Comparative study of the carcinogenic effect of BHP and BAP on NMRI mice

Green, U.; Konishi, Yoichi; Ketkar, M.B.; Althoff, J.

doi:10.1016/0304-3835(80)90096-8

Cited by 9 publications

(5 citation statements)

References 13 publications

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“…There are few reports of experimentally induced squamous cell carcinomas in the airways of mice, but spontaneous development has not been reported. (Boorman, Morgan, and Uraih 1990;Dickhaus et al 1977;Dickhaus et al 1978;Dungworth, Ernst, et al 1992;Dungworth, Hahn, et al 1992;Dungworth et al 2001;Faccini, Abbott, and Paulus 1990;Gopinath, Prentice, and Lewis 1987;Green et al 1980;Karube et al 1989;Luts et al 1991;Maekawa and Odashima 1975;Maronpot 1990;Maronpot et al 1986;Pack Al-Ugaily, and Morris 1981;Pour et al 1976;Rehm and Kelloff 1991;Rehm, Ward, and Sass 1994;Reznik 1983;St. Clair and Morgan 1992;Takahashi, Iwasaki, and Ide 1985;Yamamoto et al 1989) Adenocarcinoma ( Figure 68) Comment: Adenocarcinomas of the larynx, trachea, and bronchi are uncommon, with few reports of chemically induced tumors and in transgenic mice.…”

Section: Larynx Trachea Bronchi and Bronchiolesmentioning

confidence: 96%

“…Squamous metaplasia with normal differentiation pattern is reversible under some experimental circumstances, depending on the nature of inhaled irritant and the duration of exposure, but in other situations it may give rise to squamous papillomas or squamous cell carcinomas. (Boorman, Morgan, and Uraih 1990;Dickhaus et al 1977;Dickhaus et al 1978;Dungworth, Ernst, et al 1992;Dungworth et al 2001;Faccini, Abbott, and Paulus 1990;Gopinath, Prentice, and Lewis 1987;Green et al 1980;Karube et al 1989;Kerns et al 1983;Luts et al 1991;Maekawa and Odashima 1975;Maronpot 1990;Maronpot et al 1986;Pack, Al-Ugaily, and Morris 1981;Pour et al 1976;Rehm and Kelloff 1991;Rehm, Ward, and Sass 1994;Reznik, Schuller, and Stinson 1980;Reznik 1983;Takahashi, Iwasaki, and Ide 1985;Yamamoto et al 1989). …”

Section: Larynx Trachea Bronchi and Bronchiolesmentioning

confidence: 96%

“…Bronchial papillomas lined by uniform cuboidal to columnar cells, and whose crowded papillary structures mimic a glandular pattern, are sometimes referred to as bronchial adenomas. (Boorman and Eustis 1990;Boorman, Morgan, and Uraih 1990;Dickhaus et al 1977;Dickhaus et al 1978;Dungworth, Ernst, et al 1992;Dungworth, Hahn, et al 1992;Dungworth et al 2001;Ito et al 1989;Faccini, Abbott, and Paulus 1990;Gopinath, Prentice, and Lewis 1987;Green et al 1980;Karube et al 1989;Luts et al 1991;Maekawa and Odashima 1975;Maronpot 1990;Maronpot et al 1986;Maronpot et al 1991;Mohr et al 1990;Pack, Al-Ugaily, and Morris 1981;Pour et al 1976;Rehm and Kelloff 1991;Rehm, Ward, and Sass 1994;Reznik 1983;Takahashi, Iwasaki, and Ide 1985;Schüller 1987;Yamamoto et al 1989) Tumor, Neuroendocrine Cell, Benign: Larynx, Trachea, Bronchi, Bronchioles Synonym(s): Papilloma, neuroendocrine; Papilloma, pulmonary neuroendocrine cells (PNEC).…”

Section: Larynx Trachea Bronchi and Bronchiolesmentioning

confidence: 96%

“…Cellular atypia is also a common feature of neoplasia and may be present without hyperplasia. (Boorman, Morgan, and Uraih 1990;Dickhaus et al 1977;Dickhaus et al 1978;Dungworth, Ernst, et al 1992;Dungworth et al 2001;Faccini, Abbott, and Paulus 1990;Gopinath, Prentice, and Lewis 1987;Green et al 1980;Karube et al 1989;Kerns et al 1983;D. Lewis 1991;Luts et al 1991;Maekawa and Odashima 1975;Maronpot 1990;Maronpot et al 1986;Pack, Al-Ugaily, and Morris 1981;Pour et al 1976;Rehm and Kelloff 1991;Rehm Ward, and Sass 1994;Reznik 1983;Takahashi, Iwasaki, and Ide 1985;Yamamoto et al 1989 Comment: Severe squamous metaplasia, hyperplasia, and inflammation accompanied by proliferation of a highly vascular connective tissue stalk may occur as a sequel to blockage of laryngeal submucosal gland ducts by metaplastic duct epithelium (see Ectasia, Submucosal Glands, above).…”

Section: Larynx Trachea Bronchi and Bronchiolesmentioning

confidence: 97%

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Proliferative and Nonproliferative Lesions of the Rat and Mouse Respiratory Tract

Renne¹,

et al. 2009

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The INHAND Project (International Harmonization of Nomenclature and Diagnostic Criteria for Lesions in Rats and Mice) is a joint initiative of the Societies of Toxicologic Pathology from Europe (ESTP), Great Britain (BSTP), Japan (JSTP) and North America (STP) to develop an internationally-accepted nomenclature for proliferative and non-proliferative lesions in laboratory animals. The purpose of this publication is to provide a standardized nomenclature for classifying microscopic lesions observed in the respiratory tract of laboratory rats and mice, with color photomicrographs illustrating examples of some lesions. The standardized nomenclature presented in this document is also available electronically on the internet (http://www.goreni.org/). Sources of material included histopathology databases from government, academia, and industrial laboratories throughout the world. Content includes spontaneous developmental and aging lesions as well as lesions induced by exposure to test materials. A widely accepted and utilized international harmonization of nomenclature for respiratory tract lesions in laboratory animals will decrease confusion among regulatory and scientific research organizations in different countries and provide a common language to increase and enrich international exchanges of information among toxicologists and pathologists.

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Section: Larynx Trachea Bronchi and Bronchiolesmentioning

confidence: 96%

Section: Larynx Trachea Bronchi and Bronchiolesmentioning

confidence: 96%

Section: Larynx Trachea Bronchi and Bronchiolesmentioning

confidence: 96%

Section: Larynx Trachea Bronchi and Bronchiolesmentioning

confidence: 97%

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Proliferative and Nonproliferative Lesions of the Rat and Mouse Respiratory Tract

Renne¹,

et al. 2009

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“…À mutant frequencies in the liver of BHPtreated Parp-1 À/À mice Genomic DNA was prepared from the liver, a major target organ of BHP (Green et al, 1980). Mutant frequency of the gpt gene in the livers of nontreated mice (n ¼ 4) was 5.770.9 ( Â 10 À6 ) and 1071.8 ( Â 10 À6 ) in Parp-1 þ / þ and Parp-1 À/À mice, respectively.…”

Section: Increase In Spimentioning

confidence: 99%

Parp-1 deficiency causes an increase of deletion mutations and insertions/rearrangements in vivo after treatment with an alkylating agent

Shibata

Kamada²,

Masumura

et al. 2004

Oncogene

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Accumulated evidence suggests that Parp-1 is involved in DNA repair processes, including base excision repair, single-strand and double-strand break repairs. To understand the precise role of Parp-1 in genomic stability in vivo, we carried out mutation analysis using Parp-1 knockout (Parp-1 À/À ) mice harboring two marker genes, gpt and red/gam genes. Spontaneous mutant frequencies of both genes in the bone marrows and livers did not differ significantly between Parp-1 À/À and Parp-1 þ / þ mice (P>0.05). After treatment with an alkylating agent, Nnitrosobis(2-hydroxypropyl)amine (BHP), the mutant frequency of the red/gam genes in the liver in Parp-1 À/À mice was 1.6-fold higher than that in Parp-1 þ / þ mice (Po0.05). Categorization of the mutations revealed that deletions larger than 1 kb or those accompanying 1-5 bp insertions at the deletion junctions, as well as rearrangements, were more frequently observed in Parp-1 À/À than in Parp-1 þ / þ mice (Po0.05, respectively). In contrast, mutant frequencies of the gpt gene in the livers of Parp-1 À/À and Parp-1 þ / þ mice after BHP treatment were both elevated and there was no significant difference between the genotypes. These results indicate that Parp-1 is implicated in suppressing deletion mutations in vivo, especially those accompanying small insertions or rearrangements.

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Di(2‐Hydroxy‐N‐Propyl)Amine 53609‐64‐6

2004

Sax's Dangerous Properties of Industrial Materials

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Comparative study of the carcinogenic effect of BHP and BAP on NMRI mice

Cited by 9 publications

References 13 publications

Proliferative and Nonproliferative Lesions of the Rat and Mouse Respiratory Tract

Proliferative and Nonproliferative Lesions of the Rat and Mouse Respiratory Tract

Parp-1 deficiency causes an increase of deletion mutations and insertions/rearrangements in vivo after treatment with an alkylating agent

Di(2‐Hydroxy‐N‐Propyl)Amine 53609‐64‐6

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