Hypoploid Metaphases in Cultured Lymphocytes of Marihuana Smokers

Morishima, Akira; Henrich, Richard T.; Jayaraman, J.; Nahas, Gabriel G.

doi:10.1016/b978-0-08-023759-6.50032-9

Cited by 18 publications

(18 citation statements)

References 8 publications

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“…Nuclear blebs and chromosomal bridges are known to be associated with micronucleus development [ 156 ] and have been described after THC exposure in lymphocytes and oocytes [ 60 , 164 ]. Nuclear blebs and bridges are also seen often in association with cannabinoid exposure [ 150 , 156 ].…”

Section: Discussionmentioning

confidence: 99%

Geotemporospatial and causal inferential epidemiological overview and survey of USA cannabis, cannabidiol and cannabinoid genotoxicity expressed in cancer incidence 2003–2017: part 3 – spatiotemporal, multivariable and causal inferential pathfinding and exploratory analyses of prostate and ovarian cancers

Reece

Hulse

2022

Arch Public Health

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Background The epidemiology of cannabinoid-related cancerogenesis has not been studied with cutting edge epidemiological techniques. Building on earlier bivariate papers in this series we aimed to conduct pathfinding studies to address this gap in two tumours of the reproductive tract, prostate and ovarian cancer. Methods Age-standardized cancer incidence data for 28 tumour types (including “All (non-skin) Cancer”) was sourced from Centres for Disease Control and National Cancer Institute using SEER*Stat software across US states 2001–2017. Drug exposure was sourced from the nationally representative household survey National Survey of Drug Use and Health conducted annually by the Substance Abuse and Mental Health Services Administration 2003–2017 with response rate 74.1%. Federal seizure data provided cannabinoid concentration data. US Census Bureau provided income and ethnicity data. Inverse probability weighted mixed effects, robust and panel regression together with geospatiotemporal regression analyses were conducted in R. E-Values were also calculated. Results 19,877 age-standardized cancer rates were returned. Based on these rates and state populations this equated to 51,623,922 cancer cases over an aggregated population 2003–2017 of 124,896,418,350. Inverse probability weighted regressions for prostate and ovarian cancers confirmed causal associations robust to adjustment. Cannabidiol alone was significantly associated with prostate cancer (β-estimate = 1.61, (95%C.I. 0.99, 2.23), P = 3.75 × 10− 7). In a fully adjusted geospatiotemporal model at one spatial and two temporal years lags cannabidiol was significantly independently associated with prostate cancer (β-estimate = 2.08, (1.19, 2.98), P = 5.20 × 10− 6). Cannabidiol alone was positively associated with ovarian cancer incidence in a geospatiotemporal model (β-estimate = 0.36, (0.30, 0.42), P < 2.20 × 10− 16). The cigarette: THC: cannabidiol interaction was significant in a fully adjusted geospatiotemporal model at six years of temporal lag (β-estimate = 1.93, (1.07, 2.78), P = 9.96 × 10− 6). Minimal modelled polynomial E-Values for prostate and ovarian cancer ranged up to 5.59 × 1059 and 1.92 × 10125. Geotemporospatial modelling of these tumours showed that the cannabidiol-carcinogenesis relationship was supra-linear and highly sigmoidal (P = 1.25 × 10− 45 and 12.82 × 10− 52 for linear v. polynomial models). Conclusion Cannabinoids including THC and cannabidiol are therefore important community carcinogens additive to the effects of tobacco and greatly exceeding those of alcohol. Reproductive tract carcinogenesis necessarily implies genotoxicity and epigenotoxicity of the germ line with transgenerational potential. Pseudoexponential and causal dose-response power functions are demonstrated.

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Section: Discussionmentioning

confidence: 99%

Geotemporospatial and causal inferential epidemiological overview and survey of USA cannabis, cannabidiol and cannabinoid genotoxicity expressed in cancer incidence 2003–2017: part 3 – spatiotemporal, multivariable and causal inferential pathfinding and exploratory analyses of prostate and ovarian cancers

Reece

Hulse

2022

Arch Public Health

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“…Chromosome aberrations, notably a drumstick-shaped protru sion o f heterochromatin from the nucleus, have been reported in peripheral blood cells of long term marihuana users (17). Morishima et al (10,11) observed hypoploid metaphase cells in cultured lymphocytes obtained from marihuana users and in THC-treated lymphocytes derived from control subjects. Mouse lung cultures ex posed to marihuana smoke combined with tobacco smoke contained a statistically greater number of cells with 4N complement of DNA than cells treated exclusively with tobacco smoke (5).…”

Section: Discussionmentioning

confidence: 99%

“…Reports o f in vivo effects o f cannabis are also conflicting. Chromosome aberrations in chronic marihuana smokers have been documented (1,10,11,19). However, Nichols et al (13) and Matsuyama et al (8) could not detect such aberrations following administration o f mari huana or THC.…”

mentioning

confidence: 93%

Influence of Cannabinoids on Somatic Cells <i>in vivo</i>

Zimmerman¹,

Raj²

1980

Pharmacology

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Chromosomal and nuclear aberrations in bone marrow cells were studied in hybrid mice of genotype (C57BL x C3H)F₁ following treatment with specific cannabinoids. In the subacute series, mice were treated for 5 consecutive days with Δ⁹-tetrahydrocannabinol (THC), cannabinol or cannabidiol at a dose of 10 mg/kg, the percentage of micronuclei in cannabinoid-treated mice was 3- to 5-fold greater than in the dimethyl sulfoxide controls. In the acute series, polychromatic erythrocytes were scored after a single exposure. In one acute series there was an approximately twofold increase in the incidence of micronuclei in the cannabinoid-treated mice; in the other acute series of cannabinoid-treated animals the micronuclei values were as high as 6 times the control values. Interaction between dose and frequency of exposure was assessed for THC; the number of micronuclei was affected by THC dosage, but not by frequency of exposure. Further confirmation of nuclear aberrations was obtained from assessment of bone marrow mitosis. In this limited study of mitotic cells the incidence of metaphase aberrations in cannabinoid-treated animals was 5–7 times greater than in controls.

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“…In a study on humans, Stenchever et al (1974) noted an increase in chromosome breakage in light and heavy users of marijuana as compared with nonusers. Morishima et al (1976Morishima et al ( , 1979 demonstrated an increase in the number of cells with abnormal chromosomal complements in tissue cultures taken from marijuana smokers. In addition, Morishima et al observed that as many as 30% of the cells contained less than a normal complement of DNA, an extremely rare phenomenon.…”

Section: Effects On the Central Nervous Systemmentioning

confidence: 97%

Marijuana: A Review of Medical Research With Implications for Adolescents

Margolis

Popkin²

1980

The Personnel and Guidance Journal

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Hypoploid Metaphases in Cultured Lymphocytes of Marihuana Smokers

Cited by 18 publications

References 8 publications

Influence of Cannabinoids on Somatic Cells <i>in vivo</i>

Marijuana: A Review of Medical Research With Implications for Adolescents

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