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1. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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  • (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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2. 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]
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  • (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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3. 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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  • [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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4. 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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  • [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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5. 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

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  • [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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6. 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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7. 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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8. 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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9. 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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  • [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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10. 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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11. 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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12. Magalhães E, Eugénio L, Bernardo J, Carvalho L, Antunes M: [Pleomorphic adenoma of the trachea. Case report]. Rev Port Pneumol; 2006 Mar-Apr;12(2):177-84

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  • [Title] [Pleomorphic adenoma of the trachea. Case report].
  • [Transliterated title] Adenoma pleomórfico da traqueia. Caso clínico.
  • The authors present a case of a pleomorphic adenoma of the trachea, diagnosed during the clinical evaluation of a suspected COPD or lung cancer in a heavy smoker patient with a positive family history of oncologic diseases.
  • [MeSH-major] Adenoma, Pleomorphic / surgery. Tracheal Neoplasms / surgery

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  • (PMID = 16804633.001).
  • [ISSN] 0873-2159
  • [Journal-full-title] Revista portuguesa de pneumologia
  • [ISO-abbreviation] Rev Port Pneumol
  • [Language] por
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Portugal
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13. 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


14. 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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15. 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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16. 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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17. Herrejón A, Cervera A, Maciá M, Ferrer R, Blanquer R: [Bronchioloalveolar adenoma associated with bronchiolitis obliterans and leishmaniasis with lung involvement in acquired immunodeficiency syndrome]. Arch Bronconeumol; 2005 Apr;41(4):233-5
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  • [Title] [Bronchioloalveolar adenoma associated with bronchiolitis obliterans and leishmaniasis with lung involvement in acquired immunodeficiency syndrome].
  • [Transliterated title] Adenoma bronquioloalveolar asociado a bronquiolitis obliterante y leishmaniasis pulmonar en el sida.
  • Visceral leishmaniasis is not unusual in patients with acquired immunodeficiency syndrome (AIDS), but lung infiltration is uncommon.
  • Leishmaniasis involving the lung often manifests as interstitial pneumonitis.
  • In addition, the transbronchial biopsy findings were consistent with a diagnosis of bronchioloalveolar adenoma with radiographic evidence of multiple nodules.
  • [MeSH-major] Acquired Immunodeficiency Syndrome / complications. Adenomatosis, Pulmonary / diagnosis. Bronchiolitis Obliterans / diagnosis. Leishmaniasis / diagnosis. Lung Diseases, Parasitic / diagnosis


18. 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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19. 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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20. 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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21. 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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  • [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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22. 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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23. Saito EH, de Aaraujo LR, Carneiro LH, de Oliveira Neto AA, Correa JC, Teixeira LS: Alveolar adenoma. J Bras Pneumol; 2006 May-Jun;32(3):267-9
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  • [Title] Alveolar adenoma.
  • Alveolar adenoma is a rare benign neoplasm of the lungs, and very few cases have been described in the literature.
  • Patients with alveolar adenoma are frequently asymptomatic and are diagnosed through the accidental discovery of a singular, well-delineated nodule on a routine chest X-ray.
  • [MeSH-major] Adenoma / diagnosis. Lung Neoplasms / diagnosis

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  • (PMID = 17273617.001).
  • [ISSN] 1806-3756
  • [Journal-full-title] Jornal brasileiro de pneumologia : publicaça̋o oficial da Sociedade Brasileira de Pneumologia e Tisilogia
  • [ISO-abbreviation] J Bras Pneumol
  • [Language] eng; por
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Brazil
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24. 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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25. Kuwahara M, Nagafuchi M, Rikimaru T, Iwasaki A, Shirakusa T: Pulmonary papillary adenoma. Gen Thorac Cardiovasc Surg; 2010 Oct;58(10):542-5
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  • [Title] Pulmonary papillary adenoma.
  • We present a rare case of solitary pulmonary papillary adenoma.
  • The histological features were consistent with pulmonary papillary adenoma.
  • Only 20 cases of pulmonary papillary adenoma have been reported in the literature.
  • [MeSH-major] Adenoma / pathology. Lung Neoplasms / pathology. Solitary Pulmonary Nodule / pathology

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  • (PMID = 20941571.001).
  • [ISSN] 1863-6713
  • [Journal-full-title] General thoracic and cardiovascular surgery
  • [ISO-abbreviation] Gen Thorac Cardiovasc Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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26. 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
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  • [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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27. Nouraei SA, Ferguson MS, Clarke PM, Sandison A, Sandhu GS, Michaels L, Rhys-Evans P: Metastasizing pleomorphic salivary adenoma. Arch Otolaryngol Head Neck Surg; 2006 Jul;132(7):788-93
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  • [Title] Metastasizing pleomorphic salivary adenoma.
  • OBJECTIVE: To address questions about the etiology, behavior, optimal treatment, and prognosis of metastasizing pleomorphic adenoma (MPA), we undertook a review of the literature (1953-2005) and constructed a virtual series of all identified cases of MPA, metastatic lesions that are very occasionally identified in patients with a history of pleomorphic salivary adenoma and, on detailed pathological evaluation, found to exhibit all the histological hallmarks of the preceding benign lesions.
  • There was an overwhelming history of incomplete surgery for pleomorphic salivary adenoma.
  • Bone was the most common site for metastases (45%), followed by the head and neck (43%) and lung (36%).
  • [MeSH-major] Adenoma, Pleomorphic / pathology. Salivary Gland Neoplasms / pathology

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  • (PMID = 16847191.001).
  • [ISSN] 0886-4470
  • [Journal-full-title] Archives of otolaryngology--head & neck surgery
  • [ISO-abbreviation] Arch. Otolaryngol. Head Neck Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis
  • [Publication-country] United States
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28. 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


29. Nakamura H, Hirata T, Taguchi M, Kitamura H: Ground-glass opacities showing an adenoma-to-carcinoma sequence in the lung. Gen Thorac Cardiovasc Surg; 2008 Aug;56(8):421-3
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  • [Title] Ground-glass opacities showing an adenoma-to-carcinoma sequence in the lung.
  • We encountered a patient with three left lower lobe pulmonary tumors evident as discrete ground-glass opacities by computed tomography.
  • This case supports the hypothesis of an adenoma-to-carcinoma sequence in the lung, as the coexisting lesions represented sequential adenocarcinoma progression from a precancerous lesion, AAH, to very early-stage adenocarcinoma, noninvasive BAC.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / pathology. Cell Transformation, Neoplastic / pathology. Lung Neoplasms / pathology
  • [MeSH-minor] Adenoma / pathology. Adenoma / radiography. Aged. Female. Humans. Hyperplasia / pathology. Hyperplasia / radiography. Precancerous Conditions / pathology. Precancerous Conditions / radiography. Tomography, X-Ray Computed

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  • (PMID = 18696210.001).
  • [ISSN] 1863-6705
  • [Journal-full-title] General thoracic and cardiovascular surgery
  • [ISO-abbreviation] Gen Thorac Cardiovasc Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
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30. 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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31. 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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32. Stojsić J, Milenković B, Radojicić J, Percinkovski M: [Alveolar adenoma -- a rare lung tumour]. Srp Arh Celok Lek; 2007 Jul-Aug;135(7-8):461-4
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  • [Title] [Alveolar adenoma -- a rare lung tumour].
  • INTRODUCTION: Alveolar adenoma belongs to the group of benign epithelial tumours.
  • Histogenesis of alveolar adenoma is a combination of proliferation of alveolar pneumocytes and fibrous tissue originating from septal mesenchyma.
  • Tumourous nodule had a multicystic appearance and histologically, histochemically and immunohistochemically, an alveolar adenoma was estimated.
  • CONCLUSION: Alveolar adenoma is a rare benign lung tumour, most frequently presented as a solitary pulmonary nodule.
  • It is necessary to take into consideration alveolar adenoma, too, when a solitary pulmonary nodule is diagnosed.
  • [MeSH-major] Adenoma / diagnosis. Lung Neoplasms / diagnosis. Solitary Pulmonary Nodule / diagnosis

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  • (PMID = 17929540.001).
  • [ISSN] 0370-8179
  • [Journal-full-title] Srpski arhiv za celokupno lekarstvo
  • [ISO-abbreviation] Srp Arh Celok Lek
  • [Language] srp
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Serbia and Montenegro
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33. Manucha V, Ioffe OB: Metastasizing pleomorphic adenoma of the salivary gland. Arch Pathol Lab Med; 2008 Sep;132(9):1445-7
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  • [Title] Metastasizing pleomorphic adenoma of the salivary gland.
  • Metastasizing pleomorphic adenoma of salivary glands is a group of rare tumors that are histologically identical to benign mixed tumors and that inexplicably metastasize.
  • A review of the literature revealed that it usually occurs after multiple local recurrences, and the interval between diagnosis of primary pleomorphic adenoma and metastases ranges between 3 and 52 years.
  • The most common site for metastasis is bone, followed by the head and neck and lung.
  • [MeSH-major] Adenoma, Pleomorphic / pathology. Neoplasm Invasiveness / pathology. Salivary Gland Neoplasms / pathology. Salivary Gland Neoplasms / secondary

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  • (PMID = 18788859.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 25
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34. Sit KY, Chui WH, Wang E, Chiu SW: Multiple pulmonary metastases from benign pleomorphic adenoma. Asian Cardiovasc Thorac Ann; 2008 Jan;16(1):62-4
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  • [Title] Multiple pulmonary metastases from benign pleomorphic adenoma.
  • Metastasizing pleomorphic adenoma is a rare condition of metastasis from a histologically benign salivary gland tumor.
  • We report a case of metastasizing pleomorphic adenoma presenting with multiple bilateral lung metastases, and discuss the clinical aspects of this disease.
  • [MeSH-major] Adenoma, Pleomorphic / pathology. Incidental Findings. Lung Neoplasms / secondary. Neoplasm Recurrence, Local. Salivary Gland Neoplasms / pathology

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  • (PMID = 18245710.001).
  • [ISSN] 1816-5370
  • [Journal-full-title] Asian cardiovascular & thoracic annals
  • [ISO-abbreviation] Asian Cardiovasc Thorac Ann
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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35. Leonetti JP, Marzo SJ, Petruzzelli GJ, Herr B: Recurrent pleomorphic adenoma of the parotid gland. Otolaryngol Head Neck Surg; 2005 Sep;133(3):319-22
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  • [Title] Recurrent pleomorphic adenoma of the parotid gland.
  • OBJECTIVES: To assess the long-term results in the management of 42 patients with recurrent pleomorphic adenoma of the parotid gland.
  • STUDY DESIGN: A retrospective analysis of 42 patients who underwent parotidectomy for recurrent pleomorphic adenoma was performed to study presenting clinicoradiographic features, surgical technique, facial nerve management, and the long-term risk of recurrence.
  • The 2 patients with malignant transformation died of disseminated lung and bone metastasis.
  • Total parotidectomy or subtotal petrosectomy with facial nerve resection in selected cases may reduce the risk of multiple episodes of pleomorphic adenoma recurrence.
  • Two of 42 patients were found to have carcinoma ex-pleomorphic adenoma, both of these patients underwent prior radiotherapy, and both died of metastatic disease.
  • [MeSH-major] Adenoma, Pleomorphic / pathology. Parotid Neoplasms / pathology

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  • (PMID = 16143173.001).
  • [ISSN] 0194-5998
  • [Journal-full-title] Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery
  • [ISO-abbreviation] Otolaryngol Head Neck Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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36. Peters U, Chatterjee N, Hayes RB, Schoen RE, Wang Y, Chanock SJ, Foster CB: Variation in the selenoenzyme genes and risk of advanced distal colorectal adenoma. Cancer Epidemiol Biomarkers Prev; 2008 May;17(5):1144-54
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  • [Title] Variation in the selenoenzyme genes and risk of advanced distal colorectal adenoma.
  • We therefore investigated whether genetic variants in selenoenzymes abundantly expressed in the colon are associated with advanced colorectal adenoma, a cancer precursor.
  • METHODS: Cases with a left-sided advanced adenoma (n = 772) and matched controls (n = 777) screen negative for polyps based on sigmoidoscopy examination were randomly selected from participants in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial.
  • RESULTS: Four variants in SEPP1 were significantly associated with advanced adenoma risk.
  • Three SNPs located in the 3' region of SEPP1, which is overlapping with the promoter region of an antisense transcript, were significantly associated with adenoma risk: homozygotes at two SEPP1 loci (31,174 bp 3' of STP A>G and 43,881 bp 3' of STP G>A) were associated with increased adenoma risk [odds ratio (OR), 1.48; 95% confidence interval (95% CI), 1.00-2.19 and OR, 1.53; 95% CI, 1.05-2.22, respectively] and the variant SEPP1 44,321 bp 3' of STP C>T was associated with a reduced adenoma risk (CT versus CC OR, 0.85; 95% CI, 0.63-1.15).
  • Furthermore, we observed a significant 80% reduction for advanced colorectal adenoma risk for carriers of the variant allele at TXNRD1 IVS1-181C>G (OR, 0.20; 95% CI, 0.07-0.55; P trend = 0.004).
  • Consistent with the individual SNP results, we observed a significant overall association with adenoma risk for SEPP1 and TXNRD1 (global P = 0.02 and 0.008, respectively) but not for the four GPX genes.
  • CONCLUSION: Our study suggests that genetic variants at or near the SEPP1 and TXNRD1 loci may be associated with advanced colorectal adenoma.
  • [MeSH-major] Adenoma / enzymology. Adenoma / genetics. Colorectal Neoplasms / enzymology. Colorectal Neoplasms / genetics. Genetic Variation. Selenium

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  • (PMID = 18483336.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Selenoprotein P; EC 1.11.1.- / GPX2 protein, human; EC 1.11.1.- / GPX3 protein, human; EC 1.11.1.- / glutathione peroxidase GPX1; EC 1.11.1.12 / phospholipid-hydroperoxide glutathione peroxidase; EC 1.11.1.9 / Glutathione Peroxidase; EC 1.8.1.9 / TXNRD1 protein, human; EC 1.8.1.9 / Thioredoxin Reductase 1; H6241UJ22B / Selenium
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37. 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


38. 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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  • (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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39. 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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40. Huang WY, Chatterjee N, Chanock S, Dean M, Yeager M, Schoen RE, Hou LF, Berndt SI, Yadavalli S, Johnson CC, Hayes RB: Microsomal epoxide hydrolase polymorphisms and risk for advanced colorectal adenoma. Cancer Epidemiol Biomarkers Prev; 2005 Jan;14(1):152-7
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  • [Title] Microsomal epoxide hydrolase polymorphisms and risk for advanced colorectal adenoma.
  • Cigarette smoking is a risk factor for colorectal adenoma, a precursor of colorectal cancer.
  • Among participants randomized to the screening arm of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial, we evaluated risks for advanced adenoma in relation to cigarette use and these two EPHX1 variants.
  • We compared 772 cases with advanced adenoma (adenoma >/=1 cm or containing high-grade dysplasia or villous, including tubulovillous, elements) of the distal colon (left-sided, descending colon and sigmoid or rectum) to 777 gender- and age-matched controls who were screen-negative for left-sided adenoma.
  • Compared to those with homozygous genotypes predicting low EPHX1 activity, advanced adenoma risks tended to be elevated for carriers of (113)TyrTyr [odds ratios (OR), 1.5; 95% confidence intervals (CI), 1.0-2.2] and (139)ArgArg (OR, 1.4; 95% CI, 0.8-2.5) and for subjects who carried a greater number of the alleles ((113)Tyr or (139)Arg) associated with high predicted enzymatic activity (P(trend) = 0.03).
  • In conclusion, EPHX1 variants at codon 113 and 139 associated with high predicted enzymatic activity appear to increase risk for colorectal adenoma, particularly among recent and current smokers.
  • [MeSH-major] Adenoma / genetics. Colorectal Neoplasms / genetics. Epoxide Hydrolases / genetics. Polymorphism, Genetic. Smoking / adverse effects

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  • (PMID = 15668489.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.3.2.- / Epoxide Hydrolases
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41. 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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42. 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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43. 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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44. 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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  • (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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45. Hoellig A, Niehusmann P, Flacke S, Kristof RA: Metastasis to pituitary adenoma: case report and review of the literature. Cent Eur Neurosurg; 2009 Aug;70(3):149-53
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  • [Title] Metastasis to pituitary adenoma: case report and review of the literature.
  • We present a rare case of a metastasis to a pituitary adenoma and review 14 cases published in the literature to date.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / pathology. ACTH-Secreting Pituitary Adenoma / secondary. Pituitary Neoplasms / pathology. Pituitary Neoplasms / secondary
  • [MeSH-minor] Aged. Antineoplastic Agents / therapeutic use. Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Fatal Outcome. Humans. Lung Neoplasms / drug therapy. Lung Neoplasms / pathology. Magnetic Resonance Imaging. Male. Neoplasm Metastasis / pathology. Oculomotor Nerve / pathology. Ophthalmoplegia / etiology. Small Cell Lung Carcinoma / pathology. Tomography, X-Ray Computed

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  • [Copyright] Georg Thieme Verlag KG Stuttgart New York.
  • (PMID = 19701874.001).
  • [ISSN] 1868-4912
  • [Journal-full-title] Central European neurosurgery
  • [ISO-abbreviation] Cent Eur Neurosurg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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46. 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
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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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47. Ilhan HD, Oner FH, Sarioglu S, Lebe B, Saatci AO: Bilateral choroidal metastasis from carcinoma ex pleomorphic adenoma of the parotid gland. Clin Exp Ophthalmol; 2005 Feb;33(1):70-2
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  • [Title] Bilateral choroidal metastasis from carcinoma ex pleomorphic adenoma of the parotid gland.
  • The histological, clinical and angiographic findings are reported of a 34-year-old man with bilateral visual loss who had left parotidectomy with subsequent radiotherapy due to carcinoma ex pleomorphic adenoma of the parotid gland 1 year before.
  • At the time of ocular diagnosis, lung, pleura and pharynx metastases had recently been revealed.
  • [MeSH-major] Adenocarcinoma / secondary. Adenoma, Pleomorphic / pathology. Choroid Neoplasms / secondary. Parotid Neoplasms / pathology

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  • (PMID = 15670083.001).
  • [ISSN] 1442-6404
  • [Journal-full-title] Clinical & experimental ophthalmology
  • [ISO-abbreviation] Clin. Experiment. Ophthalmol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Coloring Agents; IX6J1063HV / Indocyanine Green
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48. 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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49. Moslehi R, Chatterjee N, Church TR, Chen J, Yeager M, Weissfeld J, Hein DW, Hayes RB: Cigarette smoking, N-acetyltransferase genes and the risk of advanced colorectal adenoma. Pharmacogenomics; 2006 Sep;7(6):819-29
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  • [Title] Cigarette smoking, N-acetyltransferase genes and the risk of advanced colorectal adenoma.
  • BACKGROUND: Cigarette use is associated with greater risk for colorectal adenoma, a colorectal cancer precursor.
  • METHODS: In the Prostate, Lung, Colorectal and Ovarian (PLCO) cancer screening trial, we compared NAT1 and NAT2 gene variant distributions for 772 cases with left-sided advanced adenoma and 777 gender and age-matched controls.
  • RESULTS: Risks for advanced colorectal adenoma were significantly increased among recent smokers (current smokers or those who quit less than 10 years ago) (odds ratio [OR] = 2.3, 95% confidence interval [CI]: 1.7-3.1) and among those who smoked more than 20 cigarettes per day (OR = 1.7, 95% CI: 1.3-2.2), compared with nonsmokers.
  • CONCLUSIONS: Our study indicated that NAT2 gene variants associated with a slow acetylator phenotype were more susceptible to the effects of tobacco smoking with respect to adenoma risk, providing leads for disease prevention.

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  • (PMID = 16981843.001).
  • [ISSN] 1462-2416
  • [Journal-full-title] Pharmacogenomics
  • [ISO-abbreviation] Pharmacogenomics
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-34627; United States / NCI NIH HHS / CA / CA034627-21; United States / Intramural NIH HHS / / ; United States / NCI NIH HHS / CA / R01 CA034627; United States / NCI NIH HHS / CA / R01 CA034627-21
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Isoenzymes; EC 2.3.1.5 / Arylamine N-Acetyltransferase; EC 2.3.1.5 / N-acetyltransferase 1; EC 2.3.1.5 / NAT2 protein, human
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50. Tarakji B, Nassani MZ, Sloan P: Immunohistochemical expression of estrogens and progesterone receptors in carcinoma ex pleomorphic adenoma-undifferentiated and adenocarcinoma types. Med Oral Patol Oral Cir Bucal; 2010 May;15(3):e432-6
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  • [Title] Immunohistochemical expression of estrogens and progesterone receptors in carcinoma ex pleomorphic adenoma-undifferentiated and adenocarcinoma types.
  • This type of cancer develops in the minor and the major salivary glands, and it sometimes metastasizes to other organs, particularly the lung.
  • OBJECTIVE: Our study aimed to characterize alteration in the immunohistochemical expression of oestrogens receptor and progesterone receptor in the tumour cells of carcinoma arising in pleomorphic adenoma.
  • STUDY DESIGN: 27 cases of carcinoma arising in pleomorphic adenoma (undifferentiated and adenocarcinoma types) were examined.
  • CONCLUSION: Our data suggest that carcinomas arising in pleomorphic adenoma were not dependent on endocrine function.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenoma, Pleomorphic / metabolism. Neoplasms, Multiple Primary / metabolism. Receptors, Estrogen / biosynthesis. Receptors, Progesterone / biosynthesis. Salivary Gland Neoplasms / metabolism

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  • (PMID = 20038908.001).
  • [ISSN] 1698-6946
  • [Journal-full-title] Medicina oral, patología oral y cirugía bucal
  • [ISO-abbreviation] Med Oral Patol Oral Cir Bucal
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Receptors, Estrogen; 0 / Receptors, Progesterone
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51. Pinsky PF, Schoen RE, Weissfeld JL, Church T, Yokochi LA, Doria-Rose VP, Prorok P: The yield of surveillance colonoscopy by adenoma history and time to examination. Clin Gastroenterol Hepatol; 2009 Jan;7(1):86-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The yield of surveillance colonoscopy by adenoma history and time to examination.
  • METHODS: A sample of subjects in the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial with abnormal flexible sigmoidoscopy and follow-up colonoscopy were queried about subsequent surveillance colonoscopy over a 10-year period.
  • Subjects with advanced adenomas, nonadvanced adenoma, nonadenomatous polyps, and no polyps at baseline were included.
  • RESULTS: At the first surveillance, 10.5% had advanced adenoma and 37% had any adenoma in the advanced adenoma group (n = 1057), compared with rates of 6.8% and 32% (nonadvanced adenoma: n = 765), 4.9% and 22% (nonadenomatous polyps: n = 658), and 3.1% and 16% (no polyps: n = 127) (P < .0001, linear trend test).
  • Mean (SD) time intervals (years) from baseline colonoscopy to first surveillance were 3.4 (2.0) for advanced adenoma, 4.3 (2.0) for nonadvanced adenoma, 4.5 (2.0) for nonadenomatous polyps, and 4.7 (2.0) for no polyps.
  • There were no increasing (or decreasing) trends in the observed rate of advanced adenoma or any adenoma with time to the initial surveillance examination in any baseline group.
  • Among subjects with a second surveillance examination, adenoma findings at both baseline and first surveillance influenced the rates of advanced adenoma and any adenoma at second surveillance.
  • The lack of association between recurrence rates and time to surveillance suggests limitations in our understanding of the biology of adenoma development.
  • [MeSH-major] Adenoma / diagnosis. Adenoma / pathology. Colonic Neoplasms / diagnosis. Colonic Neoplasms / pathology. Colonoscopy. Mass Screening / methods

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  • (PMID = 18829395.001).
  • [ISSN] 1542-7714
  • [Journal-full-title] Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association
  • [ISO-abbreviation] Clin. Gastroenterol. Hepatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
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52. Gong Z, Bostick RM, Xie D, Hurley TG, Deng Z, Dixon DA, Zhang J, Hebert JR: Genetic polymorphisms in the cyclooxygenase-1 and cyclooxygenase-2 genes and risk of colorectal adenoma. Int J Colorectal Dis; 2009 Jun;24(6):647-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic polymorphisms in the cyclooxygenase-1 and cyclooxygenase-2 genes and risk of colorectal adenoma.
  • MATERIALS AND METHODS: In a community-, colonoscopy-based case-control study with 162 incident, sporadic colorectal adenoma cases and 211 controls, we investigated associations of two promoter polymorphisms (-842 A > G in COX1 and -765 G > C in COX2) and two polymorphisms in the 3'-UTR of COX2 (8473 T > C and 9850 A > G) with risk of adenomas.
  • Multiple logistic regression models were used to estimate odds ratios (OR) and 95% confidence intervals (CI) of colorectal adenoma after adjusting for potential confounders.
  • CONCLUSION: These results suggest that the C allele of COX2 8473 T > C polymorphism may interact with NSAIDs to reduce risk for colorectal adenoma.

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  • (PMID = 19205707.001).
  • [ISSN] 1432-1262
  • [Journal-full-title] International journal of colorectal disease
  • [ISO-abbreviation] Int J Colorectal Dis
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01CA-51932; United States / NCRR NIH HHS / RR / P20 RR017698; United States / NCRR NIH HHS / RR / RR017698; United States / NCI NIH HHS / CA / R01 CA134609; United States / NCI NIH HHS / CA / U01 CA114601; United States / NCI NIH HHS / CA / 1 U01 CA114601-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] EC 1.14.99.1 / Cyclooxygenase 1; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS1 protein, human; EC 1.14.99.1 / PTGS2 protein, human
  • [Other-IDs] NLM/ NIHMS377403; NLM/ PMC3461962
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53. Hou L, Chatterjee N, Huang WY, Baccarelli A, Yadavalli S, Yeager M, Bresalier RS, Chanock SJ, Caporaso NE, Ji BT, Weissfeld JL, Hayes RB: CYP1A1 Val462 and NQO1 Ser187 polymorphisms, cigarette use, and risk for colorectal adenoma. Carcinogenesis; 2005 Jun;26(6):1122-8
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  • [Title] CYP1A1 Val462 and NQO1 Ser187 polymorphisms, cigarette use, and risk for colorectal adenoma.
  • Cigarette use is a risk factor for colorectal adenoma, a known precursor of colorectal cancer.
  • We investigated the association of cigarette smoking with risk for advanced colorectal adenoma in relation to the CYP1A1 Val(462) and NQO1 Ser(187) polymorphic variants.
  • Subjects were 725 non-Hispanic Caucasian cases with advanced colorectal adenoma of the distal colon (descending colon, sigmoid and rectum) and 729 gender- and ethnicity-matched controls, randomly selected from participants in the prostate, lung, colorectal and ovarian cancer screening trial.
  • Subjects carrying either CYP1A1 Val(462) or NQO1 Ser(187) alleles were weakly associated with risk of colorectal adenoma; however, subjects carrying both CYP1A1 Val(462) and NQO1 Ser(187) alleles showed increased risks (OR = 2.2, 95% CI = 1.1-4.5), particularly among recent (including current) (OR = 17.4, 95% CI = 3.8-79.8, P for interaction = 0.02) and heavy cigarette smokers (>20 cigarettes/day) (OR = 21.1, 95% CI = 3.9-114.4, P for interaction = 0.03) compared with non-smokers who did not carry either of these variants.
  • In analysis of adenoma subtypes, the combined gene variants were most strongly associated with the presence of multiple adenoma (P = 0.002).
  • In summary, joint carriage of CYP1A1 Val(462) and NQO1 Ser(187) alleles, particularly in smokers, was related to colorectal adenoma risk, with a propensity for formation of multiple lesions.
  • [MeSH-major] Adenoma / genetics. Colorectal Neoplasms / genetics. Cytochrome P-450 CYP1A1 / genetics. NAD(P)H Dehydrogenase (Quinone) / genetics. Polymorphism, Genetic. Smoking / adverse effects

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  • (PMID = 15731166.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.14.14.1 / Cytochrome P-450 CYP1A1; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human
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54. Berndt SI, Huang WY, Fallin MD, Helzlsouer KJ, Platz EA, Weissfeld JL, Church TR, Welch R, Chanock SJ, Hayes RB: Genetic variation in base excision repair genes and the prevalence of advanced colorectal adenoma. Cancer Res; 2007 Feb 1;67(3):1395-404
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  • [Title] Genetic variation in base excision repair genes and the prevalence of advanced colorectal adenoma.
  • To examine the relationship between genetic variation in BER genes and colorectal adenoma risk, we conducted a case-control study of 767 cases of advanced colorectal adenoma and 773 controls from the baseline screening exam of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial.
  • Cases included participants diagnosed with advanced left-sided adenoma, and controls were subjects without evidence of a left-sided polyp by sigmoidoscopy, frequency-matched to cases on race and gender.
  • Twenty single nucleotide polymorphisms were genotyped in four BER genes (APEX1, PARP1, POLB, and XRCC1), and conditional logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (95% CI) for the association with colorectal adenoma.
  • The APEX1 51H variant was associated with a borderline significant decreased risk of colorectal adenoma (OR, 0.66; 95% CI, 0.44-1.00), and the XRCC1 399Q variant was inversely associated with risk among Caucasians (OR, 0.80; 95% CI, 0.64-0.99).
  • Homozygotes at two PARP1 loci (A284A and IVS13+118G>A) were also associated with a decreased risk of colorectal adenoma compared with wild-type carriers (OR, 0.70; 95% CI, 0.49-0.98 for both), which was restricted to advanced adenomas displaying histologically aggressive characteristics (OR, 0.51; 95% CI, 0.33-0.78, P = 0.002 for PARP1 A284A).
  • This study suggests that polymorphisms in APEX1, XRCC1, and PARP1 may be associated with advanced colorectal adenoma.

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  • (PMID = 17283177.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Intramural
  • [Publication-country] United States
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55. Ricchetti T, Paci M, Cavazza A, Ferrari G, Annessi V, De Franco S, Sgarbi G: A case of metastatic epithelioid angiosarcoma in the lamina propria of a sigmoid tubulovillous adenoma. Tumori; 2005 Mar-Apr;91(2):210-2

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  • [Title] A case of metastatic epithelioid angiosarcoma in the lamina propria of a sigmoid tubulovillous adenoma.
  • It is generally a secondary tumor and the preferred sites of such metastases are the heart, pericardium, lung, breast, liver, spleen, bone, and brain.
  • In rare cases the lung has been described as the primary site.
  • We report a case of epithelioid angiosarcoma with multiple bilateral lung infiltration, bone metastasis, and metastasis of the lamina propria of a tubulovillous adenoma of the colon.
  • [MeSH-major] Adenoma / pathology. Basement Membrane / pathology. Epithelioid Cells / pathology. Hemangiosarcoma / pathology. Hemangiosarcoma / secretion. Sigmoid Neoplasms / pathology

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  • (PMID = 15948556.001).
  • [ISSN] 0300-8916
  • [Journal-full-title] Tumori
  • [ISO-abbreviation] Tumori
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD31
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56. 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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57. Gunter MJ, Hayes RB, Chatterjee N, Yeager M, Welch R, Schoen RE, Yakochi L, Schatzkin A, Peters U: Insulin resistance-related genes and advanced left-sided colorectal adenoma. Cancer Epidemiol Biomarkers Prev; 2007 Apr;16(4):703-8
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  • [Title] Insulin resistance-related genes and advanced left-sided colorectal adenoma.
  • METHODS: We investigated whether single nucleotide polymorphisms (SNP) in the INS, INSR, IRS1, and IRS2 genes are associated with risk of advanced left-sided colorectal adenoma, a cancer precursor.
  • We analyzed 20 SNPs in a largely Caucasian study population comprising 766 cases with advanced adenomas of the distal colon and 771 controls, all of whom had undergone flexible sigmoidoscopy as part of the screening arm of the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial.
  • RESULTS: Overall, we found limited evidence for a role of gene variants of the insulin signaling pathway and prevalence of advanced colorectal adenoma.
  • We observed a statistically significant interaction between INSR genotypes and body mass index (BMI) with colorectal adenoma prevalence (P value for global test = 0.003) and suggestion of an interaction between INSR genotypes and glycemic load (P value for global test = 0.06); however, exploration of the interaction of BMI and glycemic load with the individual SNPs in INSR did not suggest a single SNP that may explain the significance of these global tests of interaction and did not yield any consistent patterns.
  • CONCLUSION: These findings do not provide strong evidence for associations between polymorphic variation in genes of the insulin signaling pathway and advanced left-sided colorectal adenoma.
  • Evidence for interaction between INSR variants and BMI and glycemic load for risk of advanced left-sided colorectal adenoma requires independent confirmation, and genotyping of INSR across a broader region and at greater density may be necessary to fully elucidate the nature of these interactions.

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  • (PMID = 17416760.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Insulin
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58. 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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  • [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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59. 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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60. Ali IU, Luke BT, Dean M, Greenwald P: Allellic variants in regulatory regions of cyclooxygenase-2: association with advanced colorectal adenoma. Br J Cancer; 2005 Oct 17;93(8):953-9
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  • [Title] Allellic variants in regulatory regions of cyclooxygenase-2: association with advanced colorectal adenoma.
  • In a nested case-control study, four polymorphisms in the Cox-2 gene (two in the promoter, -663 insertion/deletion, GT/(GT) and -798 A/G; one in intron 5-5229, T/G; one in 3'untranslated region (UTR)-8494, T/C) were genotyped in 726 cases of colorectal adenomas and 729 age- and gender-matched controls in the prostate, lung, colorectal, and ovarian (PLCO) cancer screening trial.
  • There was no significant association between the Cox-2 polymorphisms and adenoma development in the overall population.
  • However, in males, the relatively rare heterozygous genotype GT/(GT) at -663 in the promoter and the variant homozygous genotype G/G at intron 5-5229 appeared to have inverse associations (odds ratio (OR)=0.59, confidence interval (CI): 0.34-1.02 and OR=0.48, CI: 0.24-0.99, respectively), whereas the heterozygous genotype T/C at 3'UTR-8494 had a positive association (OR=1.31, CI: 1.01-1.71) with adenoma development.
  • Furthermore, the haplotype carrying the risk-conferring 3'UTR-8494 variant was associated with a 35% increase in the odds for adenoma incidence in males (OR=1.35, CI: 1.07-1.70), but the one with a risk allele at 3'UTR-8494 and a protective allele at intron 5-5229 had no effect on adenoma development (OR=0.85, CI: 0.66-1.09).
  • Gender-related differences in adenoma risk were also noted with tobacco usage and protective effects of NSAIDs.

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  • (PMID = 16205694.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / N01CO12400; United States / NCI NIH HHS / CO / N01-CO-12400; United States / NCI NIH HHS / BC / Z01 BC005652-15
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Other-IDs] NLM/ NIHMS8260; NLM/ PMC1369968
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61. Moore LE, Huang WY, Chatterjee N, Gunter M, Chanock S, Yeager M, Welch B, Pinsky P, Weissfeld J, Hayes RB: GSTM1, GSTT1, and GSTP1 polymorphisms and risk of advanced colorectal adenoma. Cancer Epidemiol Biomarkers Prev; 2005 Jul;14(7):1823-7
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  • [Title] GSTM1, GSTT1, and GSTP1 polymorphisms and risk of advanced colorectal adenoma.
  • Cigarette smoking is a risk factor for colon adenoma.
  • We examined the prevalence of GSTM1 and GSTT1 gene deletions, and two GSTP1 polymorphisms in 772 cases with advanced colorectal adenomas (>1 cm, villous elements or high-grade dysplasia) of the distal colon (descending or sigmoid colon or rectum) and 777 sigmoidoscopy negative controls enrolled in the screening arm of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial.
  • Advanced adenoma risk was increased in current/former smokers (OR, 1.4; 95% CI, 1.2-1.8).
  • [MeSH-major] Adenoma / genetics. Colorectal Neoplasms / genetics. Glutathione Transferase / genetics. Isoenzymes / genetics. Polymorphism, Genetic

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  • (PMID = 16030123.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Isoenzymes; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / GSTP1 protein, human; EC 2.5.1.18 / Glutathione S-Transferase pi; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1
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62. 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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  • (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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63. Ohba S, Fujimori M, Ito S, Matsumoto F, Hata M, Takayanagi H, Wada R, Ikeda K: A case report of metastasizing myoepithelial carcinoma of the parotid gland arising in a recurrent pleomorphic adenoma. Auris Nasus Larynx; 2009 Feb;36(1):123-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case report of metastasizing myoepithelial carcinoma of the parotid gland arising in a recurrent pleomorphic adenoma.
  • Myoepithelial carcinoma, arising in a recurrent or in a pre-existing pleomorphic adenoma of the parotid gland is an extremely rare cancer.
  • We herein report the case of myoepithelial carcinoma occurring in a recurrent pleomorphic adenoma, which showed a high metastatic potential.
  • A 53-year-old male, who had undergone a superficial parotidectomy of the pleomorphic adenoma 2 years previously, presented with recurrent parotid swelling and with multiple coin lesions in the lung.
  • A total parotidectomy and a thoracoscopic biopsy of the lung lesion revealed both lesions to be myoepithelial carcinoma.
  • [MeSH-major] Adenoma, Pleomorphic / pathology. Lung Neoplasms / secondary. Myoepithelioma / pathology. Neoplasms, Second Primary / pathology. Parotid Neoplasms / pathology. Solitary Pulmonary Nodule / secondary

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  • (PMID = 18650039.001).
  • [ISSN] 1879-1476
  • [Journal-full-title] Auris, nasus, larynx
  • [ISO-abbreviation] Auris Nasus Larynx
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
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64. Daugherty SE, Platz EA, Shugart YY, Fallin MD, Isaacs WB, Chatterjee N, Welch R, Huang WY, Hayes RB: Variants in the alpha-Methylacyl-CoA racemase gene and the association with advanced distal colorectal adenoma. Cancer Epidemiol Biomarkers Prev; 2007 Aug;16(8):1536-42
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  • [Title] Variants in the alpha-Methylacyl-CoA racemase gene and the association with advanced distal colorectal adenoma.
  • METHODS: We conducted a case-control study of 725 advanced distal colorectal adenoma cases and 729 frequency-matched controls from the screening arm of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial.
  • RESULTS: The 201L allele of S201L [TT versus CC: odds ratio (OR), 1.74; 95% confidence interval (95% CI), 1.15-2.62; TC versus CC: OR, 1.17; 95% CI, 0.93-1.49] and the 277E allele of K277E (GG versus AA: OR, 1.66; 95% CI, 1.03-2.68; GA versus AA: OR, 1.21; 95% CI, 0.96-1.53) were associated with increased risk of advanced distal colorectal adenoma (both P(trend) </= 0.02); the TGTGCG haplotype of six informative single nucleotide polymorphisms was also associated with increased risk (OR, 1.27; 95% CI, 1.03-1.55).
  • Regular ibuprofen users who were homozygous for the variant allele at either M9V or D175G were at reduced risk for adenoma (both P(interaction) < 0.05).
  • CONCLUSION: Our study identified variants in AMACR associated with advanced distal colorectal adenoma and pointed to potential interactions with ibuprofen use.
  • [MeSH-major] Adenoma / enzymology. Colonic Neoplasms / enzymology. Genetic Variation / genetics. Racemases and Epimerases / genetics. Rectal Neoplasms / enzymology

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  • (PMID = 17684125.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CO / N01-CO-12400; United States / NCI NIH HHS / CA / T32 CA09314; United States / Intramural NIH HHS / /
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 30KYC7MIAI / Aspartic Acid; 3KX376GY7L / Glutamic Acid; 452VLY9402 / Serine; AE28F7PNPL / Methionine; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase; GMW67QNF9C / Leucine; HG18B9YRS7 / Valine; K3Z4F929H6 / Lysine; TE7660XO1C / Glycine; WK2XYI10QM / Ibuprofen
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65. Nakamura H, Adachi Y, Arai T, Miwa K, Haruki T, Fujioka S, Taniguchi Y: A small alveolar adenoma resected by thoracoscopic surgery. Ann Thorac Surg; 2009 Mar;87(3):956-7
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  • [Title] A small alveolar adenoma resected by thoracoscopic surgery.
  • Alveolar adenoma (AA) is a rare lung benign tumor originated from type II pneumocytes.
  • It presents as a well-defined nodule in clinical images, but is difficult to differentiate from early-stage lung cancer.
  • We treated a 58-year-old woman with a small-sized AA measuring 8 x 6 mm in the upper lobe of the left lung by performing a thoracoscopic resection.
  • There have been no reported cases of recurrence after a resection of AA, but a subsequent increase in such cases is expected, and we believe that it is necessary to understand the characteristics of this typical benign lung tumor.
  • [MeSH-major] Adenoma / surgery. Lung Neoplasms / surgery. Thoracoscopy

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  • (PMID = 19231437.001).
  • [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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66. Kozakiewicz J, Teodorowicz E, Haczyńska-Partyka A, Myrcik G, Lange D, Szwabowicz M: [Adenoma oxyphillicum an extremely rare case of tumour of the larynx end cancer lungs which are going together]. Otolaryngol Pol; 2007;61(3):311-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Adenoma oxyphillicum an extremely rare case of tumour of the larynx end cancer lungs which are going together].
  • There was presented an exstremely rare case of adenoma oxyphillicum of the larynx coexisting with the lung carcinoma.
  • It consisted such matters as detailed graphical examination, spliting of larynx, and radiotherapy and chemiotherapy of lung cancer.
  • The authors want to call attention to limited use fullness of competent lungs X-ray in a-p projection in recognizing the early stadium of lung cancer.
  • [MeSH-major] Adenoma, Oxyphilic / diagnosis. Adenoma, Oxyphilic / surgery. Laryngeal Neoplasms / diagnosis. Laryngeal Neoplasms / surgery. Lung Neoplasms / radiography. Lung Neoplasms / therapy. Neoplasms, Second Primary / radiography. Neoplasms, Second Primary / therapy

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  • (PMID = 17847787.001).
  • [ISSN] 0030-6657
  • [Journal-full-title] Otolaryngologia polska = The Polish otolaryngology
  • [ISO-abbreviation] Otolaryngol Pol
  • [Language] pol
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Poland
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67. 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
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  • [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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68. Barmeyer C, Ye JH, Sidani S, Geibel J, Binder HJ, Rajendran VM: Characteristics of rat downregulated in adenoma (rDRA) expressed in HEK 293 cells. Pflugers Arch; 2007 Jun;454(3):441-50
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  • [Title] Characteristics of rat downregulated in adenoma (rDRA) expressed in HEK 293 cells.
  • These studies proposed that anion exchanger (AE)-1 isoform encodes the former as both apical membrane DIDS-sensitive CL(-)-HCO(3)(-) exchange, and AE1 specific mRNA are present only in surface cells and are downregulated in Na-depleted rats, whereas downregulated in adenoma (DRA) encodes the latter as both DIDS-resistant Cl(-)-OH(-) exchange, and DRA-specific proteins are present in apical membranes of both surface and crypt cells and are not altered in Na(+)-depleted rats.
  • Studies were, therefore, initiated to identify the function of rat DRA (rDRA) in vitro. rDRA cDNA isolated from rat distal colon encodes a 757-amino-acid protein which has 96 and 81% homology with mDRA and hDRA, respectively. rDRA-specific mRNA expression was detectable only in specific segments of the digestive tract (duodenum, ileum, cecum, proximal colon, and distal colon) but not in the stomach, jejunum, or in the kidney, brain, heart, and lung.

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  • (PMID = 17492310.001).
  • [ISSN] 0031-6768
  • [Journal-full-title] Pflügers Archiv : European journal of physiology
  • [ISO-abbreviation] Pflugers Arch.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AF337809
  • [Grant] United States / NIDDK NIH HHS / DK / DK60069; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antiporters; 0 / Bicarbonates; 0 / Chlorides; 0 / DNA Primers; 0 / Fatty Acids, Volatile; 0 / Recombinant Proteins; 0 / Slc26a3 protein, rat; Q1O6DSW23R / 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid
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69. Zhang Y, Gomez-Fernandez CR, Jorda M, Ganjei-Azar P: Fine-needle aspiration (FNA) and pleural fluid cytology diagnosis of benign metastasizing pleomorphic adenoma of the parotid gland in the lung: a case report and review of literature. Diagn Cytopathol; 2009 Nov;37(11):828-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fine-needle aspiration (FNA) and pleural fluid cytology diagnosis of benign metastasizing pleomorphic adenoma of the parotid gland in the lung: a case report and review of literature.
  • Benign metastasizing pleomorphic adenoma is a rare neoplasm, in which the benign appearing pleomorphic adenoma, without any histological evidence of malignancy, metastasizes to distant sites including lung.
  • In the absence of clinical history of a pre-existing myoepithelial neoplasm, the presence of myoepithelial cells in the lung or any other organs besides salivary glands may create diagnostic difficulty.
  • Here we present the cytologic findings of such a metastatic tumor found in the lung FNA and pleural fluid specimens from a 64-year-old woman, with a history of local recurrent salivary gland pleomorphic adenomas, who presented with multiple bilateral pulmonary nodules and pleural effusion.
  • The diagnosis of benign metastasizing pleomorphic adenoma was made based on clinical information and cytomorphology, and confirmed by immunocytochemistry.
  • [MeSH-major] Adenoma, Pleomorphic / pathology. Biopsy, Fine-Needle. Lung Neoplasms / secondary. Parotid Neoplasms / pathology. Pleural Effusion, Malignant / pathology

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  • (PMID = 19582818.001).
  • [ISSN] 1097-0339
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 15
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70. Jiang YN, Li YH, Ke MW, Tseng TY, Tang YB, Huang MC, Cheng WT, Ju YT: Caveolin-1 sensitizes rat pituitary adenoma GH3 cells to bromocriptine induced apoptosis. Cancer Cell Int; 2007;7:1
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Caveolin-1 sensitizes rat pituitary adenoma GH3 cells to bromocriptine induced apoptosis.
  • Rat pituitary adenoma GH3 cells, which express endogenous caveolin-1, exhibit increased apoptosis and shrinkage after exposure to bromocriptine.
  • CONCLUSION: Our results reveal that caveolin-1 increases sensitivity for apoptosis induction in pituitary adenoma GH3 cells and may contribute to tumor shrinkage after clinical bromocriptine treatment.

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  • [Cites] Expert Rev Anticancer Ther. 2006 Sep;6 Suppl 9:S29-35 [17004854.001]
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  • (PMID = 17331262.001).
  • [ISSN] 1475-2867
  • [Journal-full-title] Cancer cell international
  • [ISO-abbreviation] Cancer Cell Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1832175
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71. Wong HL, Peters U, Hayes RB, Huang WY, Schatzkin A, Bresalier RS, Velie EM, Brody LC: Polymorphisms in the adenomatous polyposis coli (APC) gene and advanced colorectal adenoma risk. Eur J Cancer; 2010 Sep;46(13):2457-66
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Polymorphisms in the adenomatous polyposis coli (APC) gene and advanced colorectal adenoma risk.
  • We studied the association of eight APC single nucleotide polymorphisms (SNPs), possibly associated with functional consequences, and previously identified gene-environment (dietary fat intake and hormone replacement therapy (HRT) use) interactions, in relation to advanced colorectal adenoma in 758 cases and 767 sex- and race-matched controls, randomly selected from the screening arm of the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial.
  • Cases had at least one verified advanced adenoma of the distal colon; controls, a negative sigmoidoscopy.
  • We did not observe an association between genotypes for any of the eight APC SNPs and advanced distal adenoma risk (P(global gene-based)=0.92).
  • However, the risk for advanced distal adenoma was threefold higher for one rare haplotype (cases: 2.7%; controls: 1.6%) (odds ratio (OR)=3.27; 95% confidence interval (CI)=1.08-9.88).
  • The genetic association between D1822V and advanced distal adenoma was confined to persons consuming a high-fat diet (P(interaction)=0.03).
  • In our large, nested case-control study of advanced distal adenoma and clinically verified adenoma-free controls, we observed no association between specific APC SNPs and advanced adenoma.
  • Fat intake modified the APC D1822V-adenoma association, but further studies are warranted.

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
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  • (PMID = 20510605.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 HG000120-12
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dietary Fats
  • [Other-IDs] NLM/ NIHMS202303; NLM/ PMC2924917
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72. 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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73. Sharon E, Kelly RJ, Szabo E: Sustained response of carcinoma ex pleomorphic adenoma treated with trastuzumab and capecitabine. Head Neck Oncol; 2010;2:12
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  • [Title] Sustained response of carcinoma ex pleomorphic adenoma treated with trastuzumab and capecitabine.
  • BACKGROUND: Carcinoma ex pleomorphic adenoma is a rare histologic subtype of salivary gland cancer with an overall poor prognosis.
  • We report here a case of a 58-year old man with metastatic carcinoma ex pleomorphic adenoma who achieved a sustained long term response to combination therapy with trastuzumab and capecitabine.
  • CASE PRESENTATION: A 58 year old man presented with T1N2bM0 carcinoma ex pleomorphic adenoma and underwent surgery followed by adjuvant radiation therapy.
  • CONCLUSION: This case illustrates the successful long term treatment of carcinoma ex pleomorphic adenoma with targeted therapy with trastuzumab in combination with chemotherapy.
  • In the absence of definitive clinical trials which are unlikely to be performed due to the rarity of this tumor, case reports such as this one suggest potential utility for trastuzumab in combination with chemotherapy in the treatment of HER2/neu-overexpressing carcinoma ex pleomorphic adenoma.
  • [MeSH-major] Adenoma, Pleomorphic / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Salivary Gland Neoplasms / drug therapy

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  • (PMID = 20504363.001).
  • [ISSN] 1758-3284
  • [Journal-full-title] Head & neck oncology
  • [ISO-abbreviation] Head Neck Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0W860991D6 / Deoxycytidine; 6804DJ8Z9U / Capecitabine; EC 2.7.10.1 / Receptor, ErbB-2; P188ANX8CK / Trastuzumab; U3P01618RT / Fluorouracil
  • [Other-IDs] NLM/ PMC2889991
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74. Glaab R, Turina M, Achermann E, Maurer R, Went P, Schöb O: [Alveolar adenoma--a rare pulmonary mass: case report and review of the literature]. Zentralbl Chir; 2009 Sep;134(5):478-80
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  • [Title] [Alveolar adenoma--a rare pulmonary mass: case report and review of the literature].
  • Chest X-ray and CT scans showed a solitary pulmonary mass in the right lower lobe without radiographic signs of malignancy.
  • Definitive histology following thoracoscopic wedge resection showed the distinctive findings of an alveolar adenoma, a very rare benign tumour of the lung of unknown histogenesis.
  • Alveolar adenoma usually presents as a peripheral solitary lesion in asymptomatic, older patients.
  • Its histological features, the benign proliferation of alveolar epithelium and septal mesenchyme, allow for its distinction from other benign lesions of the lung.
  • [MeSH-major] Adenoma / diagnosis. Carcinoma, Bronchogenic / diagnosis. Lung Neoplasms / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Hemoptysis / etiology. Humans. Lung / pathology. Male. Middle Aged. Phlebography. Pneumonectomy. Thoracoscopy. Tomography, X-Ray Computed

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  • [Copyright] (c) Georg Thieme Verlag Stuttgart-New York.
  • (PMID = 19757349.001).
  • [ISSN] 1438-9592
  • [Journal-full-title] Zentralblatt für Chirurgie
  • [ISO-abbreviation] Zentralbl Chir
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 5
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75. Rodríguez-Fernández J, Mateos-Micas M, Martínez-Tello FJ, Berjón J, Montalvo JJ, Forteza-González G, Galan-Hernández R: Metastatic benign pleomorphic adenoma. Report of a case and review of the literature. Med Oral Patol Oral Cir Bucal; 2008 Mar;13(3):E193-6
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  • [Title] Metastatic benign pleomorphic adenoma. Report of a case and review of the literature.
  • Pleomorphic adenoma (PA), originally called mixed tumour, is the most common neoplasm of the salivary glands and is generally accepted as benign biologically.
  • The aim of this paper is to report one case of metastatic histological benign pleomorphic adenoma, and to consider the clinical, pathological and therapeutic consequences of these rare tumours as well as its possible causes and mechanisms for its behaviour.
  • [MeSH-major] Adenoma, Pleomorphic / pathology. Lung Neoplasms / secondary. Salivary Gland Neoplasms / pathology

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  • (PMID = 18305442.001).
  • [ISSN] 1698-6946
  • [Journal-full-title] Medicina oral, patología oral y cirugía bucal
  • [ISO-abbreviation] Med Oral Patol Oral Cir Bucal
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Spain
  • [Number-of-references] 29
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76. 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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77. Kamiyoshihara M, Ibe T, Takeyoshi I: Pleomorphic adenoma of the main bronchus in an adult treated using a wedge bronchiectomy. Gen Thorac Cardiovasc Surg; 2009 Jan;57(1):43-5

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  • [Title] Pleomorphic adenoma of the main bronchus in an adult treated using a wedge bronchiectomy.
  • A 34-year-old woman had complained of dyspnea on exertion for 3 months and was found to have a volume loss of the left lung.
  • We performed a deep wedge resection of the main bronchus, preserving the lung parenchyma.
  • Histopathologically, the tumor specimen was compatible with pleomorphic adenoma.
  • To our knowledge, only two cases of pleomorphic adenoma arising from the main bronchus have been reported in the English-language literature, and ours is the first report of lung-preserving surgery.
  • [MeSH-major] Adenoma, Pleomorphic / surgery. Bronchial Neoplasms / surgery. Pulmonary Surgical Procedures

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  • (PMID = 19160012.001).
  • [ISSN] 1863-6705
  • [Journal-full-title] General thoracic and cardiovascular surgery
  • [ISO-abbreviation] Gen Thorac Cardiovasc Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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78. Rajput R, Bhansali A, Dutta P, Gupta SK, Radotra BD, Bhadada S: Pituitary metastasis masquerading as non-functioning pituitary adenoma in a woman with adenocarcinoma lung. Pituitary; 2006;9(2):155-7
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  • [Title] Pituitary metastasis masquerading as non-functioning pituitary adenoma in a woman with adenocarcinoma lung.
  • However, pituitary metastasis manifesting as bitemporal hemianopia as a presenting manifestation in a patient with silent adenocarcinoma of the lung, that too in a women, is quite uncommon.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenoma / diagnosis. Lung Neoplasms / diagnosis. Pituitary Neoplasms / diagnosis

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  • (PMID = 16832588.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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79. de Decker S, Bovy C, Deflandre J, Moonen M, Van Nes MC: Treatment of a nephrotic syndrome by endoscopic removal of a villous adenoma of the duodenum. Gastroenterol Clin Biol; 2010 Nov;34(11):625-8
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  • [Title] Treatment of a nephrotic syndrome by endoscopic removal of a villous adenoma of the duodenum.
  • We report the case of a patient diagnosed with a villous adenoma of the duodenum showing high degree dysplasia who developed a nephrotic syndrome (NS) due to a membranous nephropathy (MN), demonstrated by renal biopsy.
  • Only the endoscopic resection of the duodenal adenoma could control the NS.
  • Tumours most often identified are those of lung, prostate and digestive tract.
  • [MeSH-major] Adenoma, Villous / surgery. Duodenal Neoplasms / surgery. Duodenoscopy. Nephrotic Syndrome / surgery

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  • [Copyright] Copyright © 2010 Elsevier Masson SAS. All rights reserved.
  • (PMID = 20850233.001).
  • [ISSN] 0399-8320
  • [Journal-full-title] Gastroentérologie clinique et biologique
  • [ISO-abbreviation] Gastroenterol. Clin. Biol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] France
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80. Yoshino N, Kubokura H, Yamauchi S, Ohaki Y, Koizumi K, Shimizu K: A true pulmonary carcinosarcoma that required diagnostic differentiation from a pleomorphic adenoma: a case report. Ann Thorac Cardiovasc Surg; 2009 Feb;15(1):42-5
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  • [Title] A true pulmonary carcinosarcoma that required diagnostic differentiation from a pleomorphic adenoma: a case report.
  • Pulmonary carcinosarcoma is a rarely encountered tumor.
  • We treated a patient who had an intrabronchial polypoid lesion that required a diagnostic differentiation from epithelial-mesenchymal mixed neoplasms inclusive of pleomorphic adenoma, and that was diagnosed by immunohistochemical staining to be a true carcinosarcoma.
  • A 69-year-old man underwent left pneumonectomy in November 2000 with a diagnosis of atelectasis resulting from a tumor obstructing the left lower lobar bronchus, and also a lung abscess.
  • The tumor was initially diagnosed as pleomorphic adenoma, since it contained both benign-looking epithelial and mesenchymal elements, but immunohistochemical staining demonstrated myoglobin-positive rhabdomyosarcomatous elements along with cytokeratin-positive squamous cell carcinoma elements.
  • A definite diagnosis of pulmonary carcinosarcoma was confirmed.
  • [MeSH-major] Adenoma, Pleomorphic / pathology. Carcinosarcoma / pathology. Lung Neoplasms / pathology
  • [MeSH-minor] Aged. Bronchoscopy. Diagnosis, Differential. Humans. Immunohistochemistry. Lung Abscess / etiology. Lung Abscess / pathology. Male. Pneumonectomy. Pulmonary Atelectasis / etiology. Pulmonary Atelectasis / pathology. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 19262449.001).
  • [ISSN] 2186-1005
  • [Journal-full-title] Annals of thoracic and cardiovascular surgery : official journal of the Association of Thoracic and Cardiovascular Surgeons of Asia
  • [ISO-abbreviation] Ann Thorac Cardiovasc Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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81. Millen AE, Subar AF, Graubard BI, Peters U, Hayes RB, Weissfeld JL, Yokochi LA, Ziegler RG, PLCO Cancer Screening Trial Project Team: Fruit and vegetable intake and prevalence of colorectal adenoma in a cancer screening trial. Am J Clin Nutr; 2007 Dec;86(6):1754-64
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fruit and vegetable intake and prevalence of colorectal adenoma in a cancer screening trial.
  • BACKGROUND: Research on the association between fruit and vegetable intake and risk of colorectal adenoma is inconclusive.
  • OBJECTIVE: We studied whether intake of fruit, vegetables, or their subgroups is associated with a lower risk of prevalent colorectal adenoma.
  • DESIGN: In men and women (aged 55-74 y) who were screened for colorectal cancer in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial (PLCO) (1993-2001), we compared 3,057 cases with at least one prevalent histologically verified adenoma of the distal large bowel with 29,413 control subjects.
  • RESULTS: Risk of distal adenoma was significantly lower among subjects in high (approximately 5.7 ps/d) versus low (approximately 1.2 ps/d) quintiles of total fruit intake (OR: 0.75; 95% CI: 0.66, 0.86, P for trend <0.001), which was not completely explained by dietary folate or fiber intake.
  • Inverse associations between adenoma and total fruit intake were observed regardless of adenoma histopathology and multiplicity.
  • However, the protective effect was seen only for colon and not rectal adenoma.
  • Total vegetable intake was not significantly associated with reduced risk of adenoma.
  • ORs for colorectal adenoma among persons with high versus low intakes of deep-yellow vegetables, dark-green vegetables, and onions and garlic were significantly related to lower risk of adenoma, although the P for trend for dark-green vegetables was not significant.
  • CONCLUSION: Diets rich in fruit and deep-yellow vegetables, dark-green vegetables, and onions and garlic are modestly associated with reduced risk of colorectal adenoma, a precursor of colorectal cancer.
  • [MeSH-major] Adenoma / epidemiology. Colorectal Neoplasms / epidemiology. Fruit. Vegetables

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  • (PMID = 18065596.001).
  • [ISSN] 0002-9165
  • [Journal-full-title] The American journal of clinical nutrition
  • [ISO-abbreviation] Am. J. Clin. Nutr.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural
  • [Publication-country] United States
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82. Gesierich W, Diwersy C, Leinsinger G, Massmann J, Präuer H, Höfler H, Fend F, Emslander HP: [Papillary adenoma of type-II pneumocytes as a rare differential diagnosis of a solitary pulmonary nodule]. Pneumologie; 2007 Nov;61(11):697-9
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  • [Title] [Papillary adenoma of type-II pneumocytes as a rare differential diagnosis of a solitary pulmonary nodule].
  • The case of a 66-year-old, asymptomatic patient with a papillary adenoma of type-II pneumocytes is reported.
  • Following the coincidental radiologic finding of a solitary pulmonary nodule, the diagnosis could be established in a bronchoscopically obtained endobronchial biopsy.
  • Papillary adenoma of type-II pneumocytes is a rare tumor, whose origin is suspected in progenitor cells of the bronchioloalveolar epithelium with the potential to differentiate towards type-II pneumocytes and clara cells.
  • [MeSH-major] Adenoma / diagnosis. Lung / pathology. Lung Neoplasms / diagnosis. Solitary Pulmonary Nodule / etiology

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  • (PMID = 17886196.001).
  • [ISSN] 1438-8790
  • [Journal-full-title] Pneumologie (Stuttgart, Germany)
  • [ISO-abbreviation] Pneumologie
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
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83. Uruga H, Fujii T, Kurosaki A, Hanada S, Takaya H, Miyamoto A, Morokawa N, Kishi K: [A case of pulmonary tumor thrombotic microangiopathy caused by carcinoma (salivary duct carcinoma) ex pleomorphic adenoma]. Nihon Kokyuki Gakkai Zasshi; 2010 Jun;48(6):463-8
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  • [Title] [A case of pulmonary tumor thrombotic microangiopathy caused by carcinoma (salivary duct carcinoma) ex pleomorphic adenoma].
  • A 53-year-old man with carcinoma (salivary duct carcinoma) ex pleomorphic adenoma was admitted to our hospital because of dyspnea.
  • Contrast-enhanced CT did not reveal any emboli in the large pulmonary arteries.
  • An echocardiogram showed severe pulmonary hypertension.
  • Tc-99m-MAA lung perfusion images showed multiple small defects in both lungs.
  • A diagnosis of pulmonary tumor thrombotic microangiopathy (PTTM) was made.
  • [MeSH-major] Carcinoma / complications. Lung Neoplasms / complications. Salivary Ducts. Salivary Gland Neoplasms / complications. Thrombotic Microangiopathies / etiology
  • [MeSH-minor] Humans. Lung / blood supply. Male. Microcirculation. Middle Aged

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  • (PMID = 20608093.001).
  • [ISSN] 1343-3490
  • [Journal-full-title] Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society
  • [ISO-abbreviation] Nihon Kokyuki Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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84. Dixon LB, Subar AF, Peters U, Weissfeld JL, Bresalier RS, Risch A, Schatzkin A, Hayes RB: Adherence to the USDA Food Guide, DASH Eating Plan, and Mediterranean dietary pattern reduces risk of colorectal adenoma. J Nutr; 2007 Nov;137(11):2443-50
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  • [Title] Adherence to the USDA Food Guide, DASH Eating Plan, and Mediterranean dietary pattern reduces risk of colorectal adenoma.
  • Our objective was to determine whether adherence to the USDA Food Guide recommendations, the DASH Eating Plan, or a Mediterranean dietary pattern is associated with reduced risk of distal colorectal adenoma.
  • In the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial, men and women aged 55-74 y were screened for colorectal cancer by sigmoidoscopy at 10 centers in the U.S.
  • After adjusting for potential confounders, men who most complied with the USDA Food Guide recommendations had a 26% reduced risk of colorectal adenoma compared with men who least complied with the recommendations (OR USDA score >or= 5 vs. <or=2 = 0.74, 95% CI = 0.64-0.85; P-trend < 0.001).
  • Women who most complied with the USDA Food Guide recommendations had an 18% reduced risk for colorectal adenoma, but subgroup analyses revealed protective associations only for current smokers (OR USDA score >or= 5 vs. <or=2 = 0.52, 95% CI = 0.31-0.89; P-trend < 0.01) or normal-weight women (OR USDA score >or= 5 vs. <or=2 = 0.74, 95% CI = 0.55-0.99; P-trend = 0.08).
  • Following the current U.S. dietary recommendations or a Mediterranean dietary pattern is associated with reduced risk of colorectal adenoma, especially in men.
  • [MeSH-major] Adenoma / prevention & control. Colorectal Neoplasms / prevention & control. Diet. Diet, Mediterranean. United States Department of Agriculture

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  • (PMID = 17951483.001).
  • [ISSN] 0022-3166
  • [Journal-full-title] The Journal of nutrition
  • [ISO-abbreviation] J. Nutr.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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85. 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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  • 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


86. Kocarnik JD, Hutter CM, Slattery ML, Berndt SI, Hsu L, Duggan DJ, Muehling J, Caan BJ, Beresford SA, Rajkovic A, Sarto GE, Marshall JR, Hammad N, Wallace RB, Makar KW, Prentice RL, Potter JD, Hayes RB, Peters U: Characterization of 9p24 risk locus and colorectal adenoma and cancer: gene-environment interaction and meta-analysis. Cancer Epidemiol Biomarkers Prev; 2010 Dec;19(12):3131-9
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  • [Title] Characterization of 9p24 risk locus and colorectal adenoma and cancer: gene-environment interaction and meta-analysis.
  • We included Caucasians with colorectal adenoma or colorectal cancer and controls from 4 studies (total 3,891 cases, 4,490 controls): the Women's Health Initiative (WHI); the Diet, Activity and Lifestyle Study (DALS); a Minnesota population-based case-control study (MinnCCS); and the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial (PLCO).
  • RESULTS: SNP rs719725 was statistically significantly associated with risk of colorectal cancer in WHI (OR per A allele 1.19; 95% CI, 1.01-1.40; P(trend) = 0.04), marginally associated with adenoma risk in PLCO (OR per A allele 1.11; 95% CI, 0.99-1.25; P(trend) = 0.07), and not associated in DALS and MinnCCS.

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  • [Copyright] ©2010 AACR.
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  • (PMID = 20978172.001).
  • [ISSN] 1538-7755
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA048998-12A2; United States / WHI NIH HHS / WH / N01 WH032112; United States / WHI NIH HHS / WH / N01 WH042122; United States / NCI NIH HHS / CA / R01 CA059045; United States / PHS HHS / / 32105-6; United States / WHI NIH HHS / WH / N01 WH32115; United States / WHI NIH HHS / WH / N01 WH042110; None / None / / N01 WH032102; United States / WHI NIH HHS / WH / N01WH22110; United States / WHI NIH HHS / WH / WH024152; United States / NIA NIH HHS / AG / R01 AG014358; United States / NIA NIH HHS / AG / R01 AG14358; United States / WHI NIH HHS / WH / N01 WH042114; United States / WHI NIH HHS / WH / N01 WH032105; United States / WHI NIH HHS / WH / N01 WH042107; United States / WHI NIH HHS / WH / N01 WH042126; United States / NCI NIH HHS / CA / P01 CA53996; United States / WHI NIH HHS / WH / N01 WH032109; United States / NCI NIH HHS / CA / P01 CA053996; United States / WHI NIH HHS / WH / N01 WH032102; None / None / / N01 WH044221; United States / WHI NIH HHS / WH / N01 WH042108-011; United States / NCI NIH HHS / CA / CA059045-05; United States / NIA NIH HHS / AG / AG014358-06; United States / PHS HHS / / 42107-26; United States / PHS HHS / / 32115; United States / WHI NIH HHS / WH / N01 WH022110; United States / WHI NIH HHS / WH / N01 WH042121; United States / WHI NIH HHS / WH / N01 WH032111; United States / WHI NIH HHS / WH / N01 WH032122; United States / NCI NIH HHS / CA / CA048998-12A2; United States / WHI NIH HHS / WH / N01 WH032118; United States / NCI NIH HHS / CA / R01 CA048998; United States / NCI NIH HHS / CA / K22 CA118421-01; United States / NCI NIH HHS / CA / R25 CA094880; United States / WHI NIH HHS / WH / N01 WH042130; United States / NIA NIH HHS / AG / R01 AG014358-06; United States / NCI NIH HHS / CA / U01 CA137088; United States / WHI NIH HHS / WH / N01 WH042115; United States / WHI NIH HHS / WH / N01 WH042131; United States / WHI NIH HHS / WH / N01 WH042119; None / None / / N01 WH032100; United States / NCI NIH HHS / CA / P01 CA053996-30; United States / WHI NIH HHS / WH / N01 WH042116; United States / PHS HHS / / 32100-2; United States / NCI NIH HHS / CA / CA118421-01; United States / PHS HHS / / 24152; United States / NCI NIH HHS / CA / R01 CA059045-05; United States / Intramural NIH HHS / / ; United States / WHI NIH HHS / WH / N01 WH042117; United States / NCI NIH HHS / CA / R01 CA48998; United States / PHS HHS / / 42129-32; United States / WHI NIH HHS / WH / N01 WH042109; United States / NIH HHS / OD / N01 WH42124; United States / NCI NIH HHS / CA / R25 CA094880-01; United States / WHI NIH HHS / WH / N01 WH032106; United States / PHS HHS / / 32118-32119; United States / WHI NIH HHS / WH / N01 WH042132; None / None / / N01 WH042113; United States / NCI NIH HHS / CA / CA053996-30; United States / WHI NIH HHS / WH / N01 WH032100; United States / PHS HHS / / 32108-9; United States / WHI NIH HHS / WH / N01 WH044221; United States / NCI NIH HHS / CA / K22 CA118421; United States / WHI NIH HHS / WH / N01 WH042112; United States / WHI NIH HHS / WH / N01 WH042125; United States / NCI NIH HHS / CA / R01 CA120582-01; United States / WHI NIH HHS / WH / N01 WH042111; United States / WHI NIH HHS / WH / N01 WH042113; United States / NCI NIH HHS / CA / CA120582-01; United States / PHS HHS / / 32122; United States / WHI NIH HHS / WH / N01 WH022110-024; United States / NCI NIH HHS / CA / R01 CA120582; United States / WHI NIH HHS / WH / N01 WH042120; United States / WHI NIH HHS / WH / N01 WH032108; United States / PHS HHS / / 44221; United States / PHS HHS / / 32111-13; United States / WHI NIH HHS / WH / N01 WH042123; United States / NCI NIH HHS / CA / CA094880-01; United States / WHI NIH HHS / WH / N01 WH032119; United States / WHI NIH HHS / WH / N01 WH042129; United States / WHI NIH HHS / WH / N01 WH032113; United States / WHI NIH HHS / WH / N01 WH024152
  • [Publication-type] Journal Article; Meta-Analysis; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS248201; NLM/ PMC3005543
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87. 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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88. 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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  • (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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89. Huang WY, Berndt SI, Kang D, Chatterjee N, Chanock SJ, Yeager M, Welch R, Bresalier RS, Weissfeld JL, Hayes RB: Nucleotide excision repair gene polymorphisms and risk of advanced colorectal adenoma: XPC polymorphisms modify smoking-related risk. Cancer Epidemiol Biomarkers Prev; 2006 Feb;15(2):306-11
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  • [Title] Nucleotide excision repair gene polymorphisms and risk of advanced colorectal adenoma: XPC polymorphisms modify smoking-related risk.
  • OBJECTIVES: Nucleotide excision repair enzymes remove bulky damage caused by environmental agents, including carcinogenic polycyclic aromatic hydrocarbons found in cigarette smoke, a risk factor for colorectal adenoma.
  • Among participants randomized to the screening arm of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial, we studied the risk of advanced colorectal adenoma in relation to cigarette smoking and selected single nucleotide polymorphisms (SNP) in the nucleotide excision repair pathway.
  • METHODS: Cases (n = 772) were subjects with left-sided advanced adenoma (>1 cm in size, high-grade dysplasia, or villous characteristics).
  • RESULTS: None of the studied SNPs were independently associated with advanced adenoma risk.
  • Smoking was related to adenoma risk and XPC polymorphisms (R492H, A499V, K939Q) modified these effects (P(interaction) from 0.03-0.003).
  • CONCLUSIONS: Examining a spectrum of polymorphic variants in nucleotide excision repair genes, we found evidence that smoking-associated risks for advanced colorectal adenoma are modified by polymorphisms in XPC, particularly haplotypes containing XPC 499V.
  • [MeSH-major] Adenoma / genetics. Colorectal Neoplasms / genetics. DNA Repair / genetics. DNA-Binding Proteins / genetics. Polymorphism, Single Nucleotide. Smoking / genetics

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  • (PMID = 16492920.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 156533-34-5 / XPC protein, human; EC 3.6.4.- / DNA Helicases
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90. Lees NP, Harrison KL, Hall CN, Margison GP, Povey AC: Human colorectal mucosal O6-alkylguanine DNA-alkyltransferase activity and DNA-N7-methylguanine levels in colorectal adenoma cases and matched referents. Gut; 2007 Mar;56(3):380-4
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  • [Title] Human colorectal mucosal O6-alkylguanine DNA-alkyltransferase activity and DNA-N7-methylguanine levels in colorectal adenoma cases and matched referents.
  • Such mutations are frequently seen in the KRAS oncogene of large colorectal adenomas, but whether adenoma or mutational risk in humans is influenced by MGMT activity and alkylating agent exposure is unclear.
  • Elevated MGMT levels were associated with an increased risk of adenoma (OR 1.17, 95% CI 1.03 to 1.33 per unit increase in activity).
  • [MeSH-major] Adenoma / genetics. Colorectal Neoplasms / genetics. Guanine / analogs & derivatives. O(6)-Methylguanine-DNA Methyltransferase / metabolism

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  • (PMID = 16891355.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / DNA, Neoplasm; 0 / Membrane Proteins; 0 / Neoplasm Proteins; 0 / SSPN protein, human; 578-76-7 / 7-methylguanine; 5Z93L87A1R / Guanine; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
  • [Other-IDs] NLM/ PMC1856833
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91. Ashktorab H, Belgrave K, Hosseinkhah F, Brim H, Nouraie M, Takkikto M, Hewitt S, Lee EL, Dashwood RH, Smoot D: Global histone H4 acetylation and HDAC2 expression in colon adenoma and carcinoma. Dig Dis Sci; 2009 Oct;54(10):2109-17
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  • [Title] Global histone H4 acetylation and HDAC2 expression in colon adenoma and carcinoma.
  • HDAC2 expression was correlated significantly with progression of adenoma to carcinoma (P = 0.002), with a discriminative power of 0.74, when comparing cancer and non-cancer cases.

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  • (PMID = 19057998.001).
  • [ISSN] 1573-2568
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA122959; United States / NCI NIH HHS / CA / CA122959-02; United States / NCI NIH HHS / CA / R01 CA122959-02; United States / PHS HHS / / A102681; United States / NCI NIH HHS / CA / R01 CA122959
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Histones; EC 3.5.1.98 / Histone Deacetylases
  • [Other-IDs] NLM/ NIHMS118762; NLM/ PMC2737733
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92. Schoen RE, Weissfeld JL, Pinsky PF, Riley T: Yield of advanced adenoma and cancer based on polyp size detected at screening flexible sigmoidoscopy. Gastroenterology; 2006 Dec;131(6):1683-9
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  • [Title] Yield of advanced adenoma and cancer based on polyp size detected at screening flexible sigmoidoscopy.
  • To examine the yield at colonoscopy when a given size lesion is observed, we assessed the yield of advanced adenoma and cancer at colonoscopy based on the size of the abnormality detected at flexible sigmoidoscopy (FSG).
  • METHODS: We used data from the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial, a randomized, controlled, community-based study of FSG.
  • For women with a polyp 0.5-0.9 cm on FSG (n = 1426), the yield in the distal colon on colonoscopy was 0.6% for cancer (number needed to screen [NNS] = 166) and 14.5% for advanced adenoma (NNS = 7).
  • In men (n = 2183), the yield was 0.7% (NNS = 142) for cancer and 15.9% (NNS = 6) for advanced adenoma.
  • [MeSH-major] Adenoma / diagnosis. Adenoma / pathology. Colonic Neoplasms / diagnosis. Colonic Neoplasms / pathology. Colonic Polyps / pathology. Sigmoidoscopy / methods

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  • [CommentIn] Gastroenterology. 2006 Dec;131(6):2006-9 [17188963.001]
  • (PMID = 17188959.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CN / N01-CN2551
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
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93. Martin JT, Alkhoury F, Helton S, Fiedler P, Sakharova O, Yood S: Metastatic adenocarcinoma within a functioning adrenal adenoma: a case report. Cases J; 2009;2:7965

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Metastatic adenocarcinoma within a functioning adrenal adenoma: a case report.
  • She had recently been diagnosed with lung adenocarcinoma.
  • Pathologic findings revealed a 5 cm adrenal adenoma with a metastatic adenocarcinoma deposit.
  • The occurrence of tumor-to-tumor metastasis is rare, and the finding of a metastasis within a functional adrenal adenoma exceptionally so.
  • Previously reported incidences of this finding in patients with lung cancer range from 0.14% to 0.63%.

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  • (PMID = 19830028.001).
  • [ISSN] 1757-1626
  • [Journal-full-title] Cases journal
  • [ISO-abbreviation] Cases J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2740135
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94. Vik A, Cui G, Isaksen V, Wik T, Hansen JB: Erythropoietin production by a hepatic adenoma in a patient with severe erythrocytosis. Acta Haematol; 2009;121(1):52-5
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  • [Title] Erythropoietin production by a hepatic adenoma in a patient with severe erythrocytosis.
  • Further investigations excluded polycythemia vera or any lung or heart disease.
  • Needle biopsies were performed and the histopathological diagnosis was hepatocellular adenoma.
  • Liver adenoma is a rare cause of erythrocytosis.
  • [MeSH-major] Adenoma / metabolism. Erythropoietin / biosynthesis. Liver Neoplasms / metabolism. Polycythemia / metabolism

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  • [Copyright] (c) 2009 S. Karger AG, Basel.
  • (PMID = 19339771.001).
  • [ISSN] 1421-9662
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 11096-26-7 / Erythropoietin
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95. Seimiya YM, Takahashi M, Furukawa T, Mizutani K, Kimura K, Haritani M: An aged bull with concurrent thyroid C cell carcinoma, adrenal pheochromocytoma and pituitary chromophobe adenoma. J Vet Med Sci; 2009 Feb;71(2):225-8
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  • [Title] An aged bull with concurrent thyroid C cell carcinoma, adrenal pheochromocytoma and pituitary chromophobe adenoma.
  • Pathological examination disclosed multiple endocrine tumors including thyroid C cell carcinoma with metastases to the cervical lymph nodes and lung, adrenal pheochromocytoma and pituitary chromophobe adenoma in the pars distalis.


96. Zhang FW, Cheng HC, Jiang CD, Deng CY, Xiong YZ, Li FE, Lei MG: Imprinted status of pleomorphic adenoma gene-like I and paternal expression gene 10 genes in pigs. J Anim Sci; 2007 Apr;85(4):886-90

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Imprinted status of pleomorphic adenoma gene-like I and paternal expression gene 10 genes in pigs.
  • In this study, the polymorphism-based approach was used to detect the expression patterns of the porcine pleomorphic adenoma gene-like I (PLAGL1) and paternal expression gene 10 (PEG10) genes.
  • Imprinting analysis indicated that the PLAGL1 and PEG10 genes were both paternally expressed in all tissues tested (heart, liver, spleen, lung, kidney, stomach, small intestine, skeletal muscle, fat, uterus, and ovary).

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  • (PMID = 17178803.001).
  • [ISSN] 1525-3163
  • [Journal-full-title] Journal of animal science
  • [ISO-abbreviation] J. Anim. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins
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97. 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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98. Kondo T: Colon invasive micropapillary carcinoma arising in tubulovillous adenoma. Pol J Pathol; 2008;59(3):183-5

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  • [Title] Colon invasive micropapillary carcinoma arising in tubulovillous adenoma.
  • This histologic pattern has been described in various organs, including the breast, lung, urinary bladder, ovary, stomach, pancreas, and major salivary glands.
  • [MeSH-major] Adenoma, Villous / pathology. Carcinoma, Papillary / pathology. Colonic Neoplasms / pathology. Neoplasms, Multiple Primary / pathology

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  • (PMID = 19097358.001).
  • [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
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99. Liu CS, Hsu HS, Li CI, Jan CI, Li TC, Lin WY, Lin T, Chen YC, Lee CC, Lin CC: Central obesity and atherogenic dyslipidemia in metabolic syndrome are associated with increased risk for colorectal adenoma in a Chinese population. BMC Gastroenterol; 2010;10:51
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  • [Title] Central obesity and atherogenic dyslipidemia in metabolic syndrome are associated with increased risk for colorectal adenoma in a Chinese population.
  • The purpose of this study was to evaluate the relationship between individual components of MetS and colorectal adenoma.
  • MetS was defined based on the America Heart Association and National Heart Lung Blood Institute criteria.
  • Among the patients with MetS, 34.6% had adenoma, 31.7% had hyperplastic polyps and 23.3% were polyp-free (p < 0.0001, Chi-square test).
  • The adjusted OR for colorectal adenoma was significantly higher in the subjects with MetS (OR, 1.31, CI: 1.09-1.57).
  • A stronger association between MetS and colorectal adenoma was found in men (OR:1.44, CI:1.16-1.80) than in women (OR:1.04, CI:0.74-1.46).
  • The adjusted OR for adenoma increased as the number of MetS components increased (p for trend = 0.0001 ).
  • When the individual components of MetS were analyzed separately, only central obesity (OR:1.36, CI:1.14-1.63), low HDL cholesterol levels (OR:1.30, CI:1.10-1.54) and high triglyceride levels (OR:1.26, CI:1.04-1.53) were independently associated with colorectal adenoma.
  • CONCLUSIONS: Of the components of MetS analyzed in this study, central obesity and dyslipidemia are independent risk factors for colorectal adenoma.
  • [MeSH-major] Adenoma / epidemiology. Adenoma / ethnology. Colorectal Neoplasms / epidemiology. Colorectal Neoplasms / ethnology. Dyslipidemias / complications. Metabolic Syndrome X / complications. Obesity, Abdominal / complications

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  • (PMID = 20507579.001).
  • [ISSN] 1471-230X
  • [Journal-full-title] BMC gastroenterology
  • [ISO-abbreviation] BMC Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2894746
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100. Baghai-Wadji M, Sianati M, Nikpour H, Koochekpour S: Pleomorphic adenoma of the trachea in an 8-year-old boy: a case report. J Pediatr Surg; 2006 Aug;41(8):e23-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pleomorphic adenoma of the trachea in an 8-year-old boy: a case report.
  • We report a case of pleomorphic adenoma of the trachea in an 8-year-old boy who required emergency surgery for severe respiratory distress.
  • Chest computed tomographic scan and bronchoscopy showed a relatively large mass in distal trachea and right main bronchus and destruction of the lung parenchyma.
  • Histopathological examination and immunohistochemical staining of tumor specimens were compatible with pleomorphic adenoma.
  • [MeSH-major] Adenoma, Pleomorphic / surgery. Bronchial Neoplasms / surgery. Thoracic Surgical Procedures / methods. Tracheal Neoplasms / surgery

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  • (PMID = 16863832.001).
  • [ISSN] 1531-5037
  • [Journal-full-title] Journal of pediatric surgery
  • [ISO-abbreviation] J. Pediatr. Surg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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