anti-rabbit Ab), as well as controls with the Ab-blocking peptides, are shown (see Methods and Results for explanation). Normal skin came from a 5-day-old mouse. Papillomas were generated by chemical carcinogenesis (as described in ref. 9), while SCCs were generated by inoculation of PDV.C57 epidermal tumor cells as described in Methods. Images of representative samples are shown. Similar results were obtained in at least two other samples. Hf, hair follicle; bl, basal layer; sbl, suprabasal layers.

The mouse tumorigenic epidermal cell lines PDV.C57 and HaCa4, and the nontransformed epidermal cell lines MCA3D (mouse) and HaCat (human), were routinely maintained in DMEM supplemented with 10% FCS. Twenty-four hours before the experiments, cells were transferred to low serum (0.5%) DMEM. Primary human keratinocytes (Biowhittaker Europe SPRL, Vervier, Belgium) were grown and cultured for the experiments in KGM-2 medium (Biowhittaker Europe SPRL). Stock solutions of cannabinoid ligands were prepared in DMSO. Control incubations had the corresponding DMSO content. No significant influence of DMSO was observed on cell viability at the final concentration used (0.1–0.2%, vol/vol).


We have recently found that in skin carcinomas EGF-R plays an important role in triggering the angiogenic switch necessary for skin tumor growth (9). Thus, we measured the expression levels and activation state of EGF-R in control and cannabinoid-treated skin tumors. While EGF-R mRNA was highly expressed in vehicle-treated tumors, in line with its known overexpression in skin carcinomas (30, 31), the levels of EGF-R mRNA in cannabinoid-treated tumors were very low (Figure ​ (Figure7a). 7 a). In addition, the degree of EGF-R activation (autophosphorylation) was markedly reduced in cannabinoid-treated tumors (Figure ​ (Figure7b). 7 b). Moreover, exposure of cultured PDV.C57 cells to WIN-55,212-2 or JWH-133 blunted EGF-R phosphorylation (Figure ​ (Figure7c), 7 c), supporting the direct impact of cannabinoids on skin tumor cells.

Cell viability in the cultures was determined by the 3-4,5-dimethylthiazol-2,5-diphenyltetrazolium bromide thiazol blue test. Apoptosis was determined by both TUNEL staining (21) and oligonucleosomal DNA fragmentation (26) according to kit manufacturer’s instructions (Boehringer Mannheim GmbH, Mannheim, Germany).

Results shown represent means ± SD. Statistical analysis was performed by ANOVA with a post hoc analysis by the Student-Neuman-Keuls test. Data in Table ​ Table1, 1 , Figure ​ Figure5a, 5 a, and Figure ​ Figure6c 6 c were analyzed by the Mann-Whitney (Wilcoxon) W test to compare medians for nonparametric data.

EGF-R participates in the regulation of key epidermal functions (35–38). Moreover, we have shown that in mouse skin carcinomas EGF-R–dependent Ha-ras activation plays a pivotal role in VEGF expression and tumor angiogenesis and growth (9). Carcinoma growth arising from subcutaneous injection of tumor epidermal cells is a biphasic process. The first phase of slow growth occurs independently of EGF-R function. Later, an angiogenic switch response mediated by the EGF-R seems to be an essential requirement for complete tumor growth, involving high VEGF levels. Other members of the EGF-R family such as HER2 may also exert their relevant anticarcinogenic role via modulation of angiogenesis (39). Here we show that cannabinoid treatment impairs EGF-R function, VEGF expression, and angiogenesis in skin tumors. It is of interest that inhibition of EGF-R function also occurred upon exposure of cultured skin tumor cells to cannabinoids, indicating that the changes observed in EGF-R activity in vivo reflect a direct impact of cannabinoids on tumor cells and are not a mere consequence of decreased tumor size. Although at present we cannot establish the mechanism for the decrease of EGF-R phosphorylation in cannabinoid-treated tumors, it is tempting to speculate that cannabinoid treatment interferes with the tumor angiogenic switch and that this, together with the direct induction of apoptosis on tumor cells, is a reason for the inhibition of tumor growth in our system.