1,1-dimethylheptyl-11-hydroxytetrahydrocannabinol and Lung Neoplasms

1,1-dimethylheptyl-11-hydroxytetrahydrocannabinol has been researched along with Lung Neoplasms in 2 studies

Research

Studies (2)

Timeframe	Studies, this research(%)	All Research%
pre-1990	0 (0.00)	18.7374
1990's	0 (0.00)	18.2507
2000's	2 (100.00)	29.6817
2010's	0 (0.00)	24.3611
2020's	0 (0.00)	2.80

Authors

Authors	Studies
Fischer, OM; Hart, S; Ullrich, A	1
Alexander, SP; Athanasiou, A; Bagiokou, D; Bates, TE; Bradshaw, TD; Calabrese, V; Clarke, AB; Clothier, RH; Constantinescu, CS; Fang, L; Kendall, DA; Kumaran, NM; Lobo, DN; Loesch, A; Smith, PA; Turner, AE; Vakilpour, S; Westwell, AD	1

Other Studies

2 other study(ies) available for 1,1-dimethylheptyl-11-hydroxytetrahydrocannabinol and Lung Neoplasms

Article	Year
Cannabinoids induce cancer cell proliferation via tumor necrosis factor alpha-converting enzyme (TACE/ADAM17)-mediated transactivation of the epidermal growth factor receptor. Cancer research, 2004, Mar-15, Volume: 64, Issue:6 Topics: ADAM Proteins; ADAM17 Protein; Amphiregulin; Apoptosis; Benzoxazines; Cannabinoids; Cell Division; Dronabinol; EGF Family of Proteins; Enzyme Activation; Epidermal Growth Factor; ErbB Receptors; Glioblastoma; Glycoproteins; Heparin-binding EGF-like Growth Factor; Humans; Intercellular Signaling Peptides and Proteins; Lung Neoplasms; Metalloendopeptidases; Mitogen-Activated Protein Kinase 1; Mitogen-Activated Protein Kinase 3; Mitogen-Activated Protein Kinases; Morpholines; Naphthalenes; Phosphorylation; Proto-Oncogene Proteins; RNA Interference; Signal Transduction; Transcriptional Activation; Tumor Cells, Cultured	2004
Cannabinoid receptor agonists are mitochondrial inhibitors: a unified hypothesis of how cannabinoids modulate mitochondrial function and induce cell death. Biochemical and biophysical research communications, 2007, Dec-07, Volume: 364, Issue:1 Topics: Apoptosis; Arachidonic Acids; Cannabinoid Receptor Agonists; Cannabinoids; Carcinoma, Non-Small-Cell Lung; Cell Line, Tumor; Dronabinol; Electron Transport Complex I; Electron Transport Complex II; Electron Transport Complex III; Endocannabinoids; Humans; Hydrogen Peroxide; Lung Neoplasms; Membrane Potential, Mitochondrial; Mitochondria; Models, Biological; Oxygen Consumption; Polyunsaturated Alkamides	2007

Article

Year

Cannabinoids induce cancer cell proliferation via tumor necrosis factor alpha-converting enzyme (TACE/ADAM17)-mediated transactivation of the epidermal growth factor receptor.

Cancer research, 2004, Mar-15, Volume: 64, Issue:6

Topics: ADAM Proteins; ADAM17 Protein; Amphiregulin; Apoptosis; Benzoxazines; Cannabinoids; Cell Division; Dronabinol; EGF Family of Proteins; Enzyme Activation; Epidermal Growth Factor; ErbB Receptors; Glioblastoma; Glycoproteins; Heparin-binding EGF-like Growth Factor; Humans; Intercellular Signaling Peptides and Proteins; Lung Neoplasms; Metalloendopeptidases; Mitogen-Activated Protein Kinase 1; Mitogen-Activated Protein Kinase 3; Mitogen-Activated Protein Kinases; Morpholines; Naphthalenes; Phosphorylation; Proto-Oncogene Proteins; RNA Interference; Signal Transduction; Transcriptional Activation; Tumor Cells, Cultured

2004

Cannabinoid receptor agonists are mitochondrial inhibitors: a unified hypothesis of how cannabinoids modulate mitochondrial function and induce cell death.

Biochemical and biophysical research communications, 2007, Dec-07, Volume: 364, Issue:1

Topics: Apoptosis; Arachidonic Acids; Cannabinoid Receptor Agonists; Cannabinoids; Carcinoma, Non-Small-Cell Lung; Cell Line, Tumor; Dronabinol; Electron Transport Complex I; Electron Transport Complex II; Electron Transport Complex III; Endocannabinoids; Humans; Hydrogen Peroxide; Lung Neoplasms; Membrane Potential, Mitochondrial; Mitochondria; Models, Biological; Oxygen Consumption; Polyunsaturated Alkamides

2007