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Results for “Cocarcinogenesis”

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At least 19 recordsLinked to original sources
PubMed1975

Foreign-body tumorigenesis by vinyl chloride vinyl acetate copolymer: no evidence for chemical cocarcinogenesis.

We investigated whether vinyl chloride monomers, released from implants of vinyl chloride vinyl acetate copolymer (VCA), exerted cocarcinogenic activity and added thereby to the mechanism of foreign-body (FB) tumorigenesis. CBA/H and CBA/H-T6 mice were used. No evidence was found to indicate that chemical carcinogenic activity partakes in tumorigenesis by VCA implants. Hence it was concluded that VCA plastic is not suitable for the study of the combined process of FB/chemical cocarcinogenesis. Furthermore, experimental results obtained with VCA film implants were representative of FB tumorigenesis in the absence of demonstrable chemical carcinogenic activity.

Acetates↗
PubMed1978

Particle-enhanced membrane uptake of a polynuclear aromatic hydrocarbon: a possible role in cocarcinogenesis.

One possible mechanism by which cocarcinogenesis occurs was investigated. The effect of a particulate, silica, upon the rate of membrane uptake of a polynuclear aromatic hydrocarbon, benz[a]anthracene (BA), was studied. The fluorescence emission spectrum and quantum yield of BA, when adsorbed to silica, underwent spectral shifts upon addition of phospholipid vesicles. These spectral changes appeared to result from the transfer of BA from the silica surface into the lipid bilayer. We used these spectral changes to measure the rates of membrane uptake of BA from the silica-adsorbed state and from the crystalline and microcrystalline states of BA. Our studies demonstrated that adsorption of BA to silica resulted in an increased rate of uptake of BA into dipalmitoyl-L-alpha-phosphatidylcholine vesicles compared to the uptake rate into these vesicles from crystalling states. Such particle-enhanced membrane uptake of chemical carcinogens may be of importance in explaining the enhanced carcinogenicity of the polynuclear aromatic hydrocarbons in the presence of particulate matter.

Adsorption↗
PubMed1979

Ureterosigmoidostomy in rats: a model for the study of bladder tumour carcinogenesis and cocarcinogenesis.

A modified Coffey I ureterosigmoidostomy has been developed in rats as a model of urinary diversion for studying bladder carcinogenesis and co-carcinogenesis. Diverted and sham-operated animals were killed at 1, 3 and 6 months. Excretory urograms revealed minimal hydroureteronephrosis in most diverted animals. Upper tract bacterial colonisation was 9 times more frequent in diverted animals. Approximately one-third of the diverted animals had focal cortical scarring; however, renal function was normal in all groups as assessed by serum creatinine and electrolytes. These studies indicate that ureterosigmoidostomy in rats is a satisfactory model of urinary diversion for studying carcinogenesis.

Animals↗
PubMed1977

Epidermal intercellular relationships during carcinogenesis and cocarcinogenesis as revealed by scanning electron microscopy.

Investigations with the scanning electron microscope were carried out on the skin of 80 NMRI mice after treating them with small doses of the carcinogenic substance DMBA and the cocarcinogenic agent TPA, respectively. The results were correlated with histologic, transmission electron microscope and autoradiographic observations. The epidermis of TPA-treated animals was markedly hyperplastic with an orderly arrangement of cell layers. Autoradiographically only the basal cells were heavily labelled. With the scanning and transmission electron microscope a reduced number of intercellular connections and dilatation of the intercellular spaces could be detected. After treatment with DMBA the epidermis was only moderately hyperplastic but severely dysplastic with 3H-thymidine-labelled cells in the upper layers. The most characteristic findings were the loss of the intercellular connections, especially the lateral ones, and a pronounced dilatation of the intercellular spaces. The results obtained with the scanning electron microscope were quantified using morphometrical methods.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1979

Cocarcinogenesis.

Explore the source record for details and available documents.

2-Acetylaminofluorene↗
PubMed1979

Biochemical evidence of cocarcinogenesis: tumor promoting agent enhances methylnitrosourea activation of rat guanylate cyclase activity.

The two-stage or cocarcinogenic hypothesis of carcinogenesis involves an initiator (carcinogen) and a promotor (cocarcinogen) being utilized in combination to produce more tumors than either would alone. This theory was tested at the cellular level utilizing Tumor Promoting Agent, 12-0-tetradecanoly-phorbol-13-acetate, (promotor) in combination with submaximal and maximal doses of methylnitrosourea (initiator). Tumor promoting agent, which can cause some tumors itself, was found to enhance the activity of guanylate cyclase (E.C.4.6.1.2.), an enzyme that has been associated with normal and abnormal growth. Tumor promoting agent when utilized in combination with submaximal stimulatory doses of methylnitrosourea had an additive effect on guanylate cyclase activity, but the agent had no further additive effect on guanylate cyclase activation when methylnitrosourea was utilized in maximal stimulatory doses. These results indicate a carcinogen acting alone without a promoter can maximally activate guanylate cyclase and would suggest that at the cellular level a promotor is not absolutely necessary for the changes observed morphologically in canerous cells. The promotor, however, did enhance the enzyme's activity when a submaximal dose of the carcinogen was used indicating that promoting agents, at least biochemically, appear capable of potentially contributing to the development of a cancerous cell.

Animals↗
PubMed1978

Hormonal induction of mammary tumor viruses and its implications for carcinogenesis.

The purpose of this study was to evaluate the possibility that hormones and mouse mammary tumor virus (MuMTV) are cocarcinogenic for mammary epithelium. Results of our investigations in vivo and in vitro suggest: (a) Hormones promote mammary carcinogenesis in BALB/c females whether MuMTV is germinally (BALB/c) or horizontally (BALB/cfC3H) transmitted; the rate of carcinogenesis in BALB/cfC3H females is substantially faster than it is in BALB/c, but the final mammary carcinoma incidence is approximately the same. The rate-limiting step in malignant transformation in BALB/c, which infectious MuMTV overcomes, is in premalignant transformation from normal. (b) One characteristic of horizontal MuMTV transmission in BALB/c that is not observed in germinal transmission is integration of new MuMTV sequences in mammary cell DNA. Integration is mammary cell specific and constant at 2 to 3 copies/cell from tumor to tumor. (c) MuMTV expression is changed in mammary epithelial cells during hormonal carcinogenesis. The nature of the change is qualitatively similar in both BALB/c and BALB/cfC3H. Expression of envelope glycopeptides (glycoprotein with a molecular weight of 52,000) is induced, which correlates with amplification of MuMTV RNA sequence content. Quantitative differences exist in induced levels in BALB/c and BALB/cfC3H. (d) MuMTV RNA and a glycoprotein with a molecular weight of 52,000 were not inducible with dexamethasone in normal mammary epithelial cells in culture. These structural components were induced in both premalignant (BALB/cfC3H) and malignant (BALB/c and BALB/cfC3H) cells. MuMTV RNA was induced by dexamethasone in normal cells pretreated with 5-iodo-2'-deoxyuridine. (e) Both premalignant and malignant cells have altered (vis-à-vis normal) surfaces, discernible by differences in reactivity with concanavalin A in hemadsorption assays. Indirect evidence suggests that the alteration includes membrane incorporation of MuMTV-related determinants of a glycoprotein with a molecular weight of 52,000. (f) Malignant cells exhibit enhanced sensitivity to insulin for reinitiation of DNA synthesis and mitosis in contact-inhibited homotypical monolayers. These findings have been organized into a hormonal cocarcinogenesis hypothesis in which expression of germinally transmitted MuMTV genes is the proximal cause of neoplastic transformation.

Animals↗
PubMed1978

Does cyclophosphamide induce bladder cancer?

An increasing incidence of bladder neoplasms temporally associated with chemotherapy, usually cyclophosphamide, is being reported. These secondary primary bladder malignancies are characteristically found in two groups of patients: those with lymphoproliferative or myeloproliferative tumors, and those with immunosuppression after organ transplantation. A case of adenocarcinoma of the bladder associated with malignant lymphoma is reported, and the known cases of second primary bladder malignancies after cyclophosphamide therapy as reported in the literature are reviewed. Studies relating to the enhanced occurrence of second primary cancers in lymphoproliferative disorders are presented. The recognized urologic toxicities of cyclophosphamide, including cytopathologic changes in animals and humans, are discussed. The observed association between immunosuppression and second primary malignancies is explored, as supported by studies on congenital immunodeficiency in humans, viral oncogenesis in experimental animals, and neoplasia after organ transplantation. Possible mechanisms of carcinogenesis associated with cyclophosphamide are reviewed, including suppression of humoral and cell-mediated immune defense mechanisms, direct carcinogenesis, or cocarcinogenesis. A plea is made for the orderly reporting and careful documentation of bladder tumors in patients receiving cyclophosphamide. It is suggested that prospective studies in these patients and in patients receiving cyclophosphamide for nonmalignant disorders would be of value in assessing the culpability of cyclophosphamide as a carcinogen.

Abdominal Neoplasms↗
PubMedDate not supplied

Immune modulation and disease patterns in population groups.

A hypothesis which explains disease prevalence among different socio-economic groups following early infantile modulation of cell-mediated immunity by infection and nutrition related stress is presented. Wealthy populations living under highly hygienic circumstances can develop their cell-mediated immunity to genetic expectation while their humoral systems remains unstimulated. Primitive populations protect the infant's immune development by breast feeding and suffer from temporary cell-mediated immune deficiencies due to intercurrent infectious disease and famine later on. Intermediary populations harbour a small percentage of people, whose cell-mediated immune system has been permanently damaged by infection in early childhood, leading to a high incidence of diseases linked to cell-mediated immune deficiency. The possible cocarcinogenesis of the cell-mediated immune deficiency following repeated gastroenteritis and persistent stimulation of B cells, leading to alpha heavy chain disease and primary intestinal lymphoma, or due to falciparum malaria in newborns and its impact on the EB virus genome in development of Burkitt's lymphoma, are discussed.

Africa↗
PubMed1975

Production of respiratory tract tumors in hamsters by benzo(a)pyrene.

Respiratory tumor induction was tested for the tumorigenic activity of benzo[a]pyrene alone. A group of 32 male and 28 female Syrian golden hamsters were given weekly intratracheal instillation of 1 mg of benzo[a]pyrene suspended in isotonic saline, for 30 weeks. Squamous cell carcinoma, adenocarcinoma, anaplastic carcinoma, adenoma, papilloma, and polyps were induced in the respiratory tract of hamsters. Tumor incidences were 42.3% in males and 57.7% in females. Respiratory carcinomas were inducible in hamsters by simple instillation of a low dose of benzo[a]pyrene without using a surface-active agent or carrier-dust. These findings may be useful as a standard data for cocarcinogenesis studies when using other modality combined with benzo[a]pyrene in experimental studies.

Adenocarcinoma↗
PubMed1979

Bowen's disease and squamous cell carcinoma. Occurrence in a patient with psoriasis after topical, systemic, and PUVA therapy.

Multiple lesions of Bowen's disease and squamous cell carcinoma on the penis and pubic areas developed in a 32-year-old patient with psoriasis who was undergoing treatment with psoralen and long-wave ultraviolet radiation (PUVA). A cumulative dose of more than 3,700 joules/sq cm of UVA had been administered over a three-year period. This case may be an early warning of possible carcinogenicity of PUVA therapy, alone or as part of sequential therapy with other agents.

Adult↗
PubMed1977

Tobacco and alcohol consumption in relation to the development of multiple primary cancers.

The relationship between tobacco and alcohol consumption and the development of additional primary cancers of the upper alimentary tract is reviewed. The chance of developing a second primary is dependent principally on the intensity (i.e., quantity and duration) of the smoking and drinking habit prior to the onset of the first neoplasm. However, results conflict regarding the effect exerted by the continuation of these habits after the first diagnosis. While tobacco smoking is considered the primary risk factor associated with cancers in this area, its interaction with alcohol creates a powerful carcinogenic effect. It is agreed that multiple primaries are selective on a site-specific basis and that risk varies with anatomic location of the first primary.

Alcohol Drinking↗
PubMed1978

Histologic findings in the tracheobronchial tree of uranium miners and non-miners with lung cancer.

The remaining tissue of the tracheobronchial tree from 210 men who died from lung cancer was studied to compare the histologic alterations leading to further sites of primary cancer. These men were uranium miners matched with nonminers for age and smoking habits. In the examination of a total of 28,928 cross-sections carcinoma in situ was found in 96% of the miners and in 92% of the nonminers. The number of slides from miners showing degree 2 or 3 atypia in areas of carcinoma in situ was about double the number found from the nonminers. Although the difference was not statistically significant, 32% of the miners had at least one section showing early primary invasive carcinoma compared with 22% of the nonminers. The data indicate that the synergistic effect of the exposure to uranium dust along with cigarette smoking increases the risk of lung cancer and that in addition to a main tumor mass, other sites of tissue alterations leading to tumor development are frequently already present in the lung.

Adult↗
PubMed1979

Alcohol as a co-factor in the etiology of cancer.

Alcohol and tobacco appear to act synergistically in the pathogenesis of epithelial cancers of the oropharynx (excluding lip), larynx, and esophagus. For the subsites within the upper aerodigestive tract, over 10,000 deaths in United States men during 1978 may be attributed to tobacco and alcohol consumption. The cancer sites for which tobacco and alcohol are major determinants occur with greater frequency in men, blacks, lower socioeconomic groups, and with increasing urbanization and increasing age (35--70 years). Because primary hepatocellular carcinoma occurs more commonly in patients with cirrhosis, chronic alcohol abuse is an important risk mechanism for carcinoma of the liver parenchyma. Although experimental animal studies have failed to demonstrate whether ethanol can independently initiate tumorigenesis, various alternative or associated biochemical and immunological mechanisms of action have been proposed.

Adult↗
PubMed1979

Asbestos, dental X-rays, tobacco, and alcohol in the epidemiology of laryngeal cancer.

A case-control study of 47 laryngeal cancers in males of three counties of Washington State was conducted. Personal interview was used to obtain information on smoking, alcohol use, exposure to asbestos, and other substances, and x-rays of the head and neck area. Smoking and alcohol consumption were found to increase risk of laryngeal cancer independently, with a clear dose-response relationship. Neither asbestos exposure nor exposure to other substances was found to significantly increase the risk of laryngeal cancer, although the relative risk with asbestos exposure was 1.75. Lifetime history of exposure to dental x-rays on five or more occasions was associated with significantly increased risk of laryngeal cancer among heavy smokers but not among light smokers. The importance of tobacco and alcohol in the epidemiology of laryngeal cancer was re-affirmed, the importance of asbestos exposure was brought into question, and a possible relationship of laryngeal cancer with exposure to dental x-rays among heavy smokers was demonstrated.

Aged↗
PubMed1979

Differential response of myofibrils and 10-nm filaments to a cocarcinogen.

Multinucleated myotubes containing large numbers of striated myofibrils and large numbers of longitudinally-oriented 10-nm filaments were treated with the cocarcinogen phorbol-12-myristate-13-acetate (PMA) for 24, 48 or 72 hours. The inhibitory effects of PMA on the accumulation of myofibrils was evident within 24 hours, and by 72 hours virtually all striated myofibrils had disappeared. In contrast, the density of the 10-nm filaments was greatly enhanced in these myofibril-depleted myotubes. These effects were not due to a generalized cytotoxicity, for PMA stimulated the replication of the presumptive myoblasts and fibroblasts present in these cultures. 24 hours after removing the PMA, these myotubes assembled a new set of striated myofibrils and the density of 10-nm filaments diminished proportionately.

Animals↗