Nasal tumours in rats after severe injury to the nasal mucosa and prolonged exposure to 10 ppm formaldehyde

Woutersen, Ruud; Garderen-Hoetmer, A. van; Bruijntjes, J.P.; Zwart, A.; Feron, V.J.

doi:10.1002/jat.2550090108

Cited by 71 publications

(32 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…These formaldehyde associated metaplastic changes are morphologically distinct from the more progressive B[a]P-associated phenotypic alterations (I 58, 165). The occurrence of epithelial cell injury enhances carcinogenesis in rats chronically exposed to formaldehyde (206). In hamsters exposed to a chronic (lifetime) dose of formaldehyde, Dalbcy (28) found that diethylnitrosamine (DEN) treated animals developed more tumors per trachea than animals exposed to DEN alone.…”

Section: Cohimunicationmentioning

confidence: 99%

Intercellular Communication in Bronchial Epithelial Cells: Review of Evidence for a Possible Role in Lung Carcinogenesis

et al. 1990

View full text Add to dashboard Cite

A challenging aspect of lung carcinogenesis is the elucidation of the mechanisms which permit initiated bronchial epithelial cells to attain a growth advantage over normal bronchial epithelial cells, and subsequently evolve into a malignant phenotype. In this review, the effects of interactions between normal and transformed cells, and the potential role of representative extrinsic factors on cell-cell communication are discussed. Evidence is presented to show how cell injury and the effects of serum and calcium may affect morphology and communication, and tumor development. A large number of autocrine-paracnne factors (e.g., TGFp, TGFa) are released by bronchial epithelial cells. These factors may inhibit or promote the proliferation of normal and transformed bronchial epithelial cells, respectively. The ability of certain injurious and tumor promoting agents (e.g., formaldehyde, TPA) to select for the transformed phenotype may involve selective cell injury, the induction of terminal differentiation and an inhibition of gap junction communication among normal BE cells.

show abstract

Section: Cohimunicationmentioning

confidence: 99%

Intercellular Communication in Bronchial Epithelial Cells: Review of Evidence for a Possible Role in Lung Carcinogenesis

et al. 1990

View full text Add to dashboard Cite

show abstract

“…Squamous cell carcinomas of the respiratory epithelium were also found in Cpb:WU (Wistar random) rats with their respiratory mucosa severely damaged by electrocoagulation and exposure to 10 ppm formaldehyde for 28 months (11). The only squamous cell carcinoma found to have metastasized to the lungs was present in a rat exposed to acetaldehyde (Plate 4).…”

Section: Introductionmentioning

confidence: 96%

Upper Respiratory Tract Tumors in Cpb:WU (Wistar Random) Rats

Feron¹,

Woutersen²,

Garderen-Hoetmer³

et al. 1990

Environmental Health Perspectives

Self Cite

View full text Add to dashboard Cite

A survey is given of upper respiratory tract tumors in Cpb:WU (Wistar random) rats. Data were collected from ten 24-to 30-month toxicity/carcinogenicity studies and from one 12-month study. Nasal tumors may lead to dyspnea, mouth breathing, and nasal discharge. These clinical signs mainly occurred in rats bearing squamous cell carcinomas. The large nasal tumors were often osteolytic, they invaded the subcutis over the premaxilla, resulting in swellings on the back of the nose, and extended into the brain. The incidence of nasal tumors in untreated male controls was 1.1% (7/661), the tumors invariably being squamous cell carcinomas. There were no nasal tumors found in untreated female controls. The type of compound-induced nasal tumor most frequently observed was adenocarcinoma (of the olfactory epithelium) followed, in order of decreasing incidence, by squamous cell carcinoma, carcinoma in situ, polypoid adenoma, Schwannoma, and carcinosarcoma. It was proposed that adenocarcinomas of the olfactory epithelium should be classified as neuroepitheliomas. It was also suggested that squamous cell carcinomas, seen in association with necrotizing inflammation of an incisor tooth, should be considered as part ofthe malocclusion syndrome. No spontaneous tracheal tumors were observed, and only one out of 422 untreated female controls (0.2 %) was seen to have a laryngeal tumor, an adenoma. Induced laryngeal tumors included carcinoma in situ, squamous cell carcinoma, and adenocarcinoma. Squamous cell carcinoma was the only type of treatment-related tracheal tumor found. The incidences of induced laryngeal and tracheal tumors were very low, and in no case were these tumors statistically significantly different from the respective incidences in controls.

show abstract

“…On the other hand, the observed histological alterations in the pulmonary epithelium ranged from acute interstitial inflammation (pnuemonitis), pulmonary fibrosis, acute purulent bronchitis, acute lung injury and chronic lung injury; similar to that reported by Kamta et al (1996). Similarly, the studies of Woutersen et al (1989) revealed nasal lesions of respiratory epithelium and yellowing of the fur. The lesions consisted rhinitis squamous metaplasia and basal cell/psuedoepithelial hyperplasia which is in agreement with the observations revealed in my studies which include yellowing of the fur and also nasal lesions in the respiratory epithelium.…”

Section: Discussionmentioning

confidence: 85%