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63. Awaya H, Takeshima Y, Amatya VJ, Ishida H, Yamasaki M, Kohno N, Inai K: Loss of expression of E-cadherin and beta-catenin is associated with progression of pulmonary adenocarcinoma. Pathol Int; 2005 Jan;55(1):14-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The expression of E-cadherin and beta-catenin was examined in 154 cases of pulmonary adenocarcinoma, including 49 cases of atypical adenomatous hyperplasia (AAH), 40 cases of bronchioloalveolar carcinoma (BAC), 42 cases of BAC-dominant type of adenocarcinoma with mixed subtypes (early MX) and 23 cases of BAC-recessive type of adenocarcinoma with mixed subtypes (overt MX), by immunohistochemistry.
  • Loss of expression of E-cadherin and beta-catenin may play an important role in the progression of pulmonary adenocarcinoma, and these events occur before structural destruction of the alveolar wall by invasion of carcinoma cell.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Cadherins / biosynthesis. Cytoskeletal Proteins / biosynthesis. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Trans-Activators / biosynthesis

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  • (PMID = 15660698.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CTNNB1 protein, human; 0 / Cadherins; 0 / Cytoskeletal Proteins; 0 / Trans-Activators; 0 / beta Catenin
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4. Ishikawa H, Koizumi N, Morita T, Tani Y, Tsuchida M, Umezu H, Naito M, Sasai K: Ultrasmall pulmonary opacities on multidetector-row high-resolution computed tomography: a prospective radiologic-pathologic examination. J Comput Assist Tomogr; 2005 Sep-Oct;29(5):621-5
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  • Each lobe had a primary lung tumor and was removed surgically.
  • Histologic diagnoses of 36 pathologic abnormalities were inflammatory lesions (n = 16), intrapulmonary lymph nodes (IPLN; n = 7), atypical adenomatous hyperplasia (AAH; n = 7), bronchioloalveolar carcinoma (BAC; n = 5), and another neoplastic lesion (n = 1).
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / radiography. Adenomatosis, Pulmonary / radiography. Lung Neoplasms / radiography. Precancerous Conditions / radiography. Tomography, X-Ray Computed / methods
  • [MeSH-minor] Adult. Female. Humans. Hyperplasia / pathology. Hyperplasia / radiography. Male. Middle Aged. Prospective Studies

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  • (PMID = 16163031.001).
  • [ISSN] 0363-8715
  • [Journal-full-title] Journal of computer assisted tomography
  • [ISO-abbreviation] J Comput Assist Tomogr
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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65. Zhang Y, Zhi XY, Chen L, Wang DY, Li Y, Wang RT, Hu M, Liu L, Qian K: [Diagnosis and treatment of atypical adenomatous pulmonary hyperplasia in lungs]. Zhonghua Yi Xue Za Zhi; 2010 Dec 21;90(47):3355-8
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  • [Title] [Diagnosis and treatment of atypical adenomatous pulmonary hyperplasia in lungs].
  • OBJECTIVE: To analyze the characteristic of atypical adenomatous hyperplasia (AAH) in lungs though its computerized tomography (CT) scan, pathology and surgical mode.
  • METHODS: The investigators retrospectively evaluated 10 atypical adenomatous hyperplasias (AAH) that were histologically confirmed and that manifested pure ground glass opacity (GGO) on thin-section helical CT scans.
  • Microscopically it manifested an apparent local pattern of alveolus epithelium hyperplasia in lungs.
  • The alveolar interval had a slight increase.
  • Local hyperplasia of fibrous cells was present with a slight degree of nucleus heteromorphism.
  • [MeSH-major] Adenoma / pathology. Lung Neoplasms / pathology. Precancerous Conditions / pathology

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  • (PMID = 21223753.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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66. Morandi L, Asioli S, Cavazza A, Pession A, Damiani S: Genetic relationship among atypical adenomatous hyperplasia, bronchioloalveolar carcinoma and adenocarcinoma of the lung. Lung Cancer; 2007 Apr;56(1):35-42
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  • [Title] Genetic relationship among atypical adenomatous hyperplasia, bronchioloalveolar carcinoma and adenocarcinoma of the lung.
  • Atypical adenomatous hyperplasia (AAH) has been recently defined by WHO as a small lesion, not exceeding 5mm in major axis, composed of slightly enlarged alveolar septa lined by pneumocytes with plump, atypical nuclei.
  • AAH is frequently found in tissue surrounding lung adenocarcinoma and is considered a precursor of this subtype of lung cancer by many Authors.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma, Bronchiolo-Alveolar / genetics. Adenomatosis, Pulmonary / genetics. Lung Neoplasms / genetics. Precancerous Conditions / genetics
  • [MeSH-minor] Aged. DNA, Mitochondrial / genetics. Female. Humans. Hyperplasia. Loss of Heterozygosity. Male. Middle Aged. Mutation. Polymerase Chain Reaction. Sequence Analysis, DNA

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  • (PMID = 17241687.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / DNA, Mitochondrial
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67. Kitamura H, Okudela K: Bronchioloalveolar neoplasia. Int J Clin Exp Pathol; 2010;4(1):97-9
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  • [Title] Bronchioloalveolar neoplasia.
  • Bronchioloalveolar carcinoma (BAC) arising in the peripheral lung is the prototype of human lung adenocar-cinoma and is considered to develop, at least in part, from its precursor atypical adenomatous hyperplasia (AAH).
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / pathology. Lung Neoplasms / pathology
  • [MeSH-minor] Adenoma / genetics. Adenoma / pathology. Animals. Disease Models, Animal. Hyperplasia / genetics. Hyperplasia / pathology. Mice. Mutation. Precancerous Conditions / genetics. Precancerous Conditions / pathology. Proto-Oncogene Proteins / genetics. Receptor, Epidermal Growth Factor / genetics. ras Proteins / genetics

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  • (PMID = 21228931.001).
  • [ISSN] 1936-2625
  • [Journal-full-title] International journal of clinical and experimental pathology
  • [ISO-abbreviation] Int J Clin Exp Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ PMC3016107
  • [Keywords] NOTNLM ; Bronchioloalveolar carcinoma / KRAS gene / atypical adenomatous hyperplasia / epidermal growth factor receptor gene / molecular targeting therapy / murine model
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68. Minami Y, Matsuno Y, Iijima T, Morishita Y, Onizuka M, Sakakibara Y, Noguchi M: Prognostication of small-sized primary pulmonary adenocarcinomas by histopathological and karyometric analysis. Lung Cancer; 2005 Jun;48(3):339-48
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  • To reveal useful prognostic factors in cases of small-sized pulmonary adenocarcinoma, we conducted a histological and karyometric analysis of 116 small-sized pulmonary adenocarcinomas measuring less than 2 cm in maximum diameter and four specimens of atypical adenomatous hyperplasia (AAH).
  • Small adenocarcinoma of the lung.
  • Lung Cancer 1995:75;2844-52].
  • There were 99 tumors of replacement-type adenocarcinoma, comprising 11 type A, localized bronchioloalveolar adenocarcinoma (LBAC); 6 type B, LBAC with alveolar collapse; and 82 type C, LBAC with foci of fibroblastic proliferation.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / pathology. Lung Neoplasms / genetics. Lung Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Nucleus / ultrastructure. Cell Proliferation. Disease-Free Survival. Female. Fibroblasts. Humans. Karyotyping. Male. Middle Aged. Neoplasm Staging / methods. Prognosis. Survival Analysis

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  • (PMID = 15893002.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
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69. Ye B, Zhang YX, Yang F, Chen HL, Xia D, Liu MQ, Lai BT: Induction of lung lesions in Wistar rats by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone and its inhibition by aspirin and phenethyl isothiocyanate. BMC Cancer; 2007;7:90
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  • [Title] Induction of lung lesions in Wistar rats by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone and its inhibition by aspirin and phenethyl isothiocyanate.
  • BACKGROUND: The development of effective chemopreventive agents against cigarette smoke-induced lung cancer could be greatly facilitated by suitable laboratory animal models, such as animals treated with the tobacco-specific lung carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK).
  • In the current study, we established a novel lung cancer model in Wistar rats treated with NNK.
  • PCNA, p63 and COX-2 expression were analyzed in the preneoplastic lung lesions.
  • RESULTS: NNK induced preneoplastic lesions in lungs, including 33.3% alveolar hyperplasia and 55.6% alveolar atypical dysplasia.
  • COX-2 expression increased similarly in alveolar hyperplasia and alveolar atypical dysplasia, while PCNA expression increased more significantly in the latter than the former.
  • In the second study, the incidences of alveolar atypical dysplasia were reduced to 10%, 10% and 0%, respectively, in the aspirin, PEITC and aspirin and PEITC groups, compared with 62.5% in the carcinogen-treated control group.
  • [MeSH-major] Anticarcinogenic Agents / therapeutic use. Aspirin / therapeutic use. Carcinogens / toxicity. Isothiocyanates / therapeutic use. Lung Neoplasms / prevention & control. Nitrosamines / toxicity
  • [MeSH-minor] Animals. Cyclooxygenase 2 / biosynthesis. Cyclooxygenase 2 / drug effects. Cyclooxygenase 2 Inhibitors. Disease Models, Animal. Female. Immunohistochemistry. Precancerous Conditions / prevention & control. Proliferating Cell Nuclear Antigen / biosynthesis. Proliferating Cell Nuclear Antigen / drug effects. Rats. Rats, Wistar. Tobacco / chemistry

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  • (PMID = 17535415.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Carcinogens; 0 / Cyclooxygenase 2 Inhibitors; 0 / Isothiocyanates; 0 / Nitrosamines; 0 / Proliferating Cell Nuclear Antigen; 64091-91-4 / 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone; 6U7TFK75KV / phenethyl isothiocyanate; EC 1.14.99.1 / Cyclooxygenase 2; R16CO5Y76E / Aspirin
  • [Other-IDs] NLM/ PMC1899177
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70. Jain D, Joshi K, Jindal SK: Precursor lesions of adenocarcinoma lung--two case reports. Indian J Pathol Microbiol; 2005 Jul;48(3):399-402
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  • [Title] Precursor lesions of adenocarcinoma lung--two case reports.
  • Although precursor lesions of bronchogenic squamous cell carcinoma are well documented, the preinvasive lesions of pulmonary adenocarcinoma are seen very rarely.
  • It has been hypothesized that there is a stepwise progression of alveolar epithelial hyperplasia to atypical alveolar hyperplasia and subsequently to malignancy in the pathogenesis of peripheral adenocarcinoma of the lung.
  • In the present paper we would like to share our experience of two cases of pulmonary adenocarcinoma with their precursor lesions in the form of atypical alveolar hyperplasia.
  • [MeSH-major] Adenocarcinoma / pathology. Lung Diseases, Interstitial / pathology. Lung Neoplasms / pathology. Precancerous Conditions / pathology. Pulmonary Alveoli / pathology
  • [MeSH-minor] Aged. Female. Humans. Hyperplasia / pathology. Male. Middle Aged

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  • (PMID = 16761769.001).
  • [ISSN] 0377-4929
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
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71. Chung JH, Choe G, Jheon S, Sung SW, Kim TJ, Lee KW, Lee JH, Lee CT: Epidermal growth factor receptor mutation and pathologic-radiologic correlation between multiple lung nodules with ground-glass opacity differentiates multicentric origin from intrapulmonary spread. J Thorac Oncol; 2009 Dec;4(12):1490-5
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  • [Title] Epidermal growth factor receptor mutation and pathologic-radiologic correlation between multiple lung nodules with ground-glass opacity differentiates multicentric origin from intrapulmonary spread.
  • INTRODUCTION: No standard guidelines detailing recommendations for the selection and treatment for multiple lung nodules with ground-glass opacity (GGO) have been established.
  • For treatment decision, we analyzed epidermal growth factor receptor (EGFR)/K-ras somatic aberrations and pathologic-radiologic correlation in multiple lung nodules presented as GGO to differentiate multifocal lesions from intrapulmonary spread.
  • METHODS: Twenty-four patients with multiple lung nodules presented as GGO were identified to investigate somatic mutations of EGFR (exon 18-21) and K-ras (codons 2, 13, and 61).
  • This series included 18 atypical adenomatous hyperplasias (AAH), 15 bronchioloalveolar carcinomas (BAC), and 23 adenocarcinomas (ADC) obtained from 24 patients.
  • RESULTS: High frequency of discordant EGFR mutations (17 of 24, 70.8%) could discriminate tumor clonality (18 of 24, 75%) of multiple lung neoplastic nodules presented as GGO.
  • These findings might be a clue to establish guidelines of the multiple neoplastic lung nodules with GGO.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / pathology. Carcinoma in Situ / pathology. Hyperplasia / pathology. Lung Neoplasms / pathology. Mutation / genetics. Precancerous Conditions / pathology. Receptor, Epidermal Growth Factor / genetics

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  • (PMID = 19844187.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.6.5.2 / ras Proteins
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