humulene and Uterine-Cervical-Neoplasms

Cannabis use is increasing legally worldwide, while its impact on cancer risk is unclear. This study was performed to investigate the relationship between cannabis use and the risk of several types of cancer.. We conducted a two-sample Mendelian randomization (MR) study to explore the causality of cannabis use on 9 site-specific types of cancer including breast cancer, cervical cancer, melanoma, colorectal cancer, laryngeal cancer, oral cancer, oropharyngeal cancer, esophageal cancer, and glioma. Genome-wide significant genetic instruments (P < 5E-06) for cannabis use were extracted from a large-scale genome-wide association meta-analysis of European ancestry, whereas cancer genetic instruments were extracted from the UK Biobank (UKB) cohort and GliomaScan consortium in the OpenGWAS database. The inverse-variance weighted (IVW) was considered the main method for MR analysis, and sensitivity analyses including MR-Egger, weighted median, MR pleiotropy residual sum, and outlier test (MR-PRESSO) were conducted to evaluate the robustness of the results.. Cannabis use was a significant promoting factor for cervical cancer (OR = 1.001265, 95% CI 1.000375-1.002155, P = 0.0053). And we also detected suggestive evidence of the causality of cannabis use on laryngeal cancer (OR = 1.000350, 95% CI 1.000027-1.000672, P = 0.0336) and breast cancer (OR = 1.003741, 95% CI 1.000052-1.007442, P = 0.0467). No evidence of a causal association of cannabis use with other site-specific types of cancer was detected. Additionally, no pleiotropy or heterogeneity was found in the sensitivity analysis.. This study indicates a causative association of cannabis use on cervical cancer, while cannabis use may increase the odds of breast cancer and laryngeal cancer, which require further evaluation in large-scale population-based studies.

Topics: Breast Neoplasms; Cannabis; Female; Genome-Wide Association Study; Humans; Laryngeal Neoplasms; Polymorphism, Single Nucleotide; Uterine Cervical Neoplasms

Topics: Animals; Asparaginase; Burkitt Lymphoma; Cannabis; Carcinogens; Clinical Trials as Topic; Contraceptives, Oral; Cyclamates; Cyclophosphamide; Cytarabine; Female; Humans; Legislation, Drug; Leukemia; Pharmacology; Psychology, Adolescent; Substance-Related Disorders; Thromboembolism; United States; United States Food and Drug Administration; Uterine Cervical Neoplasms

Cervical cancer remains a global health related issue among females of Sub-Saharan Africa, with over half a million new cases reported each year. Different therapeutic regimens have been suggested in various regions of Africa, however, over a quarter of a million women die of cervical cancer, annually. This makes it the most lethal cancer amongst black women and calls for urgent therapeutic strategies. In this study we compare the anti-proliferative effects of crude extract of Cannabis sativa and its main compound cannabidiol on different cervical cancer cell lines.. To achieve our aim, phytochemical screening, MTT assay, cell growth analysis, flow cytometry, morphology analysis, Western blot, caspase 3/7 assay, and ATP measurement assay were conducted.. Results obtained indicate that both cannabidiol and Cannabis sativa extracts were able to halt cell proliferation in all cell lines at varying concentrations. They further revealed that apoptosis was induced by cannabidiol as shown by increased subG0/G1 and apoptosis through annexin V. Apoptosis was confirmed by overexpression of p53, caspase 3 and bax. Apoptosis induction was further confirmed by morphological changes, an increase in Caspase 3/7 and a decrease in the ATP levels.. In conclusion, these data suggest that cannabidiol rather than Cannabis sativa crude extracts prevent cell growth and induce cell death in cervical cancer cell lines.

Topics: Apoptosis; Cannabidiol; Cannabis; Cell Line, Tumor; Cell Proliferation; Cell Survival; Female; HeLa Cells; Humans; Plant Extracts; Uterine Cervical Neoplasms

Topics: Cannabis; Carcinogens; Cell Nucleus; Female; Humans; Male; Protamines; Socioeconomic Factors; Spermatozoa; Uterine Cervical Neoplasms