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1. Hutt JA, Vuillemenot BR, Barr EB, Grimes MJ, Hahn FF, Hobbs CH, March TH, Gigliotti AP, Seilkop SK, Finch GL, Mauderly JL, Belinsky SA: Life-span inhalation exposure to mainstream cigarette smoke induces lung cancer in B6C3F1 mice through genetic and epigenetic pathways. Carcinogenesis; 2005 Nov;26(11):1999-2009
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  • This study demonstrated that life time whole body exposures of female B6C3F1 mice to mainstream cigarette smoke at 250 mg total particulate matter/m(3) for 6 h per day, 5 days a week induces marked increases in the incidence of focal alveolar hyperplasias, pulmonary adenomas, papillomas and adenocarcinomas.
  • [MeSH-major] DNA Methylation. Gene Silencing / drug effects. Lung / drug effects. Lung Neoplasms / chemically induced. Lung Neoplasms / genetics. Smoking / adverse effects
  • [MeSH-minor] Adenocarcinoma / chemically induced. Adenocarcinoma / genetics. Adenocarcinoma / secondary. Adenoma / chemically induced. Adenoma / genetics. Adenoma / pathology. Administration, Inhalation. Animals. Apoptosis Regulatory Proteins. Body Weight. Calcium-Calmodulin-Dependent Protein Kinases / genetics. Cell Proliferation / drug effects. Death-Associated Protein Kinases. Female. Genes, ras / drug effects. Hyperplasia / chemically induced. Hyperplasia / genetics. Hyperplasia / pathology. Incidence. Mice. Mice, Inbred Strains. Organ Size. Papilloma / chemically induced. Papilloma / genetics. Papilloma / pathology. Point Mutation. Promoter Regions, Genetic. Pulmonary Alveoli / drug effects. Pulmonary Alveoli / metabolism. Pulmonary Alveoli / pathology. Receptors, Retinoic Acid / genetics. Survival Rate

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  • [ErratumIn] Carcinogenesis. 2005 Dec;26(12):2214
  • (PMID = 15944214.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / ES08801; United States / NCRR NIH HHS / RR / RR00136CA
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Receptors, Retinoic Acid; 0 / retinoic acid receptor beta; EC 2.7.11.1 / Death-Associated Protein Kinases; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases
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2. North DW, Abdo KM, Benson JM, Dahl AR, Morris JB, Renne R, Witschi H: A review of whole animal bioassays of the carcinogenic potential of naphthalene. Regul Toxicol Pharmacol; 2008 Jul;51(2 Suppl):S6-14
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  • A statistically significant increased incidence of pulmonary alveolar/bronchiolar adenoma (a benign lesion), was observed among female mice; an observed increase among the males did not reach statistical significance.
  • A tumorigenic response was observed in both sexes of rats, in males an increased incidence of nasal respiratory epithelium adenoma (a benign rather than malignant lesion) and in females, olfactory epithelial neuroblastoma.
  • [MeSH-minor] Adenoma / chemically induced. Adenoma / pathology. Administration, Inhalation. Animals. Bronchi / drug effects. Bronchi / pathology. Esthesioneuroblastoma, Olfactory / chemically induced. Esthesioneuroblastoma, Olfactory / pathology. Female. Inhalation Exposure. Lung Neoplasms / chemically induced. Lung Neoplasms / pathology. Male. Mice. Nasal Cavity / drug effects. Nasal Cavity / pathology. Nose Neoplasms / chemically induced. Nose Neoplasms / pathology. Olfactory Mucosa / drug effects. Olfactory Mucosa / pathology. Pulmonary Alveoli / drug effects. Pulmonary Alveoli / pathology. Rats

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  • (PMID = 18364246.001).
  • [ISSN] 1096-0295
  • [Journal-full-title] Regulatory toxicology and pharmacology : RTP
  • [ISO-abbreviation] Regul. Toxicol. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens, Environmental; 0 / Naphthalenes
  • [Number-of-references] 33
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3. Hahn FF, Gigliotti AP, Hutt JA, March TH, Mauderly JL: A review of the histopathology of cigarette smoke-induced lung cancer in rats and mice. Int J Toxicol; 2007 Jul-Aug;26(4):307-13
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  • Proliferative epithelial lesions are present in the lungs of both species and are apparent antecedent lesions to benign and malignant tumors.
  • Both species have alveolar epithelia hyperplasia, alveolar adenomas, and alveolar carcinomas.
  • [MeSH-major] Adenocarcinoma / etiology. Adenoma / etiology. Lung Neoplasms / etiology. Precancerous Conditions / etiology. Pulmonary Alveoli / drug effects. Smoking / adverse effects
  • [MeSH-minor] Administration, Inhalation. Animals. Bronchi / drug effects. Bronchi / pathology. Bronchial Neoplasms / etiology. Bronchial Neoplasms / pathology. Disease Models, Animal. Female. Male. Mice. Mice, Inbred Strains. Papilloma / etiology. Papilloma / pathology. Rats. Rats, Inbred F344. Respiratory Mucosa / drug effects. Respiratory Mucosa / pathology. Species Specificity


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4. Xie XY, Shen J, Xu LY, Li EM, Shen ZY: Bronchogenic and alveologenic tumors in mice induced by N-nitrosopiperidine. Biochem Cell Biol; 2010 Aug;88(4):775-82
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  • In this study, 80 BALB/C strain mice were injected with 0.2 mmol/kg NPIP intraperitoneally for 8 weeks, and experiments were conducted for a further 16 weeks.
  • All tumors found in the experimental group originated from alveolar type II epithelial cells.
  • [MeSH-minor] Adenoma / chemically induced. Adenoma / genetics. Adenoma / pathology. Adenoma / ultrastructure. Animals. Carcinoma, Squamous Cell / chemically induced. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / pathology. Carcinoma, Squamous Cell / ultrastructure. Female. Gene Expression Regulation, Neoplastic. Genes, bcl-2. Genes, myc. Genes, p53. Genes, ras. Male. Mice. Mice, Inbred BALB C. Pulmonary Alveoli / drug effects. Pulmonary Alveoli / metabolism. Pulmonary Alveoli / pathology. Pulmonary Alveoli / ultrastructure. Telomerase / genetics. Telomerase / metabolism

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  • (PMID = 20651851.001).
  • [ISSN] 1208-6002
  • [Journal-full-title] Biochemistry and cell biology = Biochimie et biologie cellulaire
  • [ISO-abbreviation] Biochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Nitrosamines; 6N066XUL4L / N-nitrosopiperidine; EC 2.7.7.49 / Telomerase; EC 2.7.7.49 / Tert protein, mouse
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5. Tritscher AM, Mahler J, Portier CJ, Lucier GW, Walker NJ: Induction of lung lesions in female rats following chronic exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin. Toxicol Pathol; 2000 Nov-Dec;28(6):761-9
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  • TCDD treatment alone for 60 weeks caused significant increases in alveolar-bronchiolar (AB) metaplasia.
  • TCDD treatment of DEN-initiated animals for 60 weeks resulted in a significant increase in bronchiolar epithelial hyperplasia.
  • These increases were not observed in animals treated with TCDD for 30 weeks followed by corn oil for 30 weeks, indicating that the development of these lesions required continuous exposure to TCDD.
  • [MeSH-major] Bronchi / drug effects. Carcinogens / toxicity. Polychlorinated Dibenzodioxins / toxicity. Pulmonary Alveoli / drug effects. Respiratory Mucosa / drug effects
  • [MeSH-minor] Adenoma / chemically induced. Adenoma / pathology. Age Factors. Animals. Carcinogenicity Tests. Carcinoma / chemically induced. Carcinoma / pathology. Cytochrome P-450 CYP1A1 / metabolism. Diethylnitrosamine / toxicity. Drug Administration Schedule. Female. Half-Life. Hyperplasia. Lung Neoplasms / chemically induced. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Metaplasia. Precancerous Conditions / chemically induced. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. Rats. Rats, Sprague-Dawley. Receptors, Aryl Hydrocarbon / metabolism. Tissue Distribution

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  • (PMID = 11127289.001).
  • [ISSN] 0192-6233
  • [Journal-full-title] Toxicologic pathology
  • [ISO-abbreviation] Toxicol Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Polychlorinated Dibenzodioxins; 0 / Receptors, Aryl Hydrocarbon; 3IQ78TTX1A / Diethylnitrosamine; EC 1.14.14.1 / Cytochrome P-450 CYP1A1
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6. Kang Y, Prentice MA, Mariano JM, Davarya S, Linnoila RI, Moody TW, Wakefield LM, Jakowlew SB: Transforming growth factor-beta 1 and its receptors in human lung cancer and mouse lung carcinogenesis. Exp Lung Res; 2000 Dec;26(8):685-707
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  • The transforming growth factor-betas (TGF-beta s) are multifunctional proteins that inhibit the proliferation of many epithelial cells through a set of cell protein receptors that includes the TGF-beta type I (RI) and type II (RII) receptors.
  • In the present study, we have examined expression of the proteins and mRNAs for TGF-beta 1, TGF-beta RI, and TGF-beta RII in normal human lung, well-characterized non-small cell lung cancer (NSCLC) cell lines, and primary NSCLC specimens.
  • Immunohistochemical staining for TGF-beta 1, TGF-beta RI, and TGF-beta RII using specific antibodies in normal human lung showed expression of the 3 proteins in the epithelium of bronchi and bronchioles as well as in alveoli.
  • Differential expression of TGF-beta RI and TGF-beta RII proteins was detected in 5 NSCLC cell lines using Western blot analysis, with reduced levels in 3 cell lines.
  • In situ hybridization studies conducted with specific riboprobes for TGF-beta 1, TGF-beta RI, and TGF-beta RII showed corresponding localization of expression of the mRNAs in the specimens that showed positive immunostaining for the proteins.
  • To investigate the roles of TGF-beta 1, TGF-beta RI, and TGF-beta RII in chemically induced mouse lung tumorigenesis, we examined the expression of their proteins and mRNAs in 2 mouse model systems.
  • Whereas expression of the proteins and mRNAs for TGF-beta 1 and TGF-beta RI was comparable in lung adenomas and bronchioles of A/J mice treated with benzo(alpha)pyrene, decreased immunostaining and hybridization for TGF-beta RII protein and mRNA was detected in 50% of lung adenomas in these mice.
  • Interestingly, expression of TGF-beta 1 and the TGF-beta receptor proteins was similar to that of bronchioles in C57B1/6 mice and their littermates heterozygous for deletion of the TGF-beta 1 gene treated with diethylnitrosamine.
  • [MeSH-major] Adenoma / metabolism. Carcinoma, Non-Small-Cell Lung / metabolism. Lung Neoplasms / metabolism. Receptors, Transforming Growth Factor beta / metabolism. Transforming Growth Factor beta / metabolism
  • [MeSH-minor] Animals. Blotting, Western. Bronchi / drug effects. Bronchi / metabolism. Bronchi / pathology. Carcinogens / toxicity. DNA Primers / chemistry. Disease Models, Animal. Female. Humans. Immunohistochemistry. In Situ Hybridization. Mice. Mice, Inbred A. Mice, Inbred C57BL. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Transforming Growth Factor beta1. Tumor Cells, Cultured

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  • (PMID = 11195465.001).
  • [ISSN] 0190-2148
  • [Journal-full-title] Experimental lung research
  • [ISO-abbreviation] Exp. Lung Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / DNA Primers; 0 / RNA, Messenger; 0 / Receptors, Transforming Growth Factor beta; 0 / TGFB1 protein, human; 0 / Tgfb1 protein, mouse; 0 / Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1
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7. National Toxicology Program: NTP toxicology and carcinogensis studies of vanadium pentoxide (CAS No. 1314-62-1) in F344/N rats and B6C3F1 mice (inhalation). Natl Toxicol Program Tech Rep Ser; 2002 Dec;(507):1-343
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  • Alveolar and bronchiolar epithelial hyperplasia was observed in most rats exposed to 2 or 4 mg/m(3) on days 6 and 13.
  • Cell turnover rates were increased in the terminal bronchioles on days 6 and 13 and in the alveoli in the 4 mg/m(3) group on day 6 and in all exposed groups on day 13.
  • Alveolar and bronchiolar epithelial hyperplasia occurred with similar incidences and severities among the exposed groups on days 6 and 13, and time- and concentration-related increases in the incidences of interstitial inflammation and histiocytic infiltration also occurred in these groups.
  • In the alveoli, cell turnover rates were increased in an exposure concentration-related manner on day 13; cell turnover rates were increased only in the 8 mg/m(3) group on day 6.
  • Alveolar/bronchiolar neoplasms were present in exposed groups of male rats, and the incidences often exceeded the historical control ranges.
  • Alveolar/bronchiolar adenomas were present in 0.5 and 1 mg/m(3) females; one 2 mg/m(3) female also had an alveolar/bronchiolar carcinoma.
  • The incidence of alveolar/bronchiolar adenoma in the 0.5 mg/m(3) group was at the upper end of the historical control ranges.
  • The incidences of alveolar/bronchiolar neoplasms were significantly increased in all groups of exposed males and females.
  • MOLECULAR ONCOLOGY STUDIES: K-ras codon 12 mutation and loss of heterozygosity on chromosome 6 were detected in vanadium pentoxide-induced alveolar/bronchiolar carcinomas from mice.
  • CONCLUSIONS: Under the conditions of this 2-year inhalation study, there was some evidence of carcinogenic activity of vanadium pentoxide in male F344/N rats and equivocal evidence of carcinogenic activity of vanadium pentoxide in female F344/Nrats based on the occurrence of alveolar/bronchiolar neoplasms.
  • There was clear evidence of carcinogenic activity of vanadium pentoxide in male and female B6C3F1 mice based on increased incidences of alveolar/bronchiolar neoplasms. (ABSTRACT TRUNCATED)
  • [MeSH-minor] Animals. Body Burden. Body Weight / drug effects. Dose-Response Relationship, Drug. Female. Humans. Inhalation Exposure. Lung / drug effects. Lung / pathology. Lung / physiology. Male. Mice. Pulmonary Alveoli / drug effects. Rats. Rats, Inbred F344

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  • (PMID = 12533744.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Vanadium Compounds; BVG363OH7A / vanadium pentoxide
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8. Melnick RL, Nyska A, Foster PM, Roycroft JH, Kissling GE: Toxicity and carcinogenicity of the water disinfection byproduct, dibromoacetic acid, in rats and mice. Toxicology; 2007 Feb 12;230(2-3):126-36
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  • In the 2-year studies, neoplasms were induced at multiple sites in rats and mice exposed to DBA; these included mononuclear cell leukemia and abdominal cavity mesothliomas in rats, and neoplasms of the liver (hepatocellular adenoma or carcinoma and hepatoblastoma) and lung (alveolar adenoma or carcinoma) in mice.
  • These studies provide critical information for future re-evaluations of health-based drinking water standards for haloacetic acids.
  • [MeSH-minor] Administration, Oral. Animals. Carcinogenicity Tests. Female. Histocytochemistry. Liver Neoplasms / chemically induced. Liver Neoplasms / pathology. Lung Neoplasms / chemically induced. Lung Neoplasms / pathology. Male. Mice. Mice, Inbred C57BL. Organ Size / drug effects. Rats. Rats, Inbred F344. Testicular Neoplasms / chemically induced. Testicular Neoplasms / pathology. Water Purification / methods

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  • (PMID = 17157429.001).
  • [ISSN] 0300-483X
  • [Journal-full-title] Toxicology
  • [ISO-abbreviation] Toxicology
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z99 ES999999
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Acetates; 631-64-1 / dibromoacetic acid
  • [Other-IDs] NLM/ NIHMS17825; NLM/ PMC1905493
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9. Mori I, Yasuhara K, Hayashi SM, Nonoyama T, Nomura T, Yanai T, Masegi T, Mitsumori K: Aberrant expression of cyclin D1 in pulmonary proliferative lesions induced by high doses of urethane in transgenic mice carrying the human prototype c-H-ras gene. J Vet Med Sci; 2001 Mar;63(3):261-8
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  • There was neither mutation of p53 nor an increase in immunoreactivity of wild type p53 in these proliferative lesions.
  • These results suggest that cyclin D1 over-expression in alveolar/bronchiolar hyperplasias in rasH2 mice in the triple-injection group is not only indicative of a high cell proliferation rate but also of an important role in the process of malignant transformation.


10. Seike N, Wanibuchi H, Morimura K, Nishikawa T, Kishida H, Nakae D, Hirata K, Fukushima S: Lack of promoting effect due to oral administration of dimethylarsinic acid on rat lung carcinogenesis initiated with N-bis(2-hydroxypropyl)nitrosamine. Cancer Lett; 2002 Jan 25;175(2):113-9
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  • Induction of epithelial lesions, classified as alveolar epithelial hyperplasia, adenoma, and adenocarcinoma was evident in the lungs of DHPN-initiated animals, but no significant differences were found between DMA-treated groups and control groups.
  • [MeSH-minor] Administration, Oral. Animals. Carcinogens / toxicity. Cell Survival / drug effects. Lung / drug effects. Lung / pathology. Male. Mutagens / administration & dosage. Mutagens / toxicity. Pulmonary Alveoli / drug effects. Pulmonary Alveoli / pathology. Rats. Rats, Inbred F344

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  • (PMID = 11741738.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Carcinogens; 0 / Mutagens; 0 / Nitrosamines; 53609-64-6 / diisopropanolnitrosamine; 593-57-7 / dimethylarsine; 88847-89-6 / 8-oxo-7-hydrodeoxyguanosine; G9481N71RO / Deoxyguanosine
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11. Moody TW, Leyton J, Zia F, Tuthill C, Badamchian M, Goldstein AL: Thymosinalpha1 is chemopreventive for lung adenoma formation in A/J mice. Cancer Lett; 2000 Jul 31;155(2):121-7
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  • [Title] Thymosinalpha1 is chemopreventive for lung adenoma formation in A/J mice.
  • Daily administration of THNalpha1 (0.4 mg/kg, s.c.) reduced lung adenoma multiplicity significantly, by approximately 45, 40, and 17%, respectively, 2.5, 3, and 4 months after urethane injection.
  • Animals treated with THNalpha1 had a significantly greater white cell density than control A/J mice.
  • By immunocytochemistry, THNalpha1-like peptides were detected in all lung compartments including the bronchus, adenoma, bronchioles, and alveoli.
  • [MeSH-major] Adenoma / prevention & control. Lung Neoplasms / prevention & control. Thymosin / analogs & derivatives
  • [MeSH-minor] Animals. Blood / drug effects. Blotting, Western. Bronchi / metabolism. Carcinogens. Female. Immunohistochemistry. Lung / drug effects. Mice. Pulmonary Alveoli / metabolism. Radioimmunoassay. Time Factors. Tissue Distribution. Urethane

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  • (PMID = 10822126.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] IRELAND
  • [Chemical-registry-number] 0 / Carcinogens; 0 / thymalfasin; 3IN71E75Z5 / Urethane; 61512-21-8 / Thymosin
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12. Moody TW, Leyton J, Zakowicz H, Hida T, Kang Y, Jakowlew S, You L, Ozbun L, Zia H, Youngberg J, Malkinson A: Indomethacin reduces lung adenoma number in A/J mice. Anticancer Res; 2001 May-Jun;21(3B):1749-55
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Indomethacin reduces lung adenoma number in A/J mice.
  • The non-steroidal antiinflammatory drug (NSAID) indomethacin reduced significantly the number of lung adenomas 3, 4 or 8 months after urethane injection by 28, 30 and 29% respectively.
  • By immunocytochemistry, COX-2 immunoreactivity was present in the cytosol of lung adenomas, and in epithelial cells lining the bronchioli and bronchus as well as type 2 alveolar cells.
  • By RT-PCR, COX-1 and COX-2 PCR products were present in mouse lung adenomas, alveoli and bronchioli.
  • These results suggest that indomethacin may inhibit COX-1 and COX-2 in the A/J mouse lung resulting in reduced adenoma formation.
  • [MeSH-major] Adenoma / drug therapy. Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Indomethacin / pharmacology. Lung Neoplasms / drug therapy
  • [MeSH-minor] Animals. Apoptosis. Bronchi / metabolism. Carcinogens. Cyclooxygenase 1. Cyclooxygenase 2. Cytosol / metabolism. Epithelial Cells / metabolism. Female. Humans. Immunohistochemistry. Isoenzymes / biosynthesis. Membrane Proteins. Mice. Prostaglandin-Endoperoxide Synthases / biosynthesis. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Tumor Cells, Cultured. Urethane

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  • (PMID = 11497255.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Carcinogens; 0 / Isoenzymes; 0 / Membrane Proteins; 0 / RNA, Messenger; 3IN71E75Z5 / Urethane; EC 1.14.99.1 / Cyclooxygenase 1; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS1 protein, human; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; EC 1.14.99.1 / Ptgs1 protein, mouse; XXE1CET956 / Indomethacin
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13. Koujitani T, Yasuhara K, Tamura T, Onodera H, Takagi H, Takizawa T, Hirose M, Hayashi Y, Mitsumori K: Lack of modifying effects of eugenol on development of lung proliferative lesions induced by urethane in transgenic mice carrying the human prototype c-Ha-ras gene. J Toxicol Sci; 2001 Aug;26(3):129-39
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  • In both male and female rasH2 mice, alveolar/bronchiolar hyperplasias, adenomas and carcinomas were observed in all UR-treated groups.
  • In non-Tg mice, alveolar/bronchiolar hyperplasias, adenomas or carcinomas were sporadically observed in UR-treated groups of both sexes, with no significant differences in the incidences and multiplicities between the UR alone and UR + EUG groups.
  • [MeSH-major] Adenoma / chemically induced. Carcinogens / toxicity. Carcinoma / chemically induced. Eugenol / toxicity. Genes, ras. Lung Neoplasms / chemically induced
  • [MeSH-minor] Animals. Bronchi / chemistry. Bronchi / drug effects. Bronchi / pathology. Carcinogenicity Tests / methods. Cocarcinogenesis. Disease Models, Animal. Drug Synergism. Female. Fluorescent Antibody Technique, Indirect. Humans. Hyperplasia / chemically induced. Hyperplasia / pathology. Immunoenzyme Techniques. Lung / chemistry. Lung / drug effects. Lung / pathology. Male. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Mice, Transgenic. Proliferating Cell Nuclear Antigen / analysis. Pulmonary Alveoli / chemistry. Pulmonary Alveoli / drug effects. Pulmonary Alveoli / pathology. Urethane


14. Wislez M, Spencer ML, Izzo JG, Juroske DM, Balhara K, Cody DD, Price RE, Hittelman WN, Wistuba II, Kurie JM: Inhibition of mammalian target of rapamycin reverses alveolar epithelial neoplasia induced by oncogenic K-ras. Cancer Res; 2005 Apr 15;65(8):3226-35
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  • [Title] Inhibition of mammalian target of rapamycin reverses alveolar epithelial neoplasia induced by oncogenic K-ras.
  • Here, we report that mTOR inhibition blocked malignant progression in K-ras(LA1) mice, which undergo somatic activation of the K-ras oncogene and display morphologic changes in alveolar epithelial cells that recapitulate those of precursors of human lung adenocarcinoma.
  • Levels of phospho-S6(Ser236/235), a downstream mediator of mTOR, increased with malignant progression (normal alveolar epithelial cells to adenocarcinoma) in K-ras(LA1) mice and in patients with lung adenocarcinoma.
  • Atypical alveolar hyperplasia, an early neoplastic change, was prominently associated with macrophages and expressed high levels of phospho-S6(Ser236/235).
  • mTOR inhibition in K-ras(LA1) mice by treatment with the rapamycin analogue CCI-779 reduced the size and number of early epithelial neoplastic lesions (atypical alveolar hyperplasia and adenomas) and induced apoptosis of intraepithelial macrophages.
  • Lastly, conditioned medium from primary cultures of alveolar macrophages stimulated the proliferation of LKR-13 cells.
  • [MeSH-major] Adenocarcinoma / enzymology. Genes, ras / genetics. Lung Neoplasms / enzymology. Precancerous Conditions / enzymology. Protein Kinase Inhibitors / pharmacology. Protein Kinases / metabolism. Pulmonary Alveoli / pathology. Sirolimus / analogs & derivatives. Sirolimus / pharmacology
  • [MeSH-minor] Adenoma / drug therapy. Adenoma / enzymology. Adenoma / genetics. Adenoma / pathology. Animals. Cell Line, Tumor. Cell Transformation, Neoplastic / drug effects. Cell Transformation, Neoplastic / metabolism. Disease Progression. Enzyme Activation. Hyperplasia. Macrophages, Alveolar / drug effects. Macrophages, Alveolar / enzymology. Macrophages, Alveolar / pathology. Mice. Mutation. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt. Ribosomal Protein S6 Kinases / biosynthesis. TOR Serine-Threonine Kinases

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  • (PMID = 15833854.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P50 CA070907; United States / NCI NIH HHS / CA / R01 CA105155
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins; 624KN6GM2T / temsirolimus; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / Ribosomal Protein S6 Kinases; W36ZG6FT64 / Sirolimus
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