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1. Liu Y, Vikis HG, Yi Y, Futamura M, Wang Y, You M: Degradation of lung adenoma susceptibility 1, a major candidate mouse lung tumor modifier, is required for cell cycle progression. Cancer Res; 2007 Nov 1;67(21):10207-13
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Degradation of lung adenoma susceptibility 1, a major candidate mouse lung tumor modifier, is required for cell cycle progression.
  • We have previously identified murine lung adenoma susceptibility 1 (Las1) as the pulmonary adenoma susceptibility 1 candidate gene.
  • The differential degradation of Las1-A/J and Las-B6 has important implications for its intracellular function and may eventually explain Las1-A/J in lung tumorigenesis.

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  • (PMID = 17974961.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA099147; United States / NCI NIH HHS / CA / CA099187; United States / NIEHS NIH HHS / ES / ES012063; United States / NIEHS NIH HHS / ES / ES013340; United States / NIEHS NIH HHS / ES / ES014399
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Las1 protein, mouse; 0 / Tubulin; 0 / Tumor Suppressor Proteins; 0 / Ubiquitin; EC 3.4.25.1 / Proteasome Endopeptidase Complex
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2. Wang M, Zhang Z, Zhang Z, Vikis H, Yan Y, Wang Y, You M: Fine mapping and candidate gene analyses of pulmonary adenoma resistance 1, a major genetic determinant of mouse lung adenoma resistance. Cancer Res; 2007 Mar 15;67(6):2508-16
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  • [Title] Fine mapping and candidate gene analyses of pulmonary adenoma resistance 1, a major genetic determinant of mouse lung adenoma resistance.
  • Pulmonary adenoma resistance 1 (Par1) is a major genetic determinant of mouse lung adenoma resistance.
  • Genes showing differential lung tissue expression or carrying nonsynonymous single nucleotide polymorphisms were identified and discussed.
  • Our findings have narrowed the Par1 QTL region and will greatly facilitate the identification of the major genetic determinant of mouse lung adenoma resistance.
  • [MeSH-major] Adenoma / genetics. Genes, Tumor Suppressor. Lung Neoplasms / genetics

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  • (PMID = 17363568.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA099147; United States / NCI NIH HHS / CA / CA099187; United States / NIEHS NIH HHS / ES / ES012063; United States / NIEHS NIH HHS / ES / ES013340
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Tob1 protein, mouse
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3. Jin HY, Park TS: Pulmonary pleomorphic adenoma: report of a rare case. Korean J Intern Med; 2007 Jun;22(2):122-4
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  • [Title] Pulmonary pleomorphic adenoma: report of a rare case.
  • Primary pleomorphic adenoma of the lung is a type of pulmonary adenoma that is extremely rare, and it predominantly occurs in the proximal airway.
  • We recently experienced a case of a peripheral solitary pulmonary nodule that was discovered on the CT scans.
  • We performed wedge resection with video-assisted thoracoscopic surgery and we firmly diagnosed this lesion as pulmonary pleomorphic adenoma according to the histology.
  • We report here on a rare benign tumor that was diagnosed as a primary pleomorphic adenoma located in the lung periphery.
  • [MeSH-major] Adenoma, Pleomorphic / diagnosis. Lung Neoplasms / diagnosis

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  • [Cites] J Thorac Imaging. 2002 Apr;17(2):163-6 [11956369.001]
  • [Cites] Nihon Rinsho. 2002 May;60 Suppl 5:123-31 [12101640.001]
  • [Cites] Arch Pathol Lab Med. 2003 May;127(5):621-2 [12708911.001]
  • [Cites] Thorax. 1972 Nov;27(6):657-73 [4345984.001]
  • [Cites] Arch Pathol Lab Med. 1991 Apr;115(4):393-6 [2012502.001]
  • [Cites] Cancer. 1993 Apr 15;71(8):2689-97 [8453591.001]
  • [Cites] Cancer. 1994 May 15;73(10):2481-90 [7513602.001]
  • [Cites] Anticancer Res. 1998 May-Jun;18(3B):2015 -20 [9677459.001]
  • [Cites] J Thorac Cardiovasc Surg. 1965 Apr;49:663-8 [14274349.001]
  • (PMID = 17616030.001).
  • [ISSN] 1226-3303
  • [Journal-full-title] The Korean journal of internal medicine
  • [ISO-abbreviation] Korean J. Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2687611
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4. Wang M, Wang Y, You M, Devereux TR: Analysis of the Par2 modifier of pulmonary adenoma formation in mice. Exp Lung Res; 2005 Mar;31(2):193-204
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of the Par2 modifier of pulmonary adenoma formation in mice.
  • Inbred strains of mouse show various susceptibilities to spontaneous and chemical-induced lung tumorigenesis.
  • Genetic analyses have revealed that lung tumor susceptibilities of inbred mouse strains are governed by quantitative trait loci (QLTs) located on multiple chromosomes.
  • A major lung tumor resistance QLT, designated pulmonary adenoma resistance 2 (Par2), was mapped to the mouse chromosome 18 independently by several groups and accounted for up to 60% phenotype variance between susceptible A/J and more resistant BALB/c strains.
  • [MeSH-major] Adenoma / genetics. Genetic Predisposition to Disease. Lung Neoplasms / genetics. Quantitative Trait Loci

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  • (PMID = 15828125.001).
  • [ISSN] 0190-2148
  • [Journal-full-title] Experimental lung research
  • [ISO-abbreviation] Exp. Lung Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01CA099147; United States / NCI NIH HHS / CA / R01CA58554
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Number-of-references] 52
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5. Manenti G, Galvan A, Pettinicchio A, Trincucci G, Spada E, Zolin A, Milani S, Gonzalez-Neira A, Dragani TA: Mouse genome-wide association mapping needs linkage analysis to avoid false-positive Loci. PLoS Genet; 2009 Jan;5(1):e1000331
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We carried out genome-wide association (GWA) studies in inbred mouse strains characterized for their lung tumor susceptibility phenotypes (spontaneous or urethane-induced) with panels of 12,959 (13K) or 138,793 (140K) single-nucleotide polymorphisms (SNPs).
  • Above the statistical thresholds, we detected only SNP rs3681853 on Chromosome 5, two SNPs in the pulmonary adenoma susceptibility 1 (Pas1) locus, and SNP rs4174648 on Chromosome 16 for spontaneous tumor incidence, urethane-induced tumor incidence, and urethane-induced tumor multiplicity, respectively, with the 13K SNP panel, but only the Pas1 locus with the 140K SNP panel.
  • Genet., 38:888-95, 2006), showed no genetic effects in the two independent intercross mouse populations containing both alleles, nor was it expressed in mouse normal lung or lung tumors.
  • [MeSH-major] Chromosome Mapping. Genetic Predisposition to Disease. Genome-Wide Association Study / methods. Linkage Disequilibrium. Lung Neoplasms / genetics. Polymorphism, Single Nucleotide


6. Akan H, Yildiz L, Unal R: Carcinoma ex pleomorphic adenoma of the minor salivary gland with pulmonary metastasis. Diagn Interv Radiol; 2008 Mar;14(1):3-5
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  • [Title] Carcinoma ex pleomorphic adenoma of the minor salivary gland with pulmonary metastasis.
  • Carcinoma ex pleomorphic adenoma is an exceedingly rare neoplasm of the minor salivary gland.
  • We present a case of carcinoma ex pleomorphic adenoma with pulmonary metastasis to emphasize that patients treated for this condition should be investigated for distant metastasis.
  • [MeSH-major] Adenoma, Pleomorphic / diagnosis. Lung Neoplasms / diagnosis. Salivary Gland Neoplasms / diagnosis

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  • (PMID = 18306136.001).
  • [ISSN] 1305-3825
  • [Journal-full-title] Diagnostic and interventional radiology (Ankara, Turkey)
  • [ISO-abbreviation] Diagn Interv Radiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Turkey
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7. Liu PY, Vikis H, James M, Lu Y, Wang DL, Liu HB, Wen WD, Wang Y, You M: Identification of Las2, a major modifier gene affecting the Pas1 mouse lung tumor susceptibility locus. Cancer Res; 2009 Aug 1;69(15):6290-8
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  • [Title] Identification of Las2, a major modifier gene affecting the Pas1 mouse lung tumor susceptibility locus.
  • Lung cancer is the leading cause of cancer death worldwide.
  • Here, we describe a genome-wide association study of chemically induced lung tumorigenesis on 593 mice from 21 inbred strains using 115,904 genotyped and 1,952,918 imputed single nucleotide polymorphisms (SNPs).
  • Using a genetic background-controlled genome search, we identified a novel lung tumor susceptibility gene Las2 (Lung adenoma susceptibility 2) on distal chromosome 18.
  • Las2 showed strong association with resistance to tumor induction (rs30245983; P = 1.87 x 10(-9)) as well as epistatic interactions (P = 1.71 x 10(-3)) with the pulmonary adenoma susceptibility 1 locus, a major locus affecting mouse lung tumor development (rs13459098, P = 5.64 x 10(-27)).
  • Deletion of LAS2 was observed in approximately 40% of human lung adenocarcinomas, implying that loss of function of LAS2 may be a key step for lung tumorigenesis.
  • [MeSH-major] Lung Neoplasms / genetics. Oncogenes. Quantitative Trait Loci

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  • (PMID = 19622765.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA099147; United States / NCI NIH HHS / CA / CA099187; United States / NIEHS NIH HHS / ES / ES012063; United States / NIEHS NIH HHS / ES / ES013340
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
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8. Papla B: Papillary adenoma of the lung. Pol J Pathol; 2009;60(1):49-51
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  • [Title] Papillary adenoma of the lung.
  • The report presents a very rare case of papillary adenoma of the lung in a 61-year old man, described for the first time in the Polish literature.
  • [MeSH-major] Adenoma / diagnosis. Lung Neoplasms / diagnosis
  • [MeSH-minor] Humans. Keratins / metabolism. Male. Middle Aged. Pulmonary Surfactant-Associated Protein A / metabolism. Respiratory Mucosa / metabolism. Respiratory Mucosa / pathology

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  • (PMID = 19670704.001).
  • [ISSN] 1233-9687
  • [Journal-full-title] Polish journal of pathology : official journal of the Polish Society of Pathologists
  • [ISO-abbreviation] Pol J Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Pulmonary Surfactant-Associated Protein A; 68238-35-7 / Keratins
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9. Tucker AR, Ramsay EC, Donnell RL: Oligodendroglioma in an african lion (Panthera leo). J Zoo Wildl Med; 2008 Dec;39(4):650-4
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  • A second neoplasm, a pulmonary adenoma, was also iidentified at necropsy.
  • [MeSH-major] Adenoma / veterinary. Brain Neoplasms / veterinary. Lions. Lung Neoplasms / veterinary. Oligodendroglioma / veterinary

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  • (PMID = 19110712.001).
  • [ISSN] 1042-7260
  • [Journal-full-title] Journal of zoo and wildlife medicine : official publication of the American Association of Zoo Veterinarians
  • [ISO-abbreviation] J. Zoo Wildl. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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10. Liu P, Wang Y, Vikis H, Maciag A, Wang D, Lu Y, Liu Y, You M: Candidate lung tumor susceptibility genes identified through whole-genome association analyses in inbred mice. Nat Genet; 2006 Aug;38(8):888-95
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  • [Title] Candidate lung tumor susceptibility genes identified through whole-genome association analyses in inbred mice.
  • We performed a whole-genome association analysis of lung tumor susceptibility using dense SNP maps ( approximately 1 SNP per 20 kb) in inbred mice.
  • We reproduced the pulmonary adenoma susceptibility 1 (Pas1) locus identified in previous linkage studies and further narrowed this quantitative trait locus (QTL) to a region of less than 0.5 Mb in which at least two genes, Kras2 (Kirsten rat sarcoma oncogene 2) and Casc1 (cancer susceptibility candidate 1; also known as Las1), are strong candidates.
  • Casc1 knockout mouse tumor bioassays showed that Casc1-deficient mice were susceptible to chemical induction of lung tumors.
  • We also found three more genetic loci for lung adenoma development.
  • We found that the Lasc1 Glu102 allele preferentially promotes lung tumor cell growth.
  • [MeSH-major] Genetic Predisposition to Disease. Lung Neoplasms / genetics
  • [MeSH-minor] Adenoma / genetics. Adenoma / pathology. Alleles. Animals. Chromosome Mapping. Genome. Humans. Mice. Mice, Inbred Strains. Mice, Knockout. Polymorphism, Single Nucleotide. Quantitative Trait Loci


11. Manenti G, Galbiati F, Pettinicchio A, Spinola M, Piconese S, Leoni VP, Conti B, Ravagnani F, Incarbone M, Pastorino U, Dragani TA: A V141L polymorphism of the human LRMP gene is associated with survival of lung cancer patients. Carcinogenesis; 2006 Jul;27(7):1386-90
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  • [Title] A V141L polymorphism of the human LRMP gene is associated with survival of lung cancer patients.
  • Mouse Lrmp and Casc1 genes are candidates for the pulmonary adenoma susceptibility 1 (Pas1) locus, the major determinant of strain variation in lung tumor susceptibility.
  • These genes contain coding and non-coding single nucleotide polymorphisms (SNPs) strongly associated with lung tumor risk in mice.
  • Analysis of LRMP and CASC1 gene SNPs in 361 lung adenocarcinoma (ADCA) patients and 327 healthy controls revealed common SNPs in LRMP (V141L and S197C) and CASC1 (R33S and three intronic variations), and none showed a significant association with lung ADCA risk.
  • These findings suggest that the LRMP V141L polymorphism can predict survival in lung ADCA and that the role of LRMP and CASC1 in human lung cancer risk may differ from that in mice.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / mortality. Lung Neoplasms / genetics. Lung Neoplasms / mortality. Membrane Proteins / genetics

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  • (PMID = 16410263.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / LRMP protein, human; 0 / Membrane Proteins
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12. Manenti G, Dragani TA: Pas1 haplotype-dependent genetic predisposition to lung tumorigenesis in rodents: a meta-analysis. Carcinogenesis; 2005 May;26(5):875-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pas1 haplotype-dependent genetic predisposition to lung tumorigenesis in rodents: a meta-analysis.
  • Rodent species and strains show wide variations in susceptibility to lung tumorigenesis.
  • In mice, hierarchical clustering of 29 inbred laboratory strains by pulmonary adenoma susceptibility 1 (Pas1) locus polymorphisms separated the strains into either an A/J- or a C57BL/6J-type Pas1 haplotype.
  • A pooled analysis (including >8500 mice) of studies on spontaneous and chemically induced lung tumorigenesis in these strains revealed a significantly higher risk of spontaneous lung tumors [odds ratio (OR) 12.17; 95% confidence interval (CI) 9.00-16.45] as well as of chemically induced lung tumors (OR 15.14; 95% CI 12.51-18.31) in the A/J-type haplotype.
  • Thus, the present meta-analysis indicates a link between the genetic control of spontaneous and chemically induced lung tumor susceptibility in mice.
  • These findings might help in the interpretation of results of rodent carcinogenicity bioassays and assessing the risk of lung carcinogenesis from chemicals.
  • [MeSH-major] Genetic Predisposition to Disease. Lung Neoplasms / genetics. Neoplasms, Experimental / genetics

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  • (PMID = 15471897.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Meta-Analysis; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carcinogens
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13. Kohno T, Kunitoh H, Suzuki K, Yamamoto S, Kuchiba A, Matsuno Y, Yanagitani N, Yokota J: Association of KRAS polymorphisms with risk for lung adenocarcinoma accompanied by atypical adenomatous hyperplasias. Carcinogenesis; 2008 May;29(5):957-63
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  • [Title] Association of KRAS polymorphisms with risk for lung adenocarcinoma accompanied by atypical adenomatous hyperplasias.
  • The pulmonary adenoma susceptibility 1 (Pas1) gene affects susceptibility to the development of lung adenomas in mice with a subset of the adenomas progressing to adenocarcinoma (ADC).
  • In this study, genotype distributions for 10 polymorphisms in the human counterparts for three mouse candidate Pas1 genes, KRAS, CASC1/LAS1 and LRMP, were examined in a hospital-based case-control study consisting of 364 lung ADC cases and 253 controls.
  • All the ADC cases were subjected to lobectomy and subsequent pathological investigation of atypical adenomatous hyperplasia (AAH), a putative precursor for peripheral lung ADC, including bronchioloalveolar carcinoma, in the resected lobes.
  • None of the 10 polymorphisms examined showed significant associations with overall lung ADC risk (P > 0.05).
  • Minor haplotypes including the minor allele for the KRAS-6 polymorphism showed increased ORs for ADC accompanied by multiple AAHs, and KRAS transcripts from the minor allele for this polymorphism were more abundantly detected in lung tissues than those from the major allele.
  • Thus, KRAS polymorphisms were indicated to be involved in risk for the development of AAHs that progress to ADC by causing differential KRAS oncogene expression in the lungs.
  • [MeSH-major] Adenocarcinoma / genetics. Lung Neoplasms / genetics. Polymorphism, Genetic. Polymorphism, Single Nucleotide. Proto-Oncogene Proteins / genetics. ras Proteins / genetics
  • [MeSH-minor] Adenomatosis, Pulmonary / epidemiology. Adenomatosis, Pulmonary / genetics. Aged. Antigens, Neoplasm / genetics. Antigens, Nuclear / genetics. DNA, Neoplasm / blood. DNA, Neoplasm / genetics. DNA, Neoplasm / isolation & purification. Female. Humans. Hyperplasia / complications. Hyperplasia / epidemiology. Hyperplasia / genetics. Japan / epidemiology. Male. Middle Aged. Risk Factors. Smoking / epidemiology

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  • (PMID = 18299280.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Antigens, Nuclear; 0 / DNA, Neoplasm; 0 / KRAS protein, human; 0 / PASD1 protein, human; 0 / Proto-Oncogene Proteins; EC 3.6.5.2 / ras Proteins
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14. Yang CS, Liao J, Yang GY, Lu G: Inhibition of lung tumorigenesis by tea. Exp Lung Res; 2005 Jan-Feb;31(1):135-44
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  • [Title] Inhibition of lung tumorigenesis by tea.
  • Tea and tea constituents have been shown by different investigators to inhibit lung tumorigenesis in different animal model systems.
  • This includes lung tumorigenesis in A/J mice induced by 4-(methylnitrosamino)-1-(3pyridyl)-1-butanone (NNK), N-nitrosodiethylamine, benzo[a]pyrene, N-nitrosomethylurea, or cisplatin.
  • Inhibition of lung tumorigenesis has also been demonstrated in C3H mice treated with N-nitrosodiethylamine.
  • Black tea preparations have been shown to reduce the incidence and number of spontaneously generated lung adenocarcinomas and rhabdomyosarcoma in A/J mice, as well as inhibit the progression of lung adenoma to adenocarcinoma.
  • However, a study suggests that caffeine is the key effective constituent for the inhibitory activity of lung tumorigenesis in Fisher 344 rats by black tea.
  • [MeSH-major] Adenocarcinoma / prevention & control. Lung Neoplasms / prevention & control. Phytotherapy. Plant Extracts / therapeutic use. Tea

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  • (PMID = 15765923.001).
  • [ISSN] 0190-2148
  • [Journal-full-title] Experimental lung research
  • [ISO-abbreviation] Exp. Lung Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA56673; United States / NCI NIH HHS / CA / CA88961
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Plant Extracts; 0 / Tea; 8R1V1STN48 / Catechin
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15. Miyazaki M, Yamazaki H, Takeuchi H, Saoo K, Yokohira M, Masumura K, Nohmi T, Funae Y, Imaida K, Kamataki T: Mechanisms of chemopreventive effects of 8-methoxypsoralen against 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced mouse lung adenomas. Carcinogenesis; 2005 Nov;26(11):1947-55
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  • [Title] Mechanisms of chemopreventive effects of 8-methoxypsoralen against 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced mouse lung adenomas.
  • Recently we reported that the occurrence of lung adenoma caused by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) was completely prevented by pretreatment of female A/J mice with 8-methoxypsoralen, a potent inhibitor of cytochrome P450 (P450 or CYP) 2A [Takeuchi et al. (2003) Cancer Res., 63, 7581-7583].
  • Thus, the aim of this study was to confirm that 8-methoxypsoralen exhibits chemopreventive effects by inhibiting CYP2A in the mouse lung.
  • The involvement of CYP2A in the metabolic activation of NNK in the lung was first evidenced by the fact that the mutagenic activation of NNK by mouse lung microsomes was inhibited by 8-methoxypsoralen, coumarin and antibodies to rat CYP2A1.
  • The expression of mRNA for CYP2A5, but not for CYP2A4 or CYP2A12, in the mouse lung was proven by reverse transcriptase-polymerase chain reaction, probably indicating that CYP2A5 present in the mouse lung was involved in the metabolic activation of NNK.
  • The in vivo chemopreventive effects of 8-methoxypsoralen towards NNK-induced adenoma was seen only when the agent was given to female A/J mice prior to, but not posterior to, NNK, lending support to the idea that NNK is activated by CYP2A5 in the mouse lung as an initial step to cause adenoma.
  • The inhibition by 8-methoxypsoralen of NNK-induced adenoma was seen in a dose-dependent manner: the dose to show apparent 50% suppression was calculated to be 1.0 mg/kg.
  • To our surprise, CYP2A protein(s) was expressed in the lesion of NNK-induced lung adenomas, probably suggesting that 8-methoxypsoralen could inhibit the possible occurrence of further mutation of the adenoma cells induced by NNK.
  • Based on these lines of evidence, we propose that 8-methoxypsoralen inhibits the CYP2A5-mediated metabolic activation of NNK in the mouse lung, leading to the prevention of NNK-induced adenoma.
  • [MeSH-major] Adenoma. Carcinogens / toxicity. Cytochrome P-450 Enzyme Inhibitors. Lung Neoplasms / chemically induced. Lung Neoplasms / prevention & control. Methoxsalen / therapeutic use. Nitrosamines / toxicity

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  • [ErratumIn] Carcinogenesis. 2005 Dec;26(12):2214
  • (PMID = 15958517.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carcinogens; 0 / Coumarins; 0 / Cytochrome P-450 Enzyme Inhibitors; 0 / Escherichia coli Proteins; 0 / Nitrosamines; 0 / Proteins; 64091-91-4 / 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone; 9035-51-2 / Cytochrome P-450 Enzyme System; A4VZ22K1WT / coumarin; EC 1.- / Mixed Function Oxygenases; EC 1.14.- / Steroid Hydroxylases; EC 1.14.13.- / Cytochrome P-450 CYP2A6; EC 1.14.14.1 / Aryl Hydrocarbon Hydroxylases; EC 1.14.14.1 / Cyp2a4 protein, mouse; EC 1.14.14.1 / Cyp2a5 protein, mouse; EC 2.4.2.- / Pentosyltransferases; EC 2.4.2.22 / Gpt protein, E coli; U4VJ29L7BQ / Methoxsalen
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16. Panwar M, Samarth R, Kumar M, Yoon WJ, Kumar A: Inhibition of benzo(a)pyrene induced lung adenoma by panax ginseng extract, EFLA400, in Swiss albino mice. Biol Pharm Bull; 2005 Nov;28(11):2063-7
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  • [Title] Inhibition of benzo(a)pyrene induced lung adenoma by panax ginseng extract, EFLA400, in Swiss albino mice.
  • We used a 9-week medium term anticarcinogenicity test model of lung adenomas [Yun et al.1)].
  • Lung adenomas were induced by single subcutaneous injection in the subscapular region with 0.02 ml of benzo(a)pyrene (BP) (0.5 mg suspension in 1% aqueous gelatin) in newborn mice (less than 24 h old).
  • These genotoxicity end-points were compared with adenoma incidence at the same dose levels of BP and EFLA400.
  • The oral administration of EFLA400 (10 mg/kg body weight) showed significant reduction in number of adenomas and weight of the lungs induced by BP.
  • A significant reduction (p<0.001) in lung adenoma incidence in EFLA400-treated mice was observed as compared to the 68.3+/-2.96% lung adenoma incidence in BP-alone group.
  • [MeSH-major] Adenoma / chemically induced. Adenoma / prevention & control. Antineoplastic Agents, Phytogenic / pharmacology. Benzo(a)pyrene / antagonists & inhibitors. Benzo(a)pyrene / toxicity. Carcinogens / antagonists & inhibitors. Carcinogens / toxicity. Lung Neoplasms / chemically induced. Lung Neoplasms / prevention & control. Panax / chemistry

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  • (PMID = 16272690.001).
  • [ISSN] 0918-6158
  • [Journal-full-title] Biological & pharmaceutical bulletin
  • [ISO-abbreviation] Biol. Pharm. Bull.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antimutagenic Agents; 0 / Antineoplastic Agents, Phytogenic; 0 / Carcinogens; 0 / Plant Extracts; 3417WMA06D / Benzo(a)pyrene
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17. Goralczyk R, Bachmann H, Wertz K, Lenz B, Riss G, Buchwald Hunziker P, Greatrix B, Aebischer CP: beta-carotene-induced changes in RARbeta isoform mRNA expression patterns do not influence lung adenoma multiplicity in the NNK-initiated A/J mouse model. Nutr Cancer; 2006;54(2):252-62
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  • [Title] beta-carotene-induced changes in RARbeta isoform mRNA expression patterns do not influence lung adenoma multiplicity in the NNK-initiated A/J mouse model.
  • A number of epidemiological studies have reported associations of beta-carotene plasma levels or intake with decreased lung cancer risk.
  • However, intervention studies in smokers reported increased lung tumor rates after high long-term beta-carotene supplementation.
  • For insight into these conflicting results, we studied the influence of beta-carotene on tobacco smoke carcinogen-induced lung cancer development in the A/J-mouse using 4-(N-Methyl-N-nitro samino)-1-(3-pyridyl)-1-butanone (NNK) as the initiator and lung adenoma multiplicity as the functional endpoint.
  • Gene regulation of the putative tumor suppressor RARbeta in mouse lung was analyzed by quantitative real-time reverse transcriptase-polymerase chain reaction (RT-PCR) for its relevance in predicting the endpoint of lung cancer.
  • Despite high lung beta-carotene concentrations of up to 6 micromol/kg, tumor multiplicity was not significantly affected by the beta-carotene treatment, either in carcinogen-initiated or non-initiated mice, and was unrelated to beta-carotene dose and the time point of treatment during cancer formation.
  • All RARbeta isoforms were significantly suppressed in the lungs of NNK- and NNK plus high dose beta-carotene-treated animals.
  • In summary, we found no effect of beta-carotene on tumor formation in the NNK-initiated A/J-mouse lung cancer model with respect to dose or time point of treatment. beta-Carotene-induced changes in RARbeta isoform gene expression levels were not predictive for the number of lung tumors but were indicative of intact beta-carotene metabolism and persistent sensitivity to retinoic acid in the mice.
  • Down-regulation of RARbeta in NNK-induced adenoma-bearing lungs was similar to that observed in human lung cancer and further confirms the A/J-mouse as a valuable model for lung carcinogenesis.
  • [MeSH-major] Adenoma / prevention & control. Lung Neoplasms / prevention & control. RNA, Messenger / metabolism. Smoking / adverse effects. Vitamins / pharmacology. beta Carotene
  • [MeSH-minor] Animals. Carcinogens / toxicity. Dietary Supplements. Disease Models, Animal. Dose-Response Relationship, Drug. Humans. Lung / drug effects. Lung / pathology. Male. Mice. Nitrosamines / toxicity. Protein Isoforms. Random Allocation. Receptors, Retinoic Acid / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16898870.001).
  • [ISSN] 0163-5581
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Nitrosamines; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / Receptors, Retinoic Acid; 0 / Vitamins; 01YAE03M7J / beta Carotene; 64091-91-4 / 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone
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18. Kaspareit J, Friderichs-Gromoll S, Buse E, Habermann G: Spontaneous neoplasms observed in cynomolgus monkeys (Macaca fascicularis) during a 15-year period. Exp Toxicol Pathol; 2007 Nov;59(3-4):163-9

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  • Most of the tumors (22) in the cynomolgus monkeys were seen in endocrine organs (adrenal cortical adenoma, adrenal hemangioma, C-cell carcinoma, follicular adenoma), respiratory system (nasal cavity adenoma, pulmonary squamous cell carcinoma, bronchio-alveolar carcinoma, bronchiolar papilloma, chondromatous hamartoma) and female genital system (uterine polyp, uterine adenoma, uterine leiomyoma and teratoma of the ovary).

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  • (PMID = 17869495.001).
  • [ISSN] 0940-2993
  • [Journal-full-title] Experimental and toxicologic pathology : official journal of the Gesellschaft für Toxikologische Pathologie
  • [ISO-abbreviation] Exp. Toxicol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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19. Okubo C, Morishita Y, Minami Y, Ishiyama T, Kano J, Iijima T, Noguchi M: Phenotypic characteristics of mouse lung adenoma induced by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone. Mol Carcinog; 2005 Feb;42(2):121-6
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  • [Title] Phenotypic characteristics of mouse lung adenoma induced by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone.
  • The expression profile of adenoma induced by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in A/J mice was compared with that of normal lung tissue by suppression subtractive hybridization (SSH).
  • The mRNAs of surfactant-associated protein A (SP-A) and lysozyme showed characteristically higher transcription in the adenoma tissue than in normal lung.
  • In normal lung, alveolar type II pneumocytes were positive for both SP-A and lysozyme, indicating that tumor cells retained the phenotypic characteristics of the murine alveolar type II pneumocytes.
  • Thus, the present results indicate that the phenotype of NNK-induced A/J mouse adenoma differs from that of AAH, which is thought to be a preinvasive lesion of human adenocarcinoma.
  • [MeSH-major] Adenoma / chemically induced. Adenoma / pathology. Carcinogens. Nitrosamines
  • [MeSH-minor] Animals. Apoproteins / metabolism. DNA, Complementary / metabolism. DNA-Directed RNA Polymerases / metabolism. Female. In Situ Hybridization. Lasers. Lung / cytology. Lung / pathology. Mice. Microscopy, Electron, Transmission. Muramidase / chemistry. Muramidase / metabolism. Phenotype. Promoter Regions, Genetic. Pulmonary Surfactant-Associated Protein A / metabolism. RNA / metabolism. RNA, Messenger / metabolism. Surface-Active Agents / metabolism. Time Factors. Viral Proteins

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  • [Copyright] Copyright 2004 Wiley-Liss, Inc.
  • (PMID = 15584020.001).
  • [ISSN] 0899-1987
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoproteins; 0 / Carcinogens; 0 / DNA, Complementary; 0 / Nitrosamines; 0 / Pulmonary Surfactant-Associated Protein A; 0 / RNA, Messenger; 0 / Surface-Active Agents; 0 / Viral Proteins; 63231-63-0 / RNA; 64091-91-4 / 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone; EC 2.7.7.- / bacteriophage T7 RNA polymerase; EC 2.7.7.6 / DNA-Directed RNA Polymerases; EC 3.2.1.17 / Muramidase
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20. National Toxicology Program: NTP report on the toxicology studies of dichloroacetic acid (CAS No. 79-43-6) in genetically modified (FVB Tg.AC hemizygous) mice (dermal and drinking water studies) and carcinogenicity studies of dichloroacetic acid in genetically modified [B6.129-Trp53(tm1Brd) (N5) haploinsufficient] mice (drinking water studies). Natl Toxicol Program Genet Modif Model Rep; 2007 Apr;(11):1-168
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  • There was a modest increase in pulmonary adenomas at 39 weeks that may have been related to the dichloroacetic acid exposure in males and females exposed to 125 or 500 mg/kg.
  • The incidence of pulmonary adenoma was increased in the male mice exposed to 1,000 mg/L dichloroacetic acid for 41 weeks.
  • Two pulmonary adenomas were found in the 2,000 mg/L females at 41 weeks.
  • At 26 weeks, a pulmonary carcinoma was found in one 1,000 mg/L male, one 500 mg/L female, and one 2,000 mg/L female.
  • Under the conditions of these drinking water studies, there was an increase in the incidence of alveolar/bronchiolar adenoma in male Tg.AC hemizygous mice exposed to 1,000 mg/L for 41 weeks.
  • The marginally increased incidences of pulmonary adenomas and/or carcinomas compared to the unexposed groups found in both the dermal and drinking water studies at 39 or 41 weeks were considered to be related to dichloroacetic acid exposure.
  • [MeSH-major] Adenoma / chemically induced. Carcinoma / chemically induced. Dichloroacetic Acid / toxicity. Lung Neoplasms / chemically induced. Papilloma / chemically induced. Skin Neoplasms / chemically induced. Water Pollutants, Chemical / toxicity

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  • (PMID = 18784768.001).
  • [ISSN] 1556-5246
  • [Journal-full-title] National Toxicology Program genetically modified model report
  • [ISO-abbreviation] Natl Toxicol Program Genet Modif Model Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53; 0 / Water Pollutants, Chemical; 9LSH52S3LQ / Dichloroacetic Acid
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21. Carney JA: Carney triad: a syndrome featuring paraganglionic, adrenocortical, and possibly other endocrine tumors. J Clin Endocrinol Metab; 2009 Oct;94(10):3656-62
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  • One also had an adrenal cortical adenoma and the other pulmonary chondroma.
  • Five additional patients with gastric stromal tumor, paraganglioma, and pulmonary chondroma were found, and all were young women.
  • The gastric lesion was usually the presenting tumor (75%), followed by the lung lesion (15%) and the paraganglionic tumor (10%).
  • Twenty percent of the patients had adrenocortical adenoma(s), and 10% had esophageal leiomyoma(s).
  • The pulmonary tumors were asymptomatic and benign.
  • FOLLOW-UP: At follow-up, 80% of the patients were alive, two thirds with pulmonary chondroma, 25% with metastatic or residual gastric stromal tumor, and 5% with primary or metastatic paraganglioma.
  • CONCLUSION: The Carney triad is a chronic, persistent, indolent but sometimes fatal disorder of unknown etiology.
  • [MeSH-major] Adenoma. Adrenal Cortex Neoplasms. Chondroma. Esophageal Neoplasms. Leiomyoma. Lung Neoplasms. Multiple Endocrine Neoplasia. Neoplastic Syndromes, Hereditary / pathology. Paraganglioma

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  • (PMID = 19723753.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 23
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22. Molino C, Fabbian F, Russo G, Cantelli S, Bortot A, Galdi A, Catizone L: [MEN type 1 and chronic renal failure: a rarely reported association]. G Ital Nefrol; 2007 Jan-Feb;24(1):79-82
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  • CASE: A 70-year-old Caucasian female patient had a history of primitive hyperparathyroidism, prolactinoma, glucagonoma, adrenal adenoma and pulmonary neuroendocrine neoplasia.

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  • (PMID = 17342698.001).
  • [ISSN] 0393-5590
  • [Journal-full-title] Giornale italiano di nefrologia : organo ufficiale della Società italiana di nefrologia
  • [ISO-abbreviation] G Ital Nefrol
  • [Language] ita
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Italy
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23. Gentschev I, Fensterle J, Schmidt A, Potapenko T, Troppmair J, Goebel W, Rapp UR: Use of a recombinant Salmonella enterica serovar Typhimurium strain expressing C-Raf for protection against C-Raf induced lung adenoma in mice. BMC Cancer; 2005 Feb 9;5:15
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  • [Title] Use of a recombinant Salmonella enterica serovar Typhimurium strain expressing C-Raf for protection against C-Raf induced lung adenoma in mice.
  • In this study we analyzed the functionality of a new live C-Raf vaccine based on an attenuated Salmonella enterica serovar Typhimurium aroA strain in two Raf dependent lung tumor mouse models.
  • The effect of the immunization with this recombinant C-Raf strain on wild-type C57BL/6 or lung tumor bearing transgenic BxB mice was analyzed using western blot and FACS analysis as well as specific tumor growth assays.
  • Most importantly, the vaccine strain significantly reduced tumor growth in two transgenic mouse models of Raf oncogene-induced lung adenomas.
  • [MeSH-major] Adenoma / prevention & control. Cancer Vaccines / immunology. Escherichia coli Proteins / immunology. Hemolysin Proteins / immunology. Lung Neoplasms / prevention & control. Proto-Oncogene Proteins c-raf / immunology. Salmonella typhimurium / immunology


24. Halldorsson A, Dissanaike S, Kaye KS: Alveolar adenoma of the lung: a clinicopathological description of a case of this very unusual tumour. J Clin Pathol; 2005 Nov;58(11):1211-4
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  • [Title] Alveolar adenoma of the lung: a clinicopathological description of a case of this very unusual tumour.
  • Alveolar adenomas are extremely rare, and are probably benign lung tumours of unknown histogenesis.
  • This report describes a case of alveolar adenoma in a 43 year old white man, who presented with pleuritic chest pain.
  • A chest x ray and computerised tomography scan demonstrated a solitary left lower lobe lung nodule.
  • Histologically, the lesion was well demarcated, dominated by large and small cysts with no normal lung parenchyma.
  • [MeSH-major] Adenoma / pathology. Lung Neoplasms / pathology

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  • [Cites] Int J Surg Pathol. 2004 Apr;12(2):155-9 [15173924.001]
  • [Cites] Pathologe. 1990 Jan;11(1):48-54 [2179944.001]
  • [Cites] Pathologe. 1996 Mar;17(2):150-3 [8650145.001]
  • [Cites] Cancer Genet Cytogenet. 1996 Jul 1;89(1):34-7 [8689607.001]
  • [Cites] Virchows Arch. 1996 Oct;429(2-3):101-8 [8917711.001]
  • [Cites] Virchows Arch. 1997 Feb;430(2):181-4 [9083522.001]
  • [Cites] Pol J Pathol. 2003;54(2):147-52 [14575424.001]
  • [Cites] Cesk Patol. 1997 May;33(2):49-52 [9340215.001]
  • [Cites] Hum Pathol. 1999 Feb;30(2):158-67 [10029443.001]
  • [Cites] Hum Pathol. 1986 Oct;17(10):1066-71 [3759064.001]
  • [Cites] Ann Pathol. 1999 Sep;19(4):325-8 [10544770.001]
  • [Cites] J Thorac Imaging. 2002 Apr;17(2):163-6 [11956369.001]
  • [Cites] Rontgenpraxis. 1997 Feb;50(2):29-30 [9173555.001]
  • (PMID = 16254114.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1770767
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25. Sak SD, Koseoglu RD, Demirag F, Akbulut H, Gungor A: Alveolar adenoma of the lung. Immunohistochemical and flow cytometric characteristics of two new cases and a review of the literature. APMIS; 2007 Dec;115(12):1443-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alveolar adenoma of the lung. Immunohistochemical and flow cytometric characteristics of two new cases and a review of the literature.
  • Alveolar adenoma is a rare and benign tumour of the lung that usually presents in asymptomatic patients as a coin lesion on chest radiography.
  • Alveolar adenoma has a characteristic multicystic histology and often resembles the normal lung parenchyma.
  • Immunohistochemical analysis may aid in the characterization of alveolar adenoma and discriminate this condition from other types of benign lesions of the lung.
  • An indolent clinical progression and absence of recurrence and metastasis after complete resection are the most important characteristics indicative of the benign nature of alveolar adenoma.
  • Few studies have been conducted at the molecular level, such as by flow cytometry, with the objective of characterizing the biological nature of alveolar adenoma.
  • Differential diagnoses include sclerosing hemangioma, papillary adenoma, lymphangioma, atypical adenomatous hyperplasia and bronchioloalveolar carcinoma.
  • [MeSH-major] Adenoma / pathology. Pulmonary Alveoli / pathology. Solitary Pulmonary Nodule / pathology
  • [MeSH-minor] Biomarkers, Tumor / analysis. Cell Proliferation. Flow Cytometry. Humans. Immunohistochemistry. Lung Neoplasms / genetics. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Male. Middle Aged. Tumor Suppressor Protein p53 / biosynthesis

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  • (PMID = 18184418.001).
  • [ISSN] 0903-4641
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Tumor Suppressor Protein p53
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26. Wang M, Futamura M, Wang Y, You M: Pas1c1 is a candidate for the mouse pulmonary adenoma susceptibility 1 locus. Oncogene; 2005 Mar 10;24(11):1958-63
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  • [Title] Pas1c1 is a candidate for the mouse pulmonary adenoma susceptibility 1 locus.
  • Similar to Pas1c1-Vb, the newly identified transcripts were only expressed in mouse lung tissues from strains carrying the Pas1-susceptible (Pas1/s) allele.
  • [MeSH-major] Adenoma / genetics. Genetic Predisposition to Disease. Lung Neoplasms / genetics. Tumor Suppressor Proteins / genetics


27. Weissferdt A, Langman G: An intracapsular carcinoma ex pleomorphic adenoma with lung metastases composed exclusively of benign elements: histological evidence of a continuum between metastasizing pleomorphic adenoma and carcinoma ex pleomorphic adenoma. Pathol Res Pract; 2010 Jul 15;206(7):480-3
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  • [Title] An intracapsular carcinoma ex pleomorphic adenoma with lung metastases composed exclusively of benign elements: histological evidence of a continuum between metastasizing pleomorphic adenoma and carcinoma ex pleomorphic adenoma.
  • Malignant mixed tumors of the salivary glands, encompassing carcinoma ex pleomorphic adenoma (ca ex PA), carcinosarcoma and metastasizing pleomorphic adenoma (mPA), are rare neoplasms.
  • Ca ex PA arises in a pre-existing pleomorphic adenoma (PA).
  • We describe the case of a 62-year-old female with an intracapsular ca ex PA of the buccal mucosa with subsequent metastases to the lung.
  • [MeSH-major] Adenoma, Pleomorphic / pathology. Lung Neoplasms / secondary. Mouth Mucosa / pathology. Salivary Gland Neoplasms / pathology

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  • [Copyright] Copyright 2009 Elsevier GmbH. All rights reserved.
  • (PMID = 19665316.001).
  • [ISSN] 1618-0631
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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28. Sharma S, Gao P, Steele VE: The chemopreventive efficacy of inhaled oltipraz particulates in the B[a]P-induced A/J mouse lung adenoma model. Carcinogenesis; 2006 Aug;27(8):1721-7
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  • [Title] The chemopreventive efficacy of inhaled oltipraz particulates in the B[a]P-induced A/J mouse lung adenoma model.
  • This study explored the efficacy of oltipraz, a dithiolthione to prevent lung cancer by delivering it directly to the lung as inhaled particulates to obtain maximum efficacy with no toxicity.
  • Two exposure regimens were used to compare the efficacies of early (Regimen-A) versus late (Regimen-B) intervention in prevention of lung tumorigenesis in A/J mice.
  • The spontaneous tumors were few in untreated A/J mice (0.7 tumors/lung), whereas there was an average of 16.5 tumors per lung in the B[a]P group (20-fold induction).
  • Evaluation of lung tumor multiplicity following exposure to oltipraz showed that oltipraz inhibited the tumor development in a dose-dependent manner (10-100 mg/m(3)) with inhibition ranging from 37 to 53% in Regimen A and 51% in Regimen B, when compared with the B[a]P group.
  • The data from this study show that oltipraz is an effective agent for lung cancer prevention, when it is delivered directly to the target tissue as aerosolized particulates.
  • [MeSH-major] Adenoma / prevention & control. Anticarcinogenic Agents / therapeutic use. Benzo(a)pyrene / toxicity. Lung Neoplasms / prevention & control. Pyrazines / therapeutic use

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  • (PMID = 16632869.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CN / N01-CN-25112
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Pyrazines; 3417WMA06D / Benzo(a)pyrene; 6N510JUL1Y / oltipraz
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29. Fitchett J, Luckraz H, Gibbs A, O'Keefe P: A rare case of primary pleomorphic adenoma in main bronchus. Ann Thorac Surg; 2008 Sep;86(3):1025-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A rare case of primary pleomorphic adenoma in main bronchus.
  • Primary pleomorphic adenoma of the lung is a rare occurrence.
  • We describe a case of a primary pleomorphic adenoma arising from the origin of the right main bronchus and include our management strategy.
  • [MeSH-major] Adenoma, Pleomorphic / surgery. Bronchial Neoplasms / surgery

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  • (PMID = 18721613.001).
  • [ISSN] 1552-6259
  • [Journal-full-title] The Annals of thoracic surgery
  • [ISO-abbreviation] Ann. Thorac. Surg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
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30. Müller-Brüsselbach S, Ebrahimsade S, Jäkel J, Eckhardt J, Rapp UR, Peters JM, Moll R, Müller R: Growth of transgenic RAF-induced lung adenomas is increased in mice with a disrupted PPARbeta/delta gene. Int J Oncol; 2007 Sep;31(3):607-11
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  • [Title] Growth of transgenic RAF-induced lung adenomas is increased in mice with a disrupted PPARbeta/delta gene.
  • In the present study, we have addressed the role of PPARbeta and PPARgamma in lung tumorigenesis in a transgenic mouse model of RAF-induced lung adenoma using two different strategies: i) crossing with PPARbeta null mice, and ii) chronic treatment with the PPARgamma agonist rosiglitazone.
  • These observations indicate i) that RAF-induced lung tumorigenesis is attenuated in mice with a disrupted Pparb gene, and ii) that chronic PPARgamma activation does not affect lung adenoma growth.
  • [MeSH-major] Adenoma / genetics. Gene Expression Regulation, Neoplastic. Lung Neoplasms / genetics. PPAR delta / genetics. PPAR-beta / genetics. Proto-Oncogene Proteins c-raf / genetics

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  • (PMID = 17671688.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Hypoglycemic Agents; 0 / PPAR delta; 0 / PPAR-beta; 0 / Thiazolidinediones; 0 / Transcription Factors; 05V02F2KDG / rosiglitazone; EC 2.7.11.1 / Proto-Oncogene Proteins c-raf
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31. Yan Y, Wang Y, Tan Q, Lubet RA, You M: Efficacy of deguelin and silibinin on benzo(a)pyrene-induced lung tumorigenesis in A/J mice. Neoplasia; 2005 Dec;7(12):1053-7
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  • [Title] Efficacy of deguelin and silibinin on benzo(a)pyrene-induced lung tumorigenesis in A/J mice.
  • We evaluated deguelin and silibinin in A/J mice treated with the tobacco-specific carcinogen benzo(a)pyrene (BP) for their ability to inhibit pulmonary adenoma formation and growth.
  • The result indicates that deguelin significantly inhibits pulmonary adenoma formation and growth in A/J mice.
  • Finding new and effective agents that can prevent lung cancer is urgently needed because cancer of the lungs remains the principal cause of cancer deaths in the United States and because effective chemoprevention of this cancer type remains elusive.
  • Thus, deguelin appears to be a promising new preventive agent for lung cancer and may be considered for further studies in other animal models and in clinical trials.

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  • [Cites] Clin Chest Med. 1993 Mar;14(1):1-15 [8462243.001]
  • [Cites] Cancer Res. 1992 May 1;52(9 Suppl):2670s-2676s [1562998.001]
  • [Cites] Cancer Res. 1994 Apr 1;54(7 Suppl):2015s-2024s [8137331.001]
  • [Cites] Carcinogenesis. 1997 Mar;18(3):575-86 [9067559.001]
  • [Cites] J Natl Cancer Inst. 1997 Apr 16;89(8):556-66 [9106644.001]
  • [Cites] J Natl Cancer Inst. 1997 Jun 4;89(11):747-9 [9182965.001]
  • [Cites] Cancer Res. 1997 Aug 15;57(16):3424-8 [9270008.001]
  • [Cites] Science. 1997 Nov 7;278(5340):1073-7 [9353183.001]
  • [Cites] Carcinogenesis. 1997 Nov;18(11):2035-42 [9395199.001]
  • [Cites] J Cell Biochem Suppl. 1997;28-29:49-63 [9589349.001]
  • [Cites] Hematol Oncol Clin North Am. 1998 Oct;12(5):1037-53 [9888020.001]
  • [Cites] Br Med J. 1952 Dec 13;2(4797):1271-86 [12997741.001]
  • [Cites] Clin Cancer Res. 2004 Dec 15;10(24):8641-7 [15623648.001]
  • [Cites] Curr Top Med Chem. 2005;5(2):109-25 [15853641.001]
  • [Cites] JAMA. 2005 Sep 28;294(12):1505-10 [16189363.001]
  • [Cites] Cancer Res. 2000 Feb 15;60(4):901-7 [10706103.001]
  • [Cites] Cancer Chemother Pharmacol. 2001 Mar;47(3):263-8 [11320671.001]
  • [Cites] Carcinogenesis. 2002 Mar;23(3):499-510 [11895866.001]
  • [Cites] Cancer Res. 2002 Jun 1;62(11):3063-9 [12036915.001]
  • [Cites] Int J Cancer. 2002 Oct 10;101(5):461-8 [12216075.001]
  • [Cites] Eur J Cancer. 2002 Dec;38(18):2446-54 [12460790.001]
  • [Cites] Int J Cancer. 2003 Mar 10;104(1):7-11 [12532413.001]
  • [Cites] J Natl Cancer Inst. 2003 Feb 19;95(4):252-3 [12591974.001]
  • [Cites] J Natl Cancer Inst. 2003 Feb 19;95(4):291-302 [12591985.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2003 Sep;12(9):933-9 [14504208.001]
  • [Cites] Clin Cancer Res. 2004 Feb 1;10(3):1074-9 [14871987.001]
  • [Cites] Biochem Pharmacol. 2004 Sep 15;68(6):1119-24 [15313408.001]
  • [Cites] N Engl J Med. 1984 Mar 8;310(10):633-8 [6363924.001]
  • [Cites] N Engl J Med. 1985 Aug 22;313(8):491-8 [3894970.001]
  • [Cites] J Endocrinol. 1990 Feb;124(2):341-5 [2155989.001]
  • [Cites] J Natl Cancer Inst. 1991 Aug 21;83(16):1142-8 [1886147.001]
  • [Cites] Acta Physiol Hung. 1991;78(1):3-9 [1763650.001]
  • [Cites] Chest. 1993 Apr;103(4 Suppl):449S-456S [8462339.001]
  • (PMID = 16354587.001).
  • [ISSN] 1522-8002
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA058554; United States / NCI NIH HHS / CA / CA058554; United States / NCI NIH HHS / CA / CA9696401
  • [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 / Silymarin; 03L9OT429T / Rotenone; 3417WMA06D / Benzo(a)pyrene; 4RKY41TBTF / silybin; K5Z93K66IE / deguelin
  • [Other-IDs] NLM/ PMC1501176
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32. Shaik AA, Hermanson DL, Xing C: Identification of methysticin as a potent and non-toxic NF-kappaB inhibitor from kava, potentially responsible for kava's chemopreventive activity. Bioorg Med Chem Lett; 2009 Oct 1;19(19):5732-6
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  • The results of our recent chemopreventive study demonstrate that kava, a beverage in the South Pacific Islands, suppresses NF-kappaB activation in lung adenoma tissues, potentially a mechanism responsible for kava's chemopreventive activity.

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  • [Cites] Chem Biol. 2001 Aug;8(8):759-66 [11514225.001]
  • [Cites] Hawaii Med J. 2000 Nov;59(11):420-2 [11149250.001]
  • [Cites] Cochrane Database Syst Rev. 2003;(1):CD003383 [12535473.001]
  • [Cites] Phytomedicine. 2003;10 Suppl 4:68-73 [12807347.001]
  • [Cites] Chem Res Toxicol. 2003 Jun;16(6):733-40 [12807356.001]
  • [Cites] Phytomedicine. 2003 May;10(4):309-17 [12809361.001]
  • [Cites] Toxicol Lett. 2004 Apr 15;150(1):85-96 [15068826.001]
  • [Cites] Planta Med. 2004 Mar;70(3):193-6 [15114493.001]
  • [Cites] Org Lett. 2004 Jul 8;6(14):2317-20 [15228268.001]
  • [Cites] J Mol Med (Berl). 2004 Jul;82(7):434-48 [15175863.001]
  • [Cites] J Chromatogr B Analyt Technol Biomed Life Sci. 2004 Dec 5;812(1-2):203-14 [15556499.001]
  • [Cites] Cancer Res. 2005 Apr 15;65(8):3479-86 [15833884.001]
  • [Cites] J Chromatogr A. 2005 Mar 4;1067(1-2):107-14 [15844515.001]
  • [Cites] Biochem Pharmacol. 2006 Apr 14;71(8):1206-18 [16464438.001]
  • [Cites] J Agric Food Chem. 2006 Apr 19;54(8):3157-62 [16608246.001]
  • [Cites] Immunol Rev. 2006 Apr;210:171-86 [16623771.001]
  • [Cites] Ann N Y Acad Sci. 2006 Aug;1072:114-22 [17057194.001]
  • [Cites] Oncogene. 2006 Oct 30;25(51):6887-99 [17072334.001]
  • [Cites] J Med Chem. 2006 Nov 30;49(24):7182-9 [17125270.001]
  • [Cites] Exp Toxicol Pathol. 2007 Jan;58(4):223-36 [17059882.001]
  • [Cites] J Med Chem. 2006 Dec 28;49(26):7731-9 [17181155.001]
  • [Cites] Br J Clin Pharmacol. 2007 Oct;64(4):415-7 [17555466.001]
  • [Cites] Food Chem Toxicol. 2008 Jan;46(1):168-74 [17822821.001]
  • [Cites] Exp Biol Med (Maywood). 2008 Jan;233(1):21-31 [18156302.001]
  • [Cites] J Nat Med. 2008 Apr;62(2):188-94 [18404321.001]
  • [Cites] J Agric Food Chem. 2008 May 28;56(10):3876-83 [18433100.001]
  • [Cites] Eur J Gastroenterol Hepatol. 2008 Dec;20(12):1182-93 [18989142.001]
  • [Cites] Food Chem Toxicol. 2008 Dec;46(12):3732-8 [18930106.001]
  • [Cites] Cancer Prev Res (Phila). 2008 Nov;1(6):430-8 [19138990.001]
  • [Cites] Cancer Prev Res (Phila). 2008 Nov;1(6):439-51 [19138991.001]
  • [Cites] Oncogene. 1999 Nov 22;18(49):6896-909 [10602465.001]
  • [Cites] J Immunol. 2000 Jun 1;164(11):5815-25 [10820260.001]
  • [Cites] J Immunol. 2000 Jun 15;164(12):6509-19 [10843709.001]
  • [Cites] J Biol Chem. 2000 Nov 17;275(46):36062-6 [10967126.001]
  • [Cites] Phytochemistry. 2002 Feb;59(4):429-33 [11830162.001]
  • (PMID = 19716299.001).
  • [ISSN] 1464-3405
  • [Journal-full-title] Bioorganic & medicinal chemistry letters
  • [ISO-abbreviation] Bioorg. Med. Chem. Lett.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R03 CA125844-02; United States / NCI NIH HHS / CA / CA125844-02; United States / NCI NIH HHS / CA / R03CA125844; United States / NCI NIH HHS / CA / R03 CA125844; United States / NCI NIH HHS / CA / R01 CA142649
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Antineoplastic Agents, Phytogenic; 0 / NF-kappa B; 0 / Pyrans; M832AIJ6HX / methysticin
  • [Other-IDs] NLM/ NIHMS137399; NLM/ PMC2756981
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33. Galbiati F, Pettinicchio A, Dragani TA, Manenti G: Allelic effects of mouse Pas1 candidate genes in human lung cancer cell lines. Cancer Lett; 2006 Dec 8;244(2):176-81
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  • [Title] Allelic effects of mouse Pas1 candidate genes in human lung cancer cell lines.
  • Four of the six genes constituting the mouse Pulmonary adenoma susceptibility 1 (Pas1) locus haplotype carry amino acid variants: Lrmp, Casc1, Ghiso, and Lmna-rs1.
  • In vitro colony formation assay of human lung cancer cell lines A549 and NCI-H520 transfected with the allelic variants of the four genes revealed allele-specific modulations of colony numbers by Lmna-rs1 and Casc1, but not by Lrmp or Ghiso.
  • [MeSH-major] Adenoma / genetics. Alleles. Genetic Predisposition to Disease. Lung Neoplasms / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Animals. Apoptosis. Carcinoma, Non-Small-Cell Lung / genetics. Cells, Cultured. Colony-Forming Units Assay. Gene Expression Regulation, Neoplastic. Humans. Kidney / metabolism. Male. Membrane Proteins / genetics. Mice. Mice, Inbred A. Mice, Inbred C57BL. Microscopy, Fluorescence. Poly(ADP-ribose) Polymerases / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Transfection

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  • (PMID = 16458428.001).
  • [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 / Las1 protein, mouse; 0 / Lmna-rs1 protein, mouse; 0 / Lrmp protein, mouse; 0 / Membrane Proteins; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases
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34. Pan M, Chu M, Sun Y, Song X, Zhu J: [Preparation and characterization of quantum dots-peptides bioconjugations and their specificity related to recognizing tumor cells]. Sheng Wu Yi Xue Gong Cheng Xue Za Zhi; 2007 Jun;24(3):577-81
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  • The QDs-peptides conjugates could specifically recognize the lung adenoma cancer cells (SPCA-1), but did not recognize promyelocytic leukemia cells (HL-60).
  • [MeSH-major] Adenocarcinoma / pathology. Lung Neoplasms / pathology. Peptides / chemistry. Photochemistry / methods. Quantum Dots

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  • (PMID = 17713265.001).
  • [ISSN] 1001-5515
  • [Journal-full-title] Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi
  • [ISO-abbreviation] Sheng Wu Yi Xue Gong Cheng Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / LyP-1 protein, mouse; 0 / Oligopeptides; 0 / Peptides; 0 / Peptides, Cyclic; 99896-85-2 / arginyl-glycyl-aspartic acid
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35. Zaffaroni D, Spinola M, Galvan A, Falvella FS, Pazzaglia S, Saran A, Mancuso MT, Galbiati F, Pignatiello C, Cabrera W, Ibanez O, Manenti G, Dragani TA: Met proto-oncogene juxtamembrane rare variations in mouse and humans: differential effects of Arg and Cys alleles on mouse lung tumorigenesis. Oncogene; 2005 Feb 3;24(6):1084-90
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  • [Title] Met proto-oncogene juxtamembrane rare variations in mouse and humans: differential effects of Arg and Cys alleles on mouse lung tumorigenesis.
  • Analysis of seven candidate genes mapping in the 1-Mb region of the mouse pulmonary adenoma resistance 4 (Par4) locus revealed a single amino-acid change, consisting in a nonconservative Arg968Cys variation in the juxtamembrane domain of the Met proto-oncogene-encoded protein.
  • Analysis of genomic DNA of 126 lung adenocarcinoma patients for the Met juxtamembrane domain revealed the same Arg/Cys variation at the mouse homologous position in one patient; two other patients carried additional variants in the same domain, suggesting a potential role for rare MET juxtamembrane variants in human lung cancer.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / physiopathology. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / physiopathology. Cell Transformation, Neoplastic. Genetic Predisposition to Disease. Lung Neoplasms / genetics. Lung Neoplasms / physiopathology. Proto-Oncogene Proteins / genetics. Receptors, Growth Factor / genetics

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  • (PMID = 15592501.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AY439333/ AY544984/ AY551821/ AY551822/ AY558815/ AY558816/ AY558817/ AY558818/ AY558819/ AY558820
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / Receptors, Growth Factor; 0 / Receptors, Thrombin; 0 / protease-activated receptor 4; 94ZLA3W45F / Arginine; EC 2.7.10.1 / MET protein, human; EC 2.7.10.1 / Proto-Oncogene Proteins c-met; K848JZ4886 / Cysteine
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36. To MD, Perez-Losada J, Mao JH, Hsu J, Jacks T, Balmain A: A functional switch from lung cancer resistance to susceptibility at the Pas1 locus in Kras2LA2 mice. Nat Genet; 2006 Aug;38(8):926-30
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  • [Title] A functional switch from lung cancer resistance to susceptibility at the Pas1 locus in Kras2LA2 mice.
  • Pulmonary adenoma susceptibility 1 (Pas1) is the major mouse lung cancer susceptibility locus on chromosome 6 (ref. 1).
  • Kras2 is a common target of somatic mutation in chemically induced mouse lung tumors and is a candidate Pas1 gene. M. spretus mice (SPRET/Ei) carry a Pas1 resistance haplotype for chemically induced lung tumors.
  • We propose that the Pas1 modifier effect is due to Kras2, and that a sensitive balance between the expression levels of wild-type and mutant alleles determines lung tumor susceptibility.

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  • [CommentIn] Nat Genet. 2006 Aug;38(8):864-5 [16874325.001]
  • (PMID = 16823377.001).
  • [ISSN] 1061-4036
  • [Journal-full-title] Nature genetics
  • [ISO-abbreviation] Nat. Genet.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01CA84306; United States / NCI NIH HHS / CA / R01 CA111834-02; United States / NCI NIH HHS / CA / U01CA84244; United States / NCI NIH HHS / CA / R01 CA111834-01A2; United States / NCI NIH HHS / CA / U01 CA084306; United States / NCI NIH HHS / CA / U01 CA141455; United States / NCI NIH HHS / CA / R01 CA111834-03; United States / NCI NIH HHS / CA / R01 CA111834; United States / NCI NIH HHS / CA / R01 CA111834-04; United States / NCI NIH HHS / CA / U01 CA084244
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 3IN71E75Z5 / Urethane; EC 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
  • [Other-IDs] NLM/ NIHMS174190; NLM/ PMC4461000
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37. Yan Y, Wang Y, Tan Q, Hara Y, Yun TK, Lubet RA, You M: Efficacy of polyphenon E, red ginseng, and rapamycin on benzo(a)pyrene-induced lung tumorigenesis in A/J mice. Neoplasia; 2006 Jan;8(1):52-8
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  • [Title] Efficacy of polyphenon E, red ginseng, and rapamycin on benzo(a)pyrene-induced lung tumorigenesis in A/J mice.
  • The objective of this investigation was to determine the efficacy of several novel agents in preventing lung tumorigenesis in mice.
  • We evaluated polyphenon E, red ginseng, and rapamycin in A/J mice treated with the tobacco-specific carcinogen benzo(a)pyrene for their ability to inhibit pulmonary adenoma formation and growth.
  • This result provided key evidence in support of a phase II clinical chemoprevention trial of lung cancer.
  • The mammalian target of rapamycin inhibitor rapamycin showed significant efficacy against lung tumor growth in the tumor progression protocol and reduced tumor load by 84%.
  • The results of these investigations demonstrate that polyphenon E, red ginseng, and rapamycin significantly inhibit pulmonary adenoma formation and growth in A/J mice.

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  • [Cites] Lancet Oncol. 2001 Jan;2(1):49-55 [11905620.001]
  • [Cites] Eur J Biochem. 2002 Nov;269(22):5338-49 [12423332.001]
  • [Cites] Mutat Res. 2003 Feb-Mar;523-524:63-74 [12628504.001]
  • [Cites] Clin Cancer Res. 2003 Aug 15;9(9):3312-9 [12960117.001]
  • [Cites] Eur J Cancer Prev. 2003 Oct;12(5):383-90 [14512803.001]
  • [Cites] Cancer Res. 2004 Jan 15;64(2):446-51 [14744754.001]
  • [Cites] Nature. 2004 Mar 18;428(6980):332-7 [15029198.001]
  • [Cites] Nat Rev Cancer. 2004 May;4(5):335-48 [15122205.001]
  • [Cites] Nutr Cancer. 2004;48(1):44-53 [15203377.001]
  • [Cites] J Clin Oncol. 2004 Jul 15;22(14):2954-63 [15254063.001]
  • [Cites] Clin Cancer Res. 2004 Sep 15;10(18 Pt 2):6382S-7S [15448035.001]
  • [Cites] Cancer Detect Prev. 1983;6(6):515-25 [6420059.001]
  • [Cites] N Engl J Med. 1985 Aug 22;313(8):491-8 [3894970.001]
  • [Cites] Basic Life Sci. 1986;39:131-42 [3533039.001]
  • [Cites] Int J Epidemiol. 1990 Dec;19(4):871-6 [2084014.001]
  • [Cites] J Natl Cancer Inst. 1991 Aug 21;83(16):1142-8 [1886147.001]
  • [Cites] J Toxicol Sci. 1991 Feb;16 Suppl 1:53-62 [1920544.001]
  • [Cites] Cancer Res. 1992 Apr 1;52(7):1943-7 [1551122.001]
  • [Cites] Cancer Res. 1992 May 1;52(9 Suppl):2670s-2676s [1562998.001]
  • [Cites] Cancer Res. 1992 Jul 15;52(14):3875-9 [1617663.001]
  • [Cites] Cancer Res. 1992 Dec 1;52(23):6657-65 [1423310.001]
  • [Cites] Clin Chest Med. 1993 Mar;14(1):1-15 [8462243.001]
  • [Cites] Carcinogenesis. 1997 Mar;18(3):575-86 [9067559.001]
  • [Cites] Science. 1997 Nov 7;278(5340):1073-7 [9353183.001]
  • [Cites] Carcinogenesis. 1997 Nov;18(11):2035-42 [9395199.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Feb 17;95(4):1432-7 [9465032.001]
  • [Cites] J Ethnopharmacol. 1998 Feb;60(1):71-8 [9533434.001]
  • [Cites] J Cell Biochem Suppl. 1997;28-29:49-63 [9589349.001]
  • [Cites] Exp Lung Res. 1998 Jul-Aug;24(4):629-39 [9659588.001]
  • [Cites] Int J Epidemiol. 1998 Jun;27(3):359-64 [9698120.001]
  • [Cites] Hematol Oncol Clin North Am. 1998 Oct;12(5):1037-53 [9888020.001]
  • [Cites] Biofactors. 2000;13(1-4):73-9 [11237203.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10350-5 [11504910.001]
  • [Cites] J Korean Med Sci. 2001 Dec;16 Suppl:S3-5 [11748372.001]
  • [Cites] J Korean Med Sci. 2001 Dec;16 Suppl:S38-41 [11748375.001]
  • [Cites] J Korean Med Sci. 2001 Dec;16 Suppl:S81-6 [11748382.001]
  • [Cites] Chest. 1993 Apr;103(4 Suppl):449S-456S [8462339.001]
  • [Cites] Anticancer Res. 1995 May-Jun;15(3):839-45 [7645968.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1995 Jun;4(4):401-8 [7655337.001]
  • [Cites] EMBO J. 1995 Nov 1;14(21):5279-87 [7489717.001]
  • [Cites] Fundam Appl Toxicol. 1996 Feb;29(2):244-50 [8742322.001]
  • [Cites] Br Med J. 1952 Dec 13;2(4797):1271-86 [12997741.001]
  • [Cites] Curr Cancer Drug Targets. 2004 Dec;4(8):621-35 [15578919.001]
  • [Cites] J Korean Med Sci. 2001 Dec;16 Suppl:S6-18 [11748383.001]
  • [Cites] Exp Cell Res. 1999 Nov 25;253(1):100-9 [10579915.001]
  • [Cites] Cancer Res. 2000 Feb 15;60(4):901-7 [10706103.001]
  • [Cites] Cancer Lett. 2000 Mar 13;150(1):41-8 [10755385.001]
  • [Cites] Carcinogenesis. 2000 May;21(5):915-9 [10783312.001]
  • [Cites] Nutr Cancer. 2000;36(1):66-73 [10798218.001]
  • (PMID = 16533426.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA058554; United States / NCI NIH HHS / CA / P01 CA9696401
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Anticarcinogenic Agents; 0 / Antineoplastic Agents; 0 / Tea; 0 / polyphenon E; 3417WMA06D / Benzo(a)pyrene; 8R1V1STN48 / Catechin; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ PMC1584290
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38. Fu H, He J, Mei F, Zhang Q, Hara Y, Ryota S, Lubet RA, Chen R, Chen DR, You M: Lung cancer inhibitory effect of epigallocatechin-3-gallate is dependent on its presence in a complex mixture (polyphenon E). Cancer Prev Res (Phila); 2009 Jun;2(6):531-7
Hazardous Substances Data Bank. Benzo(a)pyrene .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lung cancer inhibitory effect of epigallocatechin-3-gallate is dependent on its presence in a complex mixture (polyphenon E).
  • However, (-)-epigallocatechin-3-gallate (EGCG) alone was shown to be ineffective in preventing lung tumorigenesis in mice by aerosol administration.
  • With a relatively low dose level (4.19 mg/kg), Polyphenon E decreased tumor multiplicity by 53%, whereas Polyphenon E without EGCG at the same dose failed to inhibit lung carcinogenesis.
  • These results indicate that aerosol administration can be an effective approach in chemoprevention study, and aerosolized Polyphenon E can significantly inhibit pulmonary adenoma formation and growth in A/J mice.
  • Furthermore, in aerosolized form, EGCG, which is thought to be the most active component of Polyphenon E, has to be present with other tea catechins to show chemopreventive activity on lung tumorigenesis.
  • [MeSH-major] Adenoma / prevention & control. Anticarcinogenic Agents / therapeutic use. Catechin / analogs & derivatives. Lung Neoplasms / prevention & control. Tea / chemistry

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  • [CommentIn] Cancer Prev Res (Phila). 2009 Jun;2(6):514-7 [19470792.001]
  • (PMID = 19470785.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aerosols; 0 / Anticarcinogenic Agents; 0 / Antioxidants; 0 / Tea; 0 / polyphenon E; 3417WMA06D / Benzo(a)pyrene; 8R1V1STN48 / Catechin; BQM438CTEL / epigallocatechin gallate
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39. Palanichamy MG, Zhang YP: Potential pitfalls in MitoChip detected tumor-specific somatic mutations: a call for caution when interpreting patient data. BMC Cancer; 2010;10:597

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  • METHODS: Published entire mitochondrial genomes from head and neck, adenoid cystic carcinoma, sessile serrated adenoma, and lung primary tumor from clinical patients were examined in a phylogenetic context and compared with known, naturally occurring mutations which characterize different populations.
  • RESULTS: The phylogenetic linkage analysis of whole arrays of mtDNA mutations from patient cancerous and non-cancerous tissue confirmed that artificial recombination events occurred in studies of head and neck, adenoid cystic carcinoma, sessile serrated adenoma, and lung primary tumor.
  • [MeSH-minor] Adenoma / genetics. Carcinoma, Adenoid Cystic / genetics. Genetic Techniques. Genome. Head and Neck Neoplasms / genetics. Humans. Oligonucleotide Array Sequence Analysis. Phylogeny. Reactive Oxygen Species

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  • [Cites] Am J Hum Genet. 2002 May;70(5):1152-71 [11938495.001]
  • [Cites] PLoS One. 2009;4(12):e8493 [20041111.001]
  • [Cites] Am J Hum Genet. 2004 Dec;75(6):966-78 [15467980.001]
  • [Cites] Nat Genet. 1999 Oct;23(2):147 [10508508.001]
  • [Cites] J Med Genet. 2005 Dec;42(12):957-60 [15923271.001]
  • [Cites] Genetics. 2006 Jan;172(1):373-87 [16172508.001]
  • [Cites] Mol Biol Evol. 2006 Mar;23(3):683-90 [16361303.001]
  • [Cites] PLoS Med. 2005 Nov;2(11):e296 [16187796.001]
  • [Cites] Trends Genet. 2006 Jun;22(6):339-45 [16678300.001]
  • [Cites] Hum Mol Genet. 2006 Jul 1;15(13):2076-86 [16714301.001]
  • [Cites] Mol Cancer. 2006;5:73 [17166268.001]
  • [Cites] Mol Biol Evol. 2007 Feb;24(2):436-48 [17099056.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 May 1;104(18):7540-5 [17456604.001]
  • [Cites] Clin Cancer Res. 2007 Aug 1;13(15 Pt 1):4331-5 [17671113.001]
  • [Cites] Clin Cancer Res. 2007 Dec 15;13(24):7335-40 [18094415.001]
  • [Cites] Am J Hum Genet. 2008 May;82(5):1130-40 [18439549.001]
  • [Cites] Hum Mutat. 2009 Feb;30(2):E386-94 [18853457.001]
  • [Cites] BMC Cancer. 2009;9:113 [19371404.001]
  • [Cites] Genome Res. 2004 May;14(5):812-9 [15123581.001]
  • (PMID = 21034508.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Mitochondrial; 0 / Reactive Oxygen Species
  • [Other-IDs] NLM/ PMC2988032
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40. Li L, Xie Y, El-Sayed WM, Szakacs JG, Franklin MR, Roberts JC: Chemopreventive activity of selenocysteine prodrugs against tobacco-derived nitrosamine (NNK) induced lung tumors in the A/J mouse. J Biochem Mol Toxicol; 2005;19(6):396-405
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  • [Title] Chemopreventive activity of selenocysteine prodrugs against tobacco-derived nitrosamine (NNK) induced lung tumors in the A/J mouse.
  • This study reports the efficacy of three selenazolidine-4(R)-carboxylic acids, (2-unsubstituted, 2-oxo, and 2-methyl derivatives; SCA, OSCA, and MSCA, respectively) against tobacco-related lung tumorigenesis in a mouse model.
  • After an additional 16 weeks on the diets, two compounds, OSCA and selenocystine, significantly reduced lung adenoma multiplicity from 7.2 tumors per mouse in the NNK group to 4.5 and 4.6 tumors per mouse, respectively.
  • [MeSH-major] Carcinogens / toxicity. Lung Neoplasms / prevention & control. Nitrosamines / toxicity. Prodrugs / administration & dosage. Selenocysteine / administration & dosage. Tobacco / chemistry

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  • [Copyright] (c) 2005 Wiley Periodicals, Inc. J Biochem Mol Toxicol 19:396-405, 2005
  • (PMID = 16421895.001).
  • [ISSN] 1095-6670
  • [Journal-full-title] Journal of biochemical and molecular toxicology
  • [ISO-abbreviation] J. Biochem. Mol. Toxicol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA42014; United States / NIGMS NIH HHS / GM / R01 GM58913; United States / NCRR NIH HHS / RR / RR06262; United States / NCRR NIH HHS / RR / S10 RR14768
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Nitrosamines; 0 / Prodrugs; 0CH9049VIS / Selenocysteine; 64091-91-4 / 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone; EC 1.11.1.9 / Glutathione Peroxidase; H6241UJ22B / Selenium
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41. Lu G, Liao J, Yang G, Reuhl KR, Hao X, Yang CS: Inhibition of adenoma progression to adenocarcinoma in a 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced lung tumorigenesis model in A/J mice by tea polyphenols and caffeine. Cancer Res; 2006 Dec 01;66(23):11494-501
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of adenoma progression to adenocarcinoma in a 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced lung tumorigenesis model in A/J mice by tea polyphenols and caffeine.
  • The present study investigated the inhibitory effects of Polyphenon E [a standardized green tea polyphenol preparation containing 65% (-)-epigallocatechin-3-gallate] and caffeine on 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung tumor progression from adenoma to adenocarcinoma.
  • Female A/J mice were treated with a single dose of NNK (103 mg/kg body weight, i.p.) and kept for 20 weeks for the mice to develop lung adenomas.
  • Both treatments significantly decreased the number of visible lung tumors.
  • Histopathologic analysis indicated that Polyphenon E administration significantly reduced the incidence (by 52%) and multiplicity (by 63%) of lung adenocarcinoma.
  • In the normal lung tissues, neither agent had a significant effect on cell proliferation or apoptosis.
  • The results show that tea polyphenols (and perhaps caffeine) inhibit the progression of NNK-induced lung adenoma to adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / prevention & control. Adenoma / prevention & control. Caffeine / therapeutic use. Flavonoids / therapeutic use. Lung Neoplasms / prevention & control. Phenols / therapeutic use. Tea / chemistry
  • [MeSH-minor] Analysis of Variance. Animals. Catechin / administration & dosage. Catechin / analogs & derivatives. Catechin / therapeutic use. Cell Proliferation / drug effects. Disease Progression. Female. Immunohistochemistry. JNK Mitogen-Activated Protein Kinases / metabolism. Lung / drug effects. Lung / metabolism. Lung / pathology. Mice. Mice, Inbred Strains. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Nitrosamines / administration & dosage. Nitrosamines / toxicity. Phosphorylation / drug effects. Polyphenols. Proliferating Cell Nuclear Antigen / analysis. Time Factors

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  • (PMID = 17145898.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA72720; United States / NCI NIH HHS / CA / CA88961; United States / NIEHS NIH HHS / ES / ES50522
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Flavonoids; 0 / Nitrosamines; 0 / Phenols; 0 / Polyphenols; 0 / Proliferating Cell Nuclear Antigen; 0 / Tea; 0 / polyphenon E; 3G6A5W338E / Caffeine; 7S395EDO61 / 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone; 8R1V1STN48 / Catechin; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
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42. Kassie F, Kalscheuer S, Matise I, Ma L, Melkamu T, Upadhyaya P, Hecht SS: Inhibition of vinyl carbamate-induced pulmonary adenocarcinoma by indole-3-carbinol and myo-inositol in A/J mice. Carcinogenesis; 2010 Feb;31(2):239-45
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  • [Title] Inhibition of vinyl carbamate-induced pulmonary adenocarcinoma by indole-3-carbinol and myo-inositol in A/J mice.
  • In previous studies, we reported that indole-3-carbinol (I3C) and myo-inositol (MI) inhibit lung adenoma induced by tobacco smoke carcinogens in A/J mice.
  • In this paper, we extended our work and examined the effects of I3C (70 or 30 micromol/g diet) and MI (56 micromol/g diet) against vinyl carbamate (VC)-induced lung adenocarcinoma by administering the agents from 1 week after the second of two injections of VC until termination of the study at week 18.
  • The higher dose of I3C decreased multiplicities of tumors on the surface of the lung (26%, P = 0.0005), carcinoma incidence (38%), multiplicity (67%, P < 0.0001) and size (complete abolition of carcinoma with an area of >1.0 cm(2)) as well as adenoma with cellular pleomorphism (46%, P < 0.0001).
  • MI decreased multiplicities of pulmonary surface tumors (20%, P = 0.0005), adenoma with cellular pleomorphism (40%, P < 0.0001) and lung adenoma (52%, P < 0.0001) and the proportion of the biggest carcinoma (carcinoma with an area of >1.0 cm(2), P < 0.05).
  • Immunoblot analyses of lung tissues for potential target identification showed that I3C (70 micromol/g diet) inhibits IkappaBalpha degradation, nuclear factor-kappaB activation, expression of cyclooxygenase-2, phospho-Akt and fatty acid synthase (FAS) and activates caspase-3 and poly ADP ribose polymerase cleavage.
  • Our data show that I3C and MI inhibit lung carcinoma and provide a basis for future evaluation of these compounds in clinical trials as chemopreventive agents for current and former smokers.

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  • [Cites] Oncogene. 1999 Nov 22;18(49):6853-66 [10602461.001]
  • [Cites] Cancer Res. 2009 Jul 1;69(13):5592-600 [19531648.001]
  • [Cites] Exp Lung Res. 2000 Dec;26(8):757-72 [11195469.001]
  • [Cites] Cancer Lett. 2001 Jun 10;167(1):1-6 [11323092.001]
  • [Cites] Oncogene. 2001 May 24;20(23):2927-36 [11420705.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Sep 25;98(20):10983-5 [11572954.001]
  • [Cites] Cancer Res. 2002 Feb 1;62(3):642-6 [11830512.001]
  • [Cites] Carcinogenesis. 2002 Sep;23(9):1455-61 [12189187.001]
  • [Cites] Chest. 2003 Nov;124(5):1828-33 [14605056.001]
  • [Cites] Carcinogenesis. 2004 Feb;25(2):197-201 [14578161.001]
  • [Cites] Cancer Res. 2004 Apr 1;64(7):2307-16 [15059877.001]
  • [Cites] Semin Oncol. 2004 Apr;31(2 Suppl 7):45-52 [15179623.001]
  • [Cites] Nutr Cancer. 2004;48(1):84-94 [15203382.001]
  • [Cites] Prostate. 2004 Oct 1;61(2):153-60 [15305338.001]
  • [Cites] Cancer Res. 1990 May 1;50(9):2613-7 [2328487.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Nov 1;88(21):9543-7 [1658785.001]
  • [Cites] Carcinogenesis. 1993 Sep;14(9):1975-7 [8403228.001]
  • [Cites] Cancer Res. 1996 Nov 15;56(22):5132-5 [8912846.001]
  • [Cites] Anticancer Res. 1996 Sep-Oct;16(5A):2709-12 [8917375.001]
  • [Cites] Carcinogenesis. 1999 Jan;20(1):139-45 [9934861.001]
  • [Cites] Carcinogenesis. 2004 Nov;25(11):2053-9 [15240509.001]
  • [Cites] Front Biosci. 2005 Jan 1;10:236-43 [15574364.001]
  • [Cites] CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078.001]
  • [Cites] Ann Thorac Surg. 2005 Apr;79(4):1137-41 [15797040.001]
  • [Cites] Blood. 2005 Jul 15;106(2):641-9 [15811958.001]
  • [Cites] Cancer Res. 2005 Sep 15;65(18):8548-57 [16166336.001]
  • [Cites] Carcinogenesis. 2006 Mar;27(3):541-50 [16199440.001]
  • [Cites] Carcinogenesis. 2006 Apr;27(4):717-28 [16332727.001]
  • [Cites] Cancer Res. 2006 May 1;66(9):4952-60 [16651453.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Aug;15(8):1526-31 [16896044.001]
  • [Cites] Carcinogenesis. 2006 Oct;27(10):2116-23 [16704990.001]
  • [Cites] Mol Cancer Ther. 2006 Nov;5(11):2747-56 [17121921.001]
  • [Cites] Cancer Res. 2006 Dec 1;66(23):11494-501 [17145898.001]
  • [Cites] Cancer Res. 2007 Apr 1;67(7):3310-9 [17409440.001]
  • [Cites] Cancer Res. 2007 Jul 1;67(13):6502-11 [17616712.001]
  • [Cites] Mol Cancer Ther. 2007 Oct;6(10):2757-65 [17913854.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Nov 20;104(47):18514-9 [18000061.001]
  • [Cites] Clin Cancer Res. 2007 Dec 1;13(23):7139-45 [18056164.001]
  • [Cites] CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96 [18287387.001]
  • [Cites] Clin Cancer Res. 2008 Apr 15;14(8):2458-64 [18413838.001]
  • [Cites] Cancer Prev Res (Phila). 2008 Sep;1(4):285-97 [19138972.001]
  • [Cites] Cancer Prev Res (Phila). 2008 Dec;1(7):568-76 [19139007.001]
  • [Cites] J Natl Cancer Inst. 2009 Apr 1;101(7):519-32 [19318631.001]
  • [Cites] Cancer Prev Res (Phila). 2009 Apr;2(4):370-6 [19336734.001]
  • [Cites] Oncogene. 2000 Nov 23;19(50):5764-71 [11126363.001]
  • (PMID = 19625346.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-102502
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Indoles; 12001-76-2 / Vitamin B Complex; 3IN71E75Z5 / Urethane; 4L6452S749 / Inositol; 7Y2431GOM5 / vinyl carbamate; C11E72455F / indole-3-carbinol; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / Caspase 3
  • [Other-IDs] NLM/ PMC2812566
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43. Fenske TS, McMahon C, Edwin D, Jarvis JC, Cheverud JM, Minn M, Mathews V, Bogue MA, Province MA, McLeod HL, Graubert TA: Identification of candidate alkylator-induced cancer susceptibility genes by whole genome scanning in mice. Cancer Res; 2006 May 15;66(10):5029-38
Mouse Phenome Database (MPD). Related data set (Graubert1) available .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Cancer susceptibility was a heritable trait for the most common tumor types, lung adenocarcinoma (H(2) = 0.25), T cell lymphoma (H(2) = 0.19), and myeloid malignancies (H(2) = 0.10).
  • Quantitative trait locus mapping identified regions on chromosomes 3, 6, 9, and 15 containing candidate genes associated with lung adenoma, lung carcinoma, and lymphoma susceptibility.
  • [MeSH-minor] Animals. Ethylnitrosourea / toxicity. Genetic Predisposition to Disease. Hematologic Neoplasms / chemically induced. Hematologic Neoplasms / genetics. Lung Neoplasms / chemically induced. Lung Neoplasms / genetics. Mice. Mutagens / toxicity. Quantitative Trait Loci

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  • (PMID = 16707424.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA101937
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Antineoplastic Agents, Alkylating; 0 / Mutagens; P8M1T4190R / Ethylnitrosourea
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44. Magesh V, DurgaBhavani K, Senthilnathan P, Rajendran P, Sakthisekaran D: In vivo protective effect of crocetin on benzo(a)pyrene-induced lung cancer in Swiss albino mice. Phytother Res; 2009 Apr;23(4):533-9
Hazardous Substances Data Bank. Benzo(a)pyrene .

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  • [Title] In vivo protective effect of crocetin on benzo(a)pyrene-induced lung cancer in Swiss albino mice.
  • The objective of this investigation was to determine the efficacy of crocetin in preventing lung tumorigenesis in mice.
  • We evaluated crocetin in Swiss albino mice treated with the tobacco-specific carcinogen benzo(a)pyrene [B(a)P] for their ability to inhibit pulmonary adenoma formation and growth.
  • [MeSH-major] Adenoma / prevention & control. Antineoplastic Agents, Phytogenic / therapeutic use. Carotenoids / pharmacology. Lung Neoplasms / prevention & control
  • [MeSH-minor] Animals. Benzo(a)pyrene / adverse effects. Glycoproteins / analysis. Hexosamines / analysis. Liver / metabolism. Lung / metabolism. Lung / pathology. Male. Mice. Polyamines / analysis. Proliferating Cell Nuclear Antigen / analysis

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  • [Copyright] (c) 2008 John Wiley & Sons, Ltd.
  • (PMID = 19067387.001).
  • [ISSN] 1099-1573
  • [Journal-full-title] Phytotherapy research : PTR
  • [ISO-abbreviation] Phytother Res
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Glycoproteins; 0 / Hexosamines; 0 / Polyamines; 0 / Proliferating Cell Nuclear Antigen; 20TC155L9C / crocetin; 3417WMA06D / Benzo(a)pyrene; 36-88-4 / Carotenoids
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45. Wirschell M, Yang C, Yang P, Fox L, Yanagisawa HA, Kamiya R, Witman GB, Porter ME, Sale WS: IC97 is a novel intermediate chain of I1 dynein that interacts with tubulin and regulates interdoublet sliding. Mol Biol Cell; 2009 Jul;20(13):3044-54
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  • IC97 shares homology with the murine lung adenoma susceptibility 1 (Las1) protein--a candidate tumor suppressor gene implicated in lung tumorigenesis.

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  • [Cites] Cell Motil Cytoskeleton. 1987;8(1):68-75 [2958145.001]
  • [Cites] Genetics. 1988 Dec;120(4):965-76 [3224813.001]
  • [Cites] J Cell Biol. 1990 Feb;110(2):379-89 [2137128.001]
  • [Cites] J Mol Biol. 1990 Oct 5;215(3):403-10 [2231712.001]
  • [Cites] J Cell Biol. 1991 Feb;112(3):441-7 [1825085.001]
  • [Cites] J Biol Chem. 1991 May 5;266(13):8401-7 [1827120.001]
  • [Cites] Cell Motil Cytoskeleton. 1991;18(4):258-68 [1828714.001]
  • [Cites] J Cell Sci. 1991 Oct;100 ( Pt 2):319-28 [1836791.001]
  • [Cites] J Cell Biol. 1992 Sep;118(5):1145-62 [1387403.001]
  • [Cites] J Cell Biol. 1992 Sep;118(5):1163-76 [1387404.001]
  • [Cites] Cell Motil Cytoskeleton. 1993;25(2):158-70 [7686822.001]
  • [Cites] Cell Motil Cytoskeleton. 1994;28(3):199-204 [7954848.001]
  • [Cites] J Cell Biol. 1994 Dec;127(6 Pt 1):1683-92 [7798320.001]
  • [Cites] J Biol Chem. 1995 May 12;270(19):11445-52 [7744782.001]
  • [Cites] Mol Biol Cell. 1995 Jun;6(6):697-711 [7579689.001]
  • [Cites] Methods Cell Biol. 1995;47:487-9 [7476533.001]
  • [Cites] J Cell Biol. 1997 Jan 13;136(1):167-76 [9008711.001]
  • [Cites] J Cell Biol. 1997 Jan 13;136(1):177-91 [9008712.001]
  • [Cites] Cell Motil Cytoskeleton. 1997;37(3):232-9 [9227853.001]
  • [Cites] Mol Biol Cell. 1997 Apr;8(4):607-20 [9247642.001]
  • [Cites] J Cell Biol. 1998 Mar 9;140(5):1137-47 [9490726.001]
  • [Cites] J Cell Biol. 1998 May 18;141(4):979-92 [9585416.001]
  • [Cites] Mol Biol Cell. 1998 Dec;9(12):3335-49 [9843573.001]
  • [Cites] Mol Biol Cell. 1998 Dec;9(12):3351-65 [9843574.001]
  • [Cites] J Cell Biol. 1999 Jul 12;146(1):165-80 [10402468.001]
  • [Cites] J Cell Biol. 1999 Aug 23;146(4):801-18 [10459015.001]
  • [Cites] Mol Biol Cell. 2004 Dec;15(12):5431-42 [15469982.001]
  • [Cites] Biol Cell. 2004 Dec;96(9):681-90 [15567522.001]
  • [Cites] Biochemistry. 2004 Dec 14;43(49):15595-603 [15581372.001]
  • [Cites] Curr Biol. 2004 Dec 14;14(23):2113-8 [15589153.001]
  • [Cites] J Cell Sci. 2005 Feb 1;118(Pt 3):529-37 [15657081.001]
  • [Cites] J Cell Biol. 2005 Jul 4;170(1):103-13 [15998802.001]
  • [Cites] Science. 2006 Aug 18;313(5789):944-8 [16917055.001]
  • [Cites] J Biol Chem. 2007 Feb 23;282(8):5404-12 [17194703.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jun 12;104(24):10028-33 [17551010.001]
  • [Cites] Biophys J. 2007 Aug 1;93(3):886-94 [17496036.001]
  • [Cites] Cell Motil Cytoskeleton. 2007 Aug;64(8):569-79 [17549744.001]
  • [Cites] Cancer Res. 2007 Nov 1;67(21):10207-13 [17974961.001]
  • [Cites] Biochemistry. 2008 Jan 15;47(2):503-8 [18092820.001]
  • [Cites] Cell Motil Cytoskeleton. 2008 Mar;65(3):238-48 [18157907.001]
  • [Cites] Genes Dev. 2008 Apr 1;22(7):918-30 [18334618.001]
  • [Cites] J Cell Sci. 2008 Sep 1;121(Pt 17):2833-43 [18682495.001]
  • [Cites] Sci Signal. 2008;1(47):pe51 [19036713.001]
  • [Cites] J Cell Biol. 2008 Dec 1;183(5):923-32 [19029338.001]
  • [Cites] Mol Biol Cell. 2009 Jul;20(13):3055-63 [19420135.001]
  • [Cites] Cell Motil Cytoskeleton. 2009 Aug;66(8):425-36 [18828155.001]
  • [Cites] Cell Motil Cytoskeleton. 2009 Aug;66(8):448-56 [19021242.001]
  • [Cites] Methods Mol Biol. 2000;132:365-86 [10547847.001]
  • [Cites] J Biol Chem. 2000 Jun 23;275(25):18905-12 [10858448.001]
  • [Cites] Mol Biol Cell. 2000 Jul;11(7):2297-313 [10888669.001]
  • [Cites] J Cell Biol. 2000 Nov 27;151(5):F37-42 [11086017.001]
  • [Cites] Methods. 2000 Dec;22(4):285-98 [11133235.001]
  • [Cites] Methods. 2000 Dec;22(4):365-71 [11133242.001]
  • [Cites] J Cell Biol. 2001 Jun 11;153(6):1315-26 [11402073.001]
  • [Cites] Int Rev Cytol. 2001;210:227-68 [11580207.001]
  • [Cites] Int Rev Cytol. 2002;219:115-55 [12211628.001]
  • [Cites] Cell Motil Cytoskeleton. 2002 Oct;53(2):103-24 [12211108.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Oct 28;100(22):12642-7 [14583591.001]
  • [Cites] Cell Motil Cytoskeleton. 2004 Jan;57(1):8-17 [14648553.001]
  • [Cites] Mol Biol Cell. 2004 May;15(5):2105-15 [14978211.001]
  • [Cites] J Biol Chem. 2004 May 14;279(20):21666-76 [15020587.001]
  • [Cites] Oncogene. 2004 May 27;23(25):4495-504 [15064703.001]
  • [Cites] Mol Biol Cell. 2004 Oct;15(10):4633-46 [15304520.001]
  • [Cites] J Gen Microbiol. 1972 Aug;71(3):525-40 [4647471.001]
  • [Cites] J Cell Biol. 1981 Jan;88(1):80-8 [7204490.001]
  • [Cites] Cold Spring Harb Symp Quant Biol. 1982;46 Pt 1:157-69 [6179692.001]
  • [Cites] J Cell Biol. 1985 Jun;100(6):2008-18 [2860115.001]
  • [Cites] J Cell Biol. 1986 Nov;103(5):1895-902 [2946702.001]
  • [Cites] Methods Enzymol. 1986;134:280-90 [3821567.001]
  • [ErratumIn] Mol Biol Cell. 2009 Aug;20(15):3617
  • (PMID = 19420136.001).
  • [ISSN] 1939-4586
  • [Journal-full-title] Molecular biology of the cell
  • [ISO-abbreviation] Mol. Biol. Cell
  • [Language] ENG
  • [Databank-accession-numbers] GENBANK/ FJ156240/ FJ156241
  • [Grant] United States / NIGMS NIH HHS / GM / GM-30626; United States / NIGMS NIH HHS / GM / GM-068101; United States / NIGMS NIH HHS / GM / R01 GM051173; United States / NIGMS NIH HHS / GM / R01 GM030626; United States / NIGMS NIH HHS / GM / GM-55667; United States / NIGMS NIH HHS / GM / R37 GM030626; United States / NIGMS NIH HHS / GM / GM-051173; United States / NIGMS NIH HHS / GM / R01 GM068101; United States / NIGMS NIH HHS / GM / GM068101-04; United States / NIGMS NIH HHS / GM / R37 GM051173; United States / NIGMS NIH HHS / GM / R01 GM055667; United States / NIGMS NIH HHS / GM / GM-075446; United States / NIGMS NIH HHS / GM / F32 GM075446; United States / NIGMS NIH HHS / GM / R01 GM068101-04; United States / NIGMS NIH HHS / GM / R37 GM055667
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Algal Proteins; 0 / Protein Subunits; 0 / Tubulin; EC 3.6.4.2 / Dyneins
  • [Other-IDs] NLM/ PMC2704156
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46. Takeuchi H, Saoo K, Matsuda Y, Yokohira M, Yamakawa K, Zeng Y, Kuno T, Kamataki T, Imaida K: 8-Methoxypsoralen, a potent human CYP2A6 inhibitor, inhibits lung adenocarcinoma development induced by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone in female A/J mice. Mol Med Rep; 2009 Jul-Aug;2(4):585-8

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  • [Title] 8-Methoxypsoralen, a potent human CYP2A6 inhibitor, inhibits lung adenocarcinoma development induced by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone in female A/J mice.
  • Previously, we demonstrated that 8-methoxypsoralen (methoxsalen), a potent human cytochrome P450 2A6 (CYP2A6) inhibitor, strongly suppresses lung adenoma induction by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in female A/J mice.
  • In the present study, we examined the inhibitory effects of methoxsalen on the development of lung adenocarcinomas, as well as on adenomas and alveolar hyperplasia.
  • The experiments were terminated 52 weeks after the first methoxsalen treatment, and lung adenomas and adenocarcinomas were analyzed histopathologically.
  • These results clearly demonstrate that methoxsalen, a potent human CYP2A6 inhibitor, inhibits not only lung adenoma but also adenocarcinoma development.

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  • (PMID = 21475870.001).
  • [ISSN] 1791-3004
  • [Journal-full-title] Molecular medicine reports
  • [ISO-abbreviation] Mol Med Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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47. Kang MS, Lu H, Yasui T, Sharpe A, Warren H, Cahir-McFarland E, Bronson R, Hung SC, Kieff E: Epstein-Barr virus nuclear antigen 1 does not induce lymphoma in transgenic FVB mice. Proc Natl Acad Sci U S A; 2005 Jan 18;102(3):820-5
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  • EBNA1-transgenic lineages had a higher pulmonary adenoma prevalence than did littermate controls (39% versus 7%).
  • However, the adenoma prevalence was not higher in EBNA1-transgenic mice than has been described for FVB mice, and EBNA1 was not expressed in normal pulmonary epithelia or adenomas.

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  • [Cites] Carcinogenesis. 2000 Jul;21(7):1379-89 [10874017.001]
  • [Cites] J Virol. 1999 Dec;73(12):9827-31 [10559294.001]
  • [Cites] J Biol Chem. 2000 Sep 15;275(37):28764-73 [10849420.001]
  • [Cites] Virology. 2000 Sep 15;275(1):145-57 [11017796.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Feb 13;98(4):1865-70 [11172042.001]
  • [Cites] Jpn J Cancer Res. 2001 May;92(5):499-505 [11376558.001]
  • [Cites] J Virol. 2001 Nov;75(22):10582-92 [11602700.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Dec 18;98(26):15233-8 [11734622.001]
  • [Cites] FEBS Lett. 2002 Dec 4;532(1-2):135-42 [12459478.001]
  • [Cites] J Virol. 2003 Jun;77(12):6946-56 [12768013.001]
  • [Cites] J Biol Chem. 2003 Aug 8;278(32):29987-94 [12783858.001]
  • [Cites] Mol Cell Biol. 2003 Oct;23(19):6901-8 [12972608.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Sep 16;100(19):10989-94 [12947043.001]
  • [Cites] Nat Rev Immunol. 2003 Oct;3(10):801-12 [14523386.001]
  • [Cites] J Biol Chem. 2003 Nov 28;278(48):47753-61 [14506283.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Nov 25;100(24):14269-74 [14603034.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jan 6;101(1):239-44 [14688409.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jan 6;101(1):141-6 [14691250.001]
  • [Cites] Proc Natl Acad Sci U S A. 1984 Jun;81(12):3806-10 [6328526.001]
  • [Cites] Nature. 1984 Jul 19-25;310(5974):207-11 [6087149.001]
  • [Cites] Nature. 1985 Feb 28-Mar 6;313(6005):812-5 [2983224.001]
  • [Cites] Cell. 1985 Oct;42(3):859-68 [2996781.001]
  • [Cites] Nature. 1985 Dec 12-18;318(6046):533-8 [3906410.001]
  • [Cites] Biochem Biophys Res Commun. 1986 Feb 13;134(3):1260-8 [3004487.001]
  • [Cites] Curr Top Microbiol Immunol. 1986;132:1-8 [3491731.001]
  • [Cites] Mol Cell Biol. 1986 Nov;6(11):3838-46 [3025615.001]
  • [Cites] Cell. 1987 Apr 24;49(2):161-70 [3032447.001]
  • [Cites] J Virol. 1989 Jun;63(6):2657-66 [2542579.001]
  • [Cites] J Exp Med. 1989 Sep 1;170(3):711-26 [2504875.001]
  • [Cites] J Virol. 1990 May;64(5):2369-79 [2157891.001]
  • [Cites] J Virol. 1991 Mar;65(3):1466-78 [1847464.001]
  • [Cites] Jpn J Cancer Res. 1992 Mar;83(3):269-73 [1582889.001]
  • [Cites] J Virol. 1993 Jun;67(6):3418-26 [8388506.001]
  • [Cites] Immunity. 1994 Aug;1(5):415-21 [7533646.001]
  • [Cites] J Virol. 1995 Apr;69(4):2633-6 [7884916.001]
  • [Cites] Nature. 1995 Jun 22;375(6533):685-8 [7540727.001]
  • [Cites] Cell. 1996 Mar 8;84(5):791-800 [8625416.001]
  • [Cites] EMBO J. 1996 Jun 17;15(12):3117-26 [8670812.001]
  • [Cites] Intervirology. 1995;38(3-4):195-205 [8682617.001]
  • [Cites] J Virol. 1996 Dec;70(12):9003-7 [8971032.001]
  • [Cites] Toxicol Pathol. 1996 Nov-Dec;24(6):710-6 [8994298.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Jul 22;94(15):8156-61 [9223331.001]
  • [Cites] Virology. 1997 Sep 15;236(1):18-29 [9299613.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Nov 11;94(23):12616-21 [9356498.001]
  • [Cites] J Biol Chem. 1997 Nov 21;272(47):29873-9 [9368061.001]
  • [Cites] Nucleic Acids Res. 1998 Jan 15;26(2):631-7 [9421526.001]
  • [Cites] J Virol. 1998 Nov;72(11):9150-6 [9765461.001]
  • [Cites] J Virol. 1999 Feb;73(2):1630-6 [9882370.001]
  • [Cites] Mol Cell Biol. 1999 Mar;19(3):1651-60 [10022853.001]
  • [Cites] J Virol. 1999 Apr;73(4):2974-82 [10074147.001]
  • [Cites] J Virol. 1999 Apr;73(4):3154-61 [10074167.001]
  • [Cites] J Virol. 1999 May;73(5):4385-92 [10196336.001]
  • [Cites] Mol Cell Biol. 1999 May;19(5):3349-59 [10207059.001]
  • [Cites] J Biol Chem. 2000 Jul 21;275(29):22273-7 [10801810.001]
  • (PMID = 15640350.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA047006; United States / NCI NIH HHS / CA / R35 CA047006; United States / NCI NIH HHS / CA / CA47006
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / EBV-encoded nuclear antigen 1; 0 / Epstein-Barr Virus Nuclear Antigens; EC 3.1.3.48 / Antigens, CD45
  • [Other-IDs] NLM/ PMC545574
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48. Machida K, Urano K, Yoshimura M, Tsutsumi H, Nomura T, Usui T: Carcinogenic comparative study on rasH2 mice produced by two breeding facilities. J Toxicol Sci; 2008 Oct;33(4):493-501
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  • In the pathological examination, only benign tumors of lungs, spleen, forestomach and skin were observed in a few mice in the vehicle group of both facilities.
  • Although lung adenoma and skin papilloma/keratoacanthoma, which are major MNU induced tumors in this strain, were observed in several mice from both facilities, no significant differences were found.

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  • (PMID = 18827450.001).
  • [ISSN] 1880-3989
  • [Journal-full-title] The Journal of toxicological sciences
  • [ISO-abbreviation] J Toxicol Sci
  • [Language] eng
  • [Publication-type] Comparative Study; Letter
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Carcinogens; 684-93-5 / Methylnitrosourea
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49. Lee GH: The Kras2 oncogene and mouse lung carcinogenesis. Med Mol Morphol; 2008 Dec;41(4):199-203
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  • [Title] The Kras2 oncogene and mouse lung carcinogenesis.
  • Activating point mutations of the mouse Kras2 oncogene or its human homologue, KRAS, are critical for lung adenocarcinoma genesis, independent of the species.
  • Significantly, in the mouse, several polymorphic Kras2 alleles have been identified, which cosegregate with genetic susceptibility to chemical induction of lung tumors.
  • Moreover, a major lung tumor susceptibility locus, the Pas1 (Pulmonary adenoma susceptibility 1), was found to colocalize with Kras2 on distal chromosome 6 on linkage analysis.
  • In this review, the focus is on current knowledge regarding the relationship between Kras2 and experimental mouse lung carcinogenesis, especially from the aspect of disease predisposition.
  • Because mouse and human lung tumors share considerable similarities, the experimental information should provide clues to personalized medicine in the human setting.
  • [MeSH-major] Genetic Predisposition to Disease. Lung. Lung Neoplasms / etiology. Lung Neoplasms / genetics. Proto-Oncogene Proteins p21(ras) / genetics

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  • [Cites] J Natl Cancer Inst. 1985 Nov;75(5):971-4 [3863994.001]
  • [Cites] Proc Natl Acad Sci U S A. 1982 Jun;79(11):3637-40 [6285355.001]
  • [Cites] Nat Genet. 2006 Aug;38(8):926-30 [16823377.001]
  • [Cites] Oncogene. 1997 Sep 4;15(10):1151-9 [9294608.001]
  • [Cites] Carcinogenesis. 1997 Oct;18(10):1917-20 [9364000.001]
  • [Cites] Oncogene. 2003 Jan 23;22(3):426-32 [12545163.001]
  • [Cites] Cancer Sci. 2005 May;96(5):256-9 [15904465.001]
  • [Cites] Oncogene. 2003 Apr 17;22(15):2374-82 [12700672.001]
  • [Cites] Int J Cancer. 2005 May 1;114(5):730-7 [15609317.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Jul 1;89(13):5804-8 [1352876.001]
  • [Cites] J Natl Cancer Inst. 1983 May;70(5):931-6 [6573537.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 May;86(9):3070-4 [2654935.001]
  • [Cites] Cell. 1990 May 4;61(3):407-17 [2185890.001]
  • [Cites] Biochim Biophys Acta. 2007 Aug;1773(8):1177-95 [17428555.001]
  • [Cites] Nat Genet. 1993 Feb;3(2):132-6 [8499946.001]
  • [Cites] Nat Genet. 2001 Sep;29(1):25-33 [11528387.001]
  • [Cites] Nature. 2001 Apr 26;410(6832):1111-6 [11323676.001]
  • [Cites] Mol Carcinog. 1993;8(3):177-85 [8216736.001]
  • [Cites] Mol Carcinog. 1996 Dec;17(4):217-23 [8989915.001]
  • [Cites] J Natl Cancer Inst. 1987 Dec;79(6):1351-7 [2891865.001]
  • [Cites] Oncogene. 1997 Oct 9;15(15):1833-40 [9362450.001]
  • [Cites] Oncogene. 1990 Jul;5(7):1037-43 [2197591.001]
  • [Cites] Cancer Res. 2004 Apr 1;64(7):2307-16 [15059877.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Feb 15;91(4):1589-93 [8108449.001]
  • [Cites] Oncogene. 2004 May 27;23(25):4495-504 [15064703.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 28;103(48):18083-8 [17114294.001]
  • [Cites] Genomics. 1995 Sep 20;29(2):438-44 [8666392.001]
  • [Cites] Oncogene. 1996 Oct 17;13(8):1599-604 [8895504.001]
  • [Cites] Nature. 1999 Jun 17;399(6737):700-4 [10385124.001]
  • [Cites] Adv Cancer Res. 1995;67:83-112 [8571820.001]
  • [Cites] Cancer Res. 2000 Sep 15;60(18):5017-20 [11016621.001]
  • [Cites] Am J Clin Pathol. 1999 May;111(5):610-22 [10230351.001]
  • [Cites] Mol Cell Biol. 2006 Oct;26(20):7696-706 [17015482.001]
  • [Cites] Carcinogenesis. 1991 Feb;12(2):299-303 [1995195.001]
  • [Cites] Cancer Res. 1989 Oct 1;49(19):5305-11 [2670201.001]
  • (PMID = 19107609.001).
  • [ISSN] 1860-1480
  • [Journal-full-title] Medical molecular morphology
  • [ISO-abbreviation] Med Mol Morphol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Antigens, Nuclear; 0 / PASD1 protein, human; EC 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
  • [Number-of-references] 35
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50. Lee GH, Matsushita H: Genetic linkage between Pol iota deficiency and increased susceptibility to lung tumors in mice. Cancer Sci; 2005 May;96(5):256-9
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  • [Title] Genetic linkage between Pol iota deficiency and increased susceptibility to lung tumors in mice.
  • In fact, the mouse Pol iota gene is located within the Par2 (pulmonary adenoma resistance 2) locus on distal chromosome 18, which we have identified as a major susceptibility locus regarding urethane induction of pulmonary adenomas.
  • Taking advantage of 129X1/SvJ mice naturally deficient in Pol iota due to a nonsense mutation within the coding region of the gene, we here analyzed urethane-treated (A/J x 129X1/SvJ)F(1) x A/J backcross and (A/J x 129X1/SvJ)F(2) intercross mice and observed the defective 129X1/SvJ Pol iota allele to be genetically linked with an increased susceptibility to lung tumors relative to the A/J allele.
  • Thus, among the already known mouse Pol iota alleles, the defective 129X1/SvJ allele is associated exclusively with the highest susceptibility to lung tumors.
  • The result indicates a possibility that the Pol iota gene may participate in error-free repair of damaged DNA and prevention of lung tumor development.
  • [MeSH-major] DNA-Directed DNA Polymerase / deficiency. DNA-Directed DNA Polymerase / genetics. Genetic Predisposition to Disease / genetics. Lung Neoplasms / genetics

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  • (PMID = 15904465.001).
  • [ISSN] 1347-9032
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.7.- / DNA polymerase iota; EC 2.7.7.7 / DNA-Directed DNA Polymerase
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51. Subramanian H, Roy HK, Pradhan P, Goldberg MJ, Muldoon J, Brand RE, Sturgis C, Hensing T, Ray D, Bogojevic A, Mohammed J, Chang JS, Backman V: Nanoscale cellular changes in field carcinogenesis detected by partial wave spectroscopy. Cancer Res; 2009 Jul 1;69(13):5357-63
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  • Here we use PWS to show for the first time the increase in the disorder strength of the nanoscale architecture not only in tumor cells but also in the microscopically normal-appearing cells outside of the tumor.
  • This seems to be a general event in carcinogenesis, which is supported by our data in three types of cancer: colon, pancreatic, and lung.

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  • [Cites] Curr Opin Cell Biol. 2008 Apr;20(2):186-93 [18359618.001]
  • [Cites] Nature. 2008 May 1;453(7191):115-9 [18451862.001]
  • [Cites] BMC Genomics. 2008;9:259 [18513428.001]
  • [Cites] J Cell Biochem. 2008 Oct 15;105(3):670-7 [18773413.001]
  • [Cites] N Engl J Med. 2008 Nov 6;359(19):1995-2004 [18923165.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Dec 23;105(51):20118-23 [19073935.001]
  • [Cites] Cancer Prev Res (Phila). 2008 Nov;1(6):396-403 [19138985.001]
  • [Cites] Carcinogenesis. 2009 Apr;30(4):555-65 [19168579.001]
  • [Cites] Opt Lett. 2009 Feb 15;34(4):518-20 [19373360.001]
  • [Cites] Clin Cancer Res. 1999 Dec;5(12):3899-905 [10632318.001]
  • [Cites] Arch Intern Med. 2003 Feb 24;163(4):413-20 [12588199.001]
  • [Cites] Nat Rev Cancer. 2003 Mar;3(3):179-92 [12612653.001]
  • [Cites] Cancer Res. 2004 May 15;64(10):3694-700 [15150130.001]
  • [Cites] Biochim Biophys Acta. 1987 Jan 26;896(2):311-7 [3801474.001]
  • [Cites] Gut. 1993 Apr;34(4):525-30 [8491402.001]
  • [Cites] N Engl J Med. 1998 Oct 29;339(18):1277-84 [9791143.001]
  • [Cites] Cancer Res. 1999 May 15;59(10):2353-7 [10344743.001]
  • [Cites] Clin Cancer Res. 2005 Jan 15;11(2 Pt 1):573-83 [15701843.001]
  • [Cites] Anal Quant Cytol Histol. 2005 Jun;27(3):134-42 [16121634.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Sep;14(9):2066-75 [16172211.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Sep;14(9):2113-7 [16172218.001]
  • [Cites] Opt Lett. 2005 Sep 15;30(18):2445-7 [16196347.001]
  • [Cites] Dis Colon Rectum. 2005 Dec;48(12):2329-35 [16400515.001]
  • [Cites] Nat Genet. 2006 Apr;38(4):468-73 [16565718.001]
  • [Cites] Cancer Res. 2006 Jul 1;66(13):6553-62 [16818627.001]
  • [Cites] Nat Med. 2007 Mar;13(3):361-6 [17334370.001]
  • [Cites] J Biomed Opt. 2007 Jan-Feb;12(1):014010 [17343485.001]
  • [Cites] J Biochem Mol Biol. 2007 Mar 31;40(2):142-50 [17394762.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2007 Dec;16(12):2704-16 [18086777.001]
  • [Cites] Cancer Lett. 2008 Feb 18;260(1-2):1-10 [18164807.001]
  • (PMID = 19549915.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA128641-01A1; United States / NCI NIH HHS / CA / R01 CA112315; United States / NCI NIH HHS / CA / CA128641-01A1; United States / NCI NIH HHS / CA / R01 CA128641; United States / NCI NIH HHS / CA / R01 CA112315-04; United States / NIBIB NIH HHS / EB / R01 EB003682-04; United States / NCI NIH HHS / CA / CA112315-04; United States / NIBIB NIH HHS / EB / R01 EB003682
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MicroRNAs
  • [Other-IDs] NLM/ NIHMS162262; NLM/ PMC2802178
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52. Moody TW: Thymosin alpha1 as a chemopreventive agent in lung and breast cancer. Ann N Y Acad Sci; 2007 Sep;1112:297-304
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  • [Title] Thymosin alpha1 as a chemopreventive agent in lung and breast cancer.
  • The ability of thymosin alpha1 (Talpha1) to prevent lung and breast cancer was investigated.
  • Lung adenomas developed in A/J mice injected with carcinogens, such as urethane.
  • The lung adenoma number was reduced by 15-45% if animals were daily treated subcutaneously (s.c.) with Talpha1 (0.4 mg/kg).
  • Talpha1 (1 microM) directly inhibited the growth of mouse lung cell lines.
  • These results suggest that Talpha1 may prevent mouse lung carcinogenesis because it directly inhibits the growth of lung cancer cells.
  • These results indicate that Talpha1 is a chemopreventive agent in animal models for lung and breast carcinogenesis.
  • [MeSH-major] Anticarcinogenic Agents / therapeutic use. Lung Neoplasms / prevention & control. Mammary Neoplasms, Animal / prevention & control. Thymosin / analogs & derivatives
  • [MeSH-minor] Adenoma / prevention & control. Animals. Female. Mice. Mice, Inbred A. Rats. Rats, Inbred F344

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  • (PMID = 17567944.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / thymalfasin; 61512-21-8 / Thymosin
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53. Salinas NR, Oshima CT, Cury PM, Cordeiro JA, Bueno V: FTY720 and lung tumor development. Int Immunopharmacol; 2009 Jun;9(6):689-93
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  • [Title] FTY720 and lung tumor development.
  • Lung adenoma was induced in mice by urethane injection followed by different periods of FTY720 administration in order to evaluate lung tumor development.
  • Twenty-four weeks after urethane administration mice were evaluated for the number of leukocyte in blood, lymphocytes in spleen, and lungs were evaluated for changes in histology, PCNA and VEGF expression.
  • Lung nodules were present in higher numbers both in non treated (G1; 0.0-7.0) and FTY720 treated 8 weeks after urethane injection (G4; 0.0-6.0).
  • Therefore, our data suggest that the benefits of FTY720 treatment are time-dependent and when administered in early periods after lung tumor induction this drug could impair cancer development.
  • [MeSH-major] Adenoma / prevention & control. Immunosuppressive Agents / administration & dosage. Lung Neoplasms / prevention & control. Propylene Glycols / administration & dosage. Sphingosine / analogs & derivatives

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  • (PMID = 19146992.001).
  • [ISSN] 1878-1705
  • [Journal-full-title] International immunopharmacology
  • [ISO-abbreviation] Int. Immunopharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 0 / Proliferating Cell Nuclear Antigen; 0 / Propylene Glycols; 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, mouse; 3IN71E75Z5 / Urethane; G926EC510T / Fingolimod Hydrochloride; NGZ37HRE42 / Sphingosine
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54. Sun W, Iijima T, Kano J, Kobayashi H, Li D, Morishita Y, Okubo C, Anami Y, Noguchi M: Frequent aberrant methylation of the promoter region of sterile alpha motif domain 14 in pulmonary adenocarcinoma. Cancer Sci; 2008 Nov;99(11):2177-84
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  • [Title] Frequent aberrant methylation of the promoter region of sterile alpha motif domain 14 in pulmonary adenocarcinoma.
  • In order to identify novel hypermethylated genes in early stage lung adenocarcinoma, we carried out methylated CpG island amplification, modified suppression subtractive hybridization, and methylation-specific polymerase chain reaction to identify aberrant methylation of CpG islands in the A/J mouse lung adenoma model, which histologically mimics the early stage of human pulmonary adenocarcinoma.
  • Two of them showed downregulation of their expression in human lung adenocarcinoma.
  • Most of the lung adenocarcinoma cell lines showed suppressed expression of SAMD14 together with hypermethylation at the promoter region, although an immortalized bronchial epithelium cell line (PL16B) did not show hypermethylation and did express SAMD14.
  • Hypermethylation at the CpG site of the SAMD14 promoter region was detected frequently in early invasive adenocarcinoma (8/24, 33.3%) but not in in situ adenocarcinoma (0/7, 0%) or normal lung tissue (0/31, 0%).
  • Hypermethylation of the SAMD14 gene is a specific event in pulmonary adenocarcinogenesis and malignant progression.
  • [MeSH-major] Adenocarcinoma / genetics. DNA Methylation. Lung Neoplasms / genetics. Promoter Regions, Genetic / genetics. Tumor Suppressor Proteins / genetics

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  • (PMID = 18823374.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / KIF21A protein, human; 0 / Kif21a protein, mouse; 0 / Tumor Suppressor Proteins; EC 3.6.1.- / Kinesin
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55. Stinn W, Arts JH, Buettner A, Duistermaat E, Janssens K, Kuper CF, Haussmann HJ: Murine lung tumor response after exposure to cigarette mainstream smoke or its particulate and gas/vapor phase fractions. Toxicology; 2010 Sep 10;275(1-3):10-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Murine lung tumor response after exposure to cigarette mainstream smoke or its particulate and gas/vapor phase fractions.
  • In order to develop such a model, A/J and Swiss SWR/J mouse strains, with a genetic susceptibility to developing lung adenocarcinoma, were whole-body exposed to diluted cigarette mainstream smoke at 0, 120, and 240 mg total particulate matter per m(3) for 6h per day, 5 days per week.
  • After 5 months of smoke inhalation and an additional 4-month post-inhalation period, both mouse strains responded similarly: no increase in lung tumor multiplicity was seen at the end of the inhalation period; however, there was a concentration-dependent tumorigenic response at the end of the post-inhalation period (up to 2-fold beyond control) in mice exposed to the whole smoke or the particulate phase.
  • Tumors were characterized mainly as pulmonary adenomas.
  • In summary, these mouse strains responded to mainstream smoke inhalation with enhanced pulmonary adenoma formation.
  • [MeSH-major] Gases / adverse effects. Inhalation Exposure / adverse effects. Lung Neoplasms / pathology. Particulate Matter / adverse effects. Smoking / adverse effects. Tobacco Smoke Pollution / adverse effects

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  • [Copyright] (c) 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20594951.001).
  • [ISSN] 1879-3185
  • [Journal-full-title] Toxicology
  • [ISO-abbreviation] Toxicology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Gases; 0 / Particulate Matter; 0 / Tobacco Smoke Pollution
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56. Wang F, Li HM, Chen XF, Xie KC, Huang Q: Low dosage 5-fluorouracil increases the transfection efficiency of Ad/VEGF-A in mouse lung carcinoma cell line LA795 and inhibits tumor growth. Chin J Cancer; 2010 Jul;29(7):677-82
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  • [Title] Low dosage 5-fluorouracil increases the transfection efficiency of Ad/VEGF-A in mouse lung carcinoma cell line LA795 and inhibits tumor growth.
  • We used adenovirus vector to transfer small interfering RNA (siRNA) against vascular epithelium growth factor A (VEGF-A) molecules to mouse lung adenoma LA795 cells and used low dose of chemotherapeutic drugs to further elevate the infection efficiency of adenovirus vector in and therapeutic effect of RNAi on tumor cells.
  • [MeSH-major] Cell Proliferation. Fluorouracil / pharmacology. Lung Neoplasms / pathology. RNA, Small Interfering / genetics. Vascular Endothelial Growth Factor A / genetics

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  • (PMID = 20591220.001).
  • [ISSN] 1000-467X
  • [Journal-full-title] Chinese journal of cancer
  • [ISO-abbreviation] Chin J Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Vascular Endothelial Growth Factor A; U3P01618RT / Fluorouracil
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57. Shen J, Liu J, Xie Y, Diwan BA, Waalkes MP: Fetal onset of aberrant gene expression relevant to pulmonary carcinogenesis in lung adenocarcinoma development induced by in utero arsenic exposure. Toxicol Sci; 2007 Feb;95(2):313-20
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  • [Title] Fetal onset of aberrant gene expression relevant to pulmonary carcinogenesis in lung adenocarcinoma development induced by in utero arsenic exposure.
  • Arsenic is a human pulmonary carcinogen.
  • Our work indicates that in utero arsenic exposure in mice can induce or initiate lung cancer in female offspring.
  • To define early molecular changes, pregnant C3H mice were given 85 ppm arsenic in drinking water from days 8 to 18 of gestation and expression of selected genes in the fetal lung or in lung tumors developing in adults was examined.
  • Transplacental arsenic exposure increased estrogen receptor-alpha (ER-alpha) transcript and protein levels in the female fetal lung.
  • The insulin growth factor system, which can be influenced by ER and has been implicated in the pulmonary oncogenic process, was activated in fetal lung after gestational arsenic exposure.
  • In utero arsenic exposure also induced overexpression of alpha-fetoprotein, epidermal growth factor receptor, L-myc, and metallothionein-1 in fetal lung, all of which are associated with lung cancer.
  • Lung adenoma and adenocarcinoma from adult female mice exposed to arsenic in utero showed widespread, intense nuclear ER-alpha expression.
  • In contrast, normal adult lung and diethylnitrosamine-induced lung adenocarcinoma showed little evidence of ER-alpha expression.
  • Thus, transplacental arsenic exposure at a carcinogenic dose produced aberrant estrogen-linked pulmonary gene expression.
  • ER-alpha activation was specifically associated with arsenic-induced lung adenocarcinoma and adenoma but not with nitrosamine-induced lung tumors.
  • These data provide evidence that arsenic-induced aberrant ER signaling could disrupt early life stage genetic programing in the lung leading eventually to lung tumor formation much later in adulthood.

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  • [Cites] J Pathol. 2000 Feb;190(2):133-42 [10657010.001]
  • [Cites] Mol Cancer Ther. 2003 Nov;2(11):1243-55 [14617798.001]
  • [Cites] Toxicol Sci. 2004 Feb;77(2):249-57 [14691202.001]
  • [Cites] J Natl Cancer Inst. 2004 Mar 17;96(6):466-74 [15026472.001]
  • [Cites] Curr Oncol Rep. 2004 Jul;6(4):259-67 [15161576.001]
  • [Cites] Clin Lung Cancer. 2004 May;5(6):353-9 [15217534.001]
  • [Cites] Growth Horm IGF Res. 2004 Aug;14(4):261-9 [15231294.001]
  • [Cites] Toxicol Appl Pharmacol. 2004 Aug 1;198(3):366-76 [15276416.001]
  • [Cites] Toxicol Appl Pharmacol. 2004 Aug 1;198(3):394-404 [15276419.001]
  • [Cites] Carcinogenesis. 2004 Sep;25(9):1779-86 [15073043.001]
  • [Cites] Toxicol Appl Pharmacol. 2004 Sep 1;199(2):162-74 [15313588.001]
  • [Cites] Am J Pathol. 1998 Dec;153(6):1775-85 [9846968.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Jan 7;326(1):218-27 [15567174.001]
  • [Cites] Am J Respir Cell Mol Biol. 2005 Jan;32(1):65-71 [15514114.001]
  • [Cites] Exp Oncol. 2004 Dec;26(4):316-9 [15627066.001]
  • [Cites] J Soc Gynecol Investig. 2005 Jan;12(1):58-64 [15629674.001]
  • [Cites] Cancer Res. 2005 Feb 15;65(4):1459-70 [15735034.001]
  • [Cites] Endocr Relat Cancer. 2005 Mar;12(1):101-7 [15788642.001]
  • [Cites] Cancer Res. 2005 May 1;65(9):3796-805 [15867376.001]
  • [Cites] J Natl Cancer Inst. 2005 May 4;97(9):643-55 [15870435.001]
  • [Cites] J Clin Oncol. 2005 May 10;23(14):3212-8 [15886308.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jun 14;102(24):8644-9 [15937110.001]
  • [Cites] Toxicol Appl Pharmacol. 2005 Aug 15;206(3):288-98 [16039940.001]
  • [Cites] Cancer Res. 2005 Dec 15;65(24):11287-91 [16357134.001]
  • [Cites] Cancer Res. 2006 Feb 1;66(3):1337-45 [16452187.001]
  • [Cites] Environ Health Perspect. 2006 Mar;114(3):404-11 [16507464.001]
  • [Cites] Toxicol Sci. 2006 Jun;91(2):372-81 [16543296.001]
  • [Cites] Toxicology. 2006 Jul 5;224(1-2):147-55 [16753250.001]
  • [Cites] Environ Health Perspect. 2006 Aug;114(8):1293-6 [16882542.001]
  • [Cites] Carcinogenesis. 2004 Jan;25(1):133-41 [14514661.001]
  • [Cites] Mutat Res. 2003 Dec 10;533(1-2):37-65 [14643412.001]
  • [Cites] Toxicol Appl Pharmacol. 2006 Sep 15;215(3):295-305 [16712894.001]
  • [Cites] Cancer Lett. 2003 Jun 10;195(2):127-37 [12767520.001]
  • [Cites] Toxicol Appl Pharmacol. 2003 Jan 1;186(1):7-17 [12583988.001]
  • [Cites] Annu Rev Med. 2003;54:73-87 [12471176.001]
  • [Cites] Expert Rev Anticancer Ther. 2002 Dec;2(6):709-35 [12503217.001]
  • [Cites] Biochem Cell Biol. 2002;80(3):335-41 [12123286.001]
  • [Cites] Prostate. 2002 Aug 1;52(3):236-44 [12111698.001]
  • [Cites] Lung Cancer. 2002 May;36(2):125-32 [11955646.001]
  • [Cites] Pathol Int. 2002 Jan;52(1):46-53 [11940206.001]
  • [Cites] Mol Cell Endocrinol. 2002 Feb 25;188(1-2):125-40 [11911952.001]
  • [Cites] Toxicol Appl Pharmacol. 2001 May 1;172(3):249-61 [11312654.001]
  • [Cites] Toxicol Appl Pharmacol. 2000 Jul 1;166(1):24-35 [10873715.001]
  • [Cites] Environ Health Perspect. 2000 Jun;108 Suppl 3:573-94 [10852857.001]
  • (PMID = 17077188.001).
  • [ISSN] 1096-6080
  • [Journal-full-title] Toxicological sciences : an official journal of the Society of Toxicology
  • [ISO-abbreviation] Toxicol. Sci.
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / / NIH0011069698; United States / Intramural NIH HHS / / ; United States / PHS HHS / / NIH0011069698; United States / NCI NIH HHS / CA / N01CO12400; United States / NCI NIH HHS / CO / N01-CO-12400
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arsenites; 0 / Carcinogens, Environmental; 0 / Sodium Compounds; 48OVY2OC72 / sodium arsenite
  • [Other-IDs] NLM/ NIHMS33564; NLM/ PMC2692318
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58. Lucas da Silva LB, Ribeiro DA, Cury PM, Cordeiro JA, Bueno V: FTY720 treatment in experimentally urethane-induced lung tumors. J Exp Ther Oncol; 2008;7(1):9-15
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  • [Title] FTY720 treatment in experimentally urethane-induced lung tumors.
  • Lung adenoma was induced in mice by urethane injection followed by different periods of FTY720 administration in order to evaluate lung tumor development.
  • Twenty-four weeks after urethane administration mice were evaluated for leukocyte numbers in blood, lymphocytes in spleen, and lungs were evaluated for changes in histology and PCNA expression.
  • Lung nodules were present in higher numbers both in non treated (G1; 0.0-7.0) and FTY720 treated 8 weeks after urethane injection (G4; 0.0-6.0).
  • Therefore, our data suggest that FTY720 treatment in early periods after lung tumor induction is beneficial and impairs adenoma development.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / prevention & control. Anticarcinogenic Agents / pharmacology. Lung Neoplasms / prevention & control. Propylene Glycols / pharmacology. Sphingosine / analogs & derivatives

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  • (PMID = 18472638.001).
  • [ISSN] 1359-4117
  • [Journal-full-title] Journal of experimental therapeutics & oncology
  • [ISO-abbreviation] J. Exp. Ther. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Carcinogens; 0 / Propylene Glycols; 3IN71E75Z5 / Urethane; G926EC510T / Fingolimod Hydrochloride; NGZ37HRE42 / Sphingosine
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59. Sakiyama T, Kohno T, Mimaki S, Ohta T, Yanagitani N, Sobue T, Kunitoh H, Saito R, Shimizu K, Hirama C, Kimura J, Maeno G, Hirose H, Eguchi T, Saito D, Ohki M, Yokota J: Association of amino acid substitution polymorphisms in DNA repair genes TP53, POLI, REV1 and LIG4 with lung cancer risk. Int J Cancer; 2005 May 1;114(5):730-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association of amino acid substitution polymorphisms in DNA repair genes TP53, POLI, REV1 and LIG4 with lung cancer risk.
  • Single nucleotide polymorphisms (SNPs) were searched for in 36 genes involved in diverse DNA repair pathways, and 50 nonsynonymous (associated with amino acid changes) SNPs identified were assessed for associations with lung cancer risk by a case-control study consisting of 752 adenocarcinoma cases, 250 squamous cell carcinoma cases and 685 controls.
  • POLI is the human counterpart of PolI, a strong candidate for the Par2 (pulmonary adenoma resistance 2) gene responsible for adenoma/adenocarcinoma susceptibility in mice.
  • The present results suggest that these 4 SNPs function as genetic factors underlying lung cancer susceptibility by modulating activities to maintain the genome integrity of each individual.
  • [MeSH-major] Amino Acids / genetics. DNA Ligases / genetics. DNA Polymerase I / genetics. DNA Repair. Genes, p53. Lung Neoplasms / genetics. Nucleotidyltransferases / genetics. Polymorphism, Genetic

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  • [Copyright] 2004 Wiley-Liss, Inc.
  • (PMID = 15609317.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amino Acids; 0 / Nuclear Proteins; EC 2.7.7.- / DNA Polymerase I; EC 2.7.7.- / Nucleotidyltransferases; EC 2.7.7.- / REV1 protein, human; EC 6.5.1.- / DNA Ligases; EC 6.5.1.1 / DNA ligase (ATP)
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60. Conaway CC, Wang CX, Pittman B, Yang YM, Schwartz JE, Tian D, McIntee EJ, Hecht SS, Chung FL: Phenethyl isothiocyanate and sulforaphane and their N-acetylcysteine conjugates inhibit malignant progression of lung adenomas induced by tobacco carcinogens in A/J mice. Cancer Res; 2005 Sep 15;65(18):8548-57
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phenethyl isothiocyanate and sulforaphane and their N-acetylcysteine conjugates inhibit malignant progression of lung adenomas induced by tobacco carcinogens in A/J mice.
  • We have shown previously that naturally occurring isothiocyanates derived from cruciferous vegetables and their N-acetylcysteine conjugates inhibit lung adenoma formation induced by tobacco carcinogens in A/J mice at the post-initiation stage.
  • The tumor-inhibitory activity by these compounds is linked with activation of activator protein and induction of apoptosis in lung tissues, suggesting that these compounds may also inhibit the development of adenomas to adenocarcinomas in lung.
  • In this study, the chemopreventive activity of phenethyl isothiocyanate and sulforaphane and their N-acetylcysteine conjugates during progression of lung adenomas to malignant tumors was investigated in A/J mice.
  • Twenty weeks after the beginning of carcinogen administration, a total of 20 mice in the treatment groups were sacrificed with an average yield of 7.3 +/- 4.5 lung adenomas per mouse.
  • Four mice in each of the high-dose treatment groups were sacrificed during weeks 28 and 36 and the bioassay was terminated during week 42; lung tissues were harvested for histopathologic examination of tumors and for cell proliferation (proliferating cell nuclear antigen) and apoptosis (caspase-3) assays using immunohistochemical staining.
  • At the lower doses, phenethyl isothiocyanate and its N-acetylcysteine conjugate also inhibited the incidences of lung adenocarcinoma, however, the decreases were not statistically significant.
  • The lung tumor incidences in groups treated with sulforaphane-N-acetylcysteine in the diet were also significantly reduced to 11% or 16%.
  • Furthermore, the malignant lung tumor multiplicity was significantly reduced from 1.0 tumor/mouse in the carcinogen-treated control group to 0.3 in the sulforaphane low-dose group, 0.3 and 0.4 in the two sulforaphane-N-acetylcysteine groups, and 0.4 in the phenethyl isothiocyanate high-dose group.
  • Unlike lung adenocarcinomas, both incidences and multiplicities of lung adenomas were not much affected by treatment with isothiocyanates or their conjugates.
  • Immunohistochemical examination of the lung tumors from all time points indicated that significant reduction in proliferating cell nuclear antigen and induction of apoptosis (terminal nucleotidyl transferase-mediated nick end labeling and caspase-3) were observed in the isothiocyanate and isothiocyanate-N-acetylcysteine-treated groups that showed inhibition of the development of lung adenocarcinomas.
  • The results of the study provide a basis for future evaluation of the potential of phenethyl isothiocyanate and sulforaphane and their conjugates as chemopreventive agents in smokers and ex-smokers with early lung lesions.
  • [MeSH-major] Acetylcysteine / analogs & derivatives. Adenocarcinoma / prevention & control. Adenoma / drug therapy. Anticarcinogenic Agents / pharmacology. Isothiocyanates / pharmacology. Lung Neoplasms / prevention & control. Thiocyanates / pharmacology

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  • (PMID = 16166336.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA46535
  • [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 / Anticarcinogenic Agents; 0 / Carcinogens; 0 / Isothiocyanates; 0 / Nitrosamines; 0 / Thiocyanates; 3417WMA06D / Benzo(a)pyrene; 4478-93-7 / sulforafan; 64091-91-4 / 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone; 6U7TFK75KV / phenethyl isothiocyanate; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; WYQ7N0BPYC / Acetylcysteine
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