astrocytoma/cannabis

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The expression level of cannabinoid receptors type 1 and 2 in the different types of astrocytomas

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Astrocytomas, the most prevalent primary brain tumors, can be divided by histology and malignancy levels into four following types: pilocytic astrocytoma (grade I), diffuse fibrillary astrocytoma (grade II), anaplastic astrocytoma (grade III), and glioblastoma multiforme (grade IV). For high grade

Stimulation of cannabinoid receptor CB1 induces krox-24 expression in human astrocytoma cells.

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The recent isolation and cloning of the G protein-coupled central cannabinoid receptor (CB1) from brain tissue has provided a molecular basis to elucidate how cannabinoid compounds may mediate their psychoactive effects. Here we report the high expression of cannabinoid receptors in human

Spontaneous regression of septum pellucidum/forniceal pilocytic astrocytomas--possible role of Cannabis inhalation.

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BACKGROUND 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

Targeting astrocytomas and invading immune cells with cannabinoids: a promising therapeutic avenue.

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The last quarter century has borne witness to great advances in both the detection and treatment of numerous cancers. Even so, malignancies of the central nervous system, especially high-grade astrocytomas, continue to thwart our best efforts toward effective chemotherapeutic strategies. With

Cannabinoid and cannabinoid-like receptors in microglia, astrocytes, and astrocytomas.

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CB1 and CB2 receptors are activated by a plethora of cannabinoid compounds, be they endogenously-produced, plant-derived or synthetic. These receptors are expressed by microglia, astrocytes and astrocytomas, and their activation regulates these cells' differentiation, functions and viability. Recent

Characterization of CB1 cannabinoid receptor immunoreactivity in postmortem human brain homogenates.

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The CB1 cannabinoid receptor (CB1) is the predominant type of cannabinoid receptor in the CNS, in which it displays a unique anatomical distribution and is present at higher densities than most other known seven transmembrane domain receptors. Nevertheless, as with almost all seven transmembrane

Cyclosporine attenuates the adenylyl cyclase superactivation induced by chronic cannabinoid treatment.

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Chronic cannabinoid treatment results in the development of tolerance. Adenylyl cyclase superactivation, induced by chronic cannabinoid agonist administration, is regarded as one of the molecular mechanisms leading to tolerance. In the present study, the effect of cyclosporine on adenylyl cyclase

Cannabinoid receptors in human astroglial tumors.

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In animal models, cannabinoids are reported to inhibit the growth of tumors, including gliomas. These effects have been claimed to be mediated via cannabinoid receptors 1 and 2 (CB1, CB2). To elucidate a possible relevance for treatment of human gliomas, we investigated receptor subtype expression

High concentrations of cannabinoids activate apoptosis in human U373MG glioma cells.

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Cannabinoids bind to two G-protein-coupled receptors, CB1 and CB2, expressed by neurons and cells of the immune system, respectively. Glioma cells (astrocyte-derived brain tumor cells) express cannabinoid receptors, and numerous in vitro and in vivo studies performed in rodents have concluded that

[Cannabis and cancer].

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Several publications have recently suggested a relationship between cannabis use and certain types of cancer. We gathered information on the latest findings on the subject. A manual and computerized bibliographic search on cannabis and cancer was conducted. In users under 40 years of age, cannabis

Cannabinoid receptor activation correlates with the proapoptotic action of the β2-adrenergic agonist (R,R')-4-methoxy-1-naphthylfenoterol in HepG2 hepatocarcinoma cells.

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Inhibition of cell proliferation by fenoterol and fenoterol derivatives in 1321N1 astrocytoma cells is consistent with β(2)-adrenergic receptor (β(2)-AR) stimulation. However, the events that result in fenoterol-mediated control of cell proliferation in other cell types are not clear. Here, we

The synthetic cannabinoid R(+)WIN 55,212-2 inhibits the interleukin-1 signaling pathway in human astrocytes in a cannabinoid receptor-independent manner.

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R(+)WIN 55,212-2 is a synthetic cannabinoid that controls disease progression in models of multiple sclerosis. This is associated with its ability to reduce migration of leukocytes into the central nervous system. Because leukocyte migration is dependent on induction of adhesion molecules and

Opposing control of cannabinoid receptor stimulation on amyloid-beta-induced reactive gliosis: in vitro and in vivo evidence.

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Beside cytotoxic mechanisms impacting on neurons, amyloid beta (A beta)-induced astroglial activation is operative in Alzheimer's disease brain, suggesting that persistent inflammatory response may have a role in the illness and that positive results may be achieved by curbing the astroglial

Opposite changes in cannabinoid CB1 and CB2 receptor expression in human gliomas.

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Gliomas are the most important group of malignant primary brain tumors and one of the most aggressive forms of cancer. During the last years, several studies have demonstrated that cannabinoids induce apoptosis of glioma cells and inhibit angiogenesis of gliomas in vivo. As the effects of

Distinctive pattern of cannabinoid receptor type II (CB2) expression in adult and pediatric brain tumors.

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The efficacy of cannabinoids against high-grade glioma in animal models, mediated by two specific receptors, CB1 and CB2, raised promises for targeted treatment of the most frequent and malignant primary brain tumors. Unlike the abundantly expressed CB1, the CB2 receptor shows a restricted

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