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56. Shimada A, Kano J, Ishiyama T, Okubo C, Iijima T, Morishita Y, Minami Y, Inadome Y, Shu Y, Sugita S, Takeuchi T, Noguchi M: Establishment of an immortalized cell line from a precancerous lesion of lung adenocarcinoma, and genes highly expressed in the early stages of lung adenocarcinoma development. Cancer Sci; 2005 Oct;96(10):668-75
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Establishment of an immortalized cell line from a precancerous lesion of lung adenocarcinoma, and genes highly expressed in the early stages of lung adenocarcinoma development.
  • Atypical adenomatous hyperplasia (AAH) is classified as a precancerous lesion of lung adenocarcinoma.
  • We established an immortalized AAH cell line (PL16T) and a human non-neoplastic bronchial epithelial cell line (PL16B) from the same patient by transfection with the gene for SV40 large T antigen.
  • In normal lung tissue, both TACSTD2 and S100A2 were expressed at very low levels, but seven and five of 14 AAH were positive for TACSTD2 and S100A2, respectively.
  • The frequency of TACSTD2 positivity was increased in 16 of 22 bronchioloalveolar carcinomas (BAC) and adenocarcinoma with mixed subtype with BAC component (mixed BAC).
  • The abnormal transcription of TACSTD2 and S100A2 are thought to be unique molecular markers of the preinvasive stage of lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Antigens, Neoplasm / biosynthesis. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / pathology. Cell Adhesion Molecules / biosynthesis. Chemotactic Factors / biosynthesis. Lung Neoplasms / genetics. Lung Neoplasms / pathology. Precancerous Conditions / genetics. Precancerous Conditions / pathology. S100 Proteins / biosynthesis
  • [MeSH-minor] Female. Gene Expression Profiling. Humans. Hyperplasia. Lung / pathology. Middle Aged. Neoplasm Staging. Nucleic Acid Hybridization. Tumor Cells, Cultured

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  • (PMID = 16232198.001).
  • [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] 0 / Antigens, Neoplasm; 0 / Cell Adhesion Molecules; 0 / Chemotactic Factors; 0 / S100 Proteins; 0 / S100A2 protein, human; 0 / TACSTD2 protein, human
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57. 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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  • 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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58. Findeis-Hosey JJ, Yang Q, Spaulding BO, Wang HL, Xu H: IMP3 expression is correlated with histologic grade of lung adenocarcinoma. Hum Pathol; 2010 Apr;41(4):477-84
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  • [Title] IMP3 expression is correlated with histologic grade of lung adenocarcinoma.
  • This study aimed to determine the correlation of insulin-like growth factor II mRNA binding protein 3 expression with histologic grade of lung adenocarcinoma.
  • Eighty-nine cases, including 11 atypical adenomatous hyperplasias, 10 pure bronchioloalveolar carcinomas, 36 well-differentiated adenocarcinomas and 41 moderately or poorly differentiated adenocarcinomas, were immunohistochemically studied using a monoclonal antibody against insulin-like growth factor II mRNA binding protein 3.
  • Four (40.0%) of 10 bronchioloalveolar carcinomas and 13 (36.1%) of 36 well-differentiated adenocarcinomas exhibited insulin-like growth factor II mRNA binding protein 3 positivity with a variable degree and percentage of tumor cells staining.
  • When bronchioloalveolar carcinomas were present in a pure form or as a component of adenocarcinomas, positive insulin-like growth factor II mRNA binding protein 3 staining was always patchy, with less than 20% of tumor cells stained.
  • Overall, the frequency of positive insulin-like growth factor II mRNA binding protein 3 staining was lower in bronchioloalveolar carcinomas and well-differentiated adenocarcinomas compared to moderately/poorly differentiated adenocarcinomas (P < .01).
  • No insulin-like growth factor II mRNA binding protein 3 signal was detected in any case of atypical adenomatous hyperplasia.
  • These findings show that insulin-like growth factor II mRNA binding protein 3 is strongly and diffusely expressed in a large proportion of moderately/poorly differentiated lung adenocarcinomas, in particular in the solid component of mixed subtype adenocarcinomas, less frequently expressed in well-differentiated adenocarcinomas and bronchioloalveolar carcinomas, and negative in atypical adenomatous hyperplasias.
  • [MeSH-major] Adenocarcinoma / pathology. Lung Neoplasms / pathology. Neoplasm Proteins / biosynthesis. RNA-Binding Proteins / biosynthesis
  • [MeSH-minor] Adenocarcinoma, Bronchiolo-Alveolar / metabolism. Adenocarcinoma, Bronchiolo-Alveolar / pathology. Humans. Hyperplasia. Immunohistochemistry. Lung / metabolism. Lung / pathology. Neoplasm Invasiveness. Neoplasm Staging. Precancerous Conditions / metabolism

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  • [Copyright] Copyright 2010 Elsevier Inc.
  • (PMID = 20004948.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / IMP3 protein, human; 0 / Neoplasm Proteins; 0 / RNA-Binding Proteins
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59. Orita H, Coulter J, Tully E, Kuhajda FP, Gabrielson E: Inhibiting fatty acid synthase for chemoprevention of chemically induced lung tumors. Clin Cancer Res; 2008 Apr 15;14(8):2458-64
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  • [Title] Inhibiting fatty acid synthase for chemoprevention of chemically induced lung tumors.
  • PURPOSE: Fatty acid synthase (FAS) is overexpressed in lung cancer, and we have investigated the potential use of FAS inhibitors for chemoprevention of lung cancer.
  • EXPERIMENTAL DESIGN: Expression of FAS was evaluated in preinvasive human lung lesions (bronchial squamous dysplasia and atypical adenomatous hyperplasia) and in murine models of lung tumorigenesis [4-(methylnitrosamino)-I-(3-pyridyl)-1-butanone-induced and urethane-induced lung tumors in A/J mice].
  • RESULTS: Immunohistochemical studies show that human bronchial dysplasia and atypical adenomatous hyperplasia express high levels of FAS compared with normal lung tissues, suggesting that FAS might be a target for intervention in lung carcinogenesis.
  • FAS is also expressed at high levels in chemically induced murine lung tumors, and the numbers and sizes of those murine tumors are significantly reduced by treating carcinogen-exposed mice with pharmacologic inhibitors of FAS, C75 and C93.
  • CONCLUSIONS: We conclude that increased levels of FAS are common in human preinvasive neoplasia of the lung.
  • Based on studies in mouse models, it seems that inhibiting FAS is an effective strategy in preventing and retarding growth of lung tumors that have high expression of this enzyme.
  • [MeSH-major] Anticarcinogenic Agents / therapeutic use. Enzyme Inhibitors / therapeutic use. Fatty Acid Synthases / antagonists & inhibitors. Lung Neoplasms / prevention & control


60. 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.
  • Previous studies of human adenocarcinomas have shown that the two proteins are expressed reciprocally; SP-A and lysozyme are differential markers of atypical adenomatous hyperplasia (AAH) and non-goblet cell type adenocarcinoma, and of goblet cell type adenocarcinoma, respectively.
  • 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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61. Ruan YH, Hua HR, Gao Q, Song JL, Liang R, Jin KW: [Pathological study of lung cancer induced by Yunnan tin mine dusts in F344 rats]. Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi; 2007 Jun;25(6):331-5
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  • [Title] [Pathological study of lung cancer induced by Yunnan tin mine dusts in F344 rats].
  • OBJECTIVE: To set up animal models of the lung cancer induced by Yunnan tin mineral dusts (no radon) in F344 rats and to explore the process of carcinogenesis and pathologic alterations in various stages of malignant transformation in the animal models.
  • Pollak stein was used to evaluate the development of fibrosis of lung in the rats.
  • Along with reduction of inflammation, collagen fibrils increased at alveolar interstices.
  • Simple hyperplasia, papillary hyperplasia and metaplasia of the epithelial cells in alveolar and bronchi were observed, followed by atypical adenomatous hyperplasia and squamous dysplasia.
  • Lung cancer was induced in the end.
  • Among the 14 cases of lung cancer, 9 cases were adenocarcinoma, 2 squamous cell carcinoma and 3 mixed carcinoma.
  • No lung cancer occurred in other three control groups.
  • Lung fibrosis was found in 31 cases of in the tin mineral dust group.
  • The greater the mineral dust deposit was, the more serious the alveolar fibrosis was.
  • CONCLUSION: Yunnan tin mineral dusts without radon induce lung cancer in rates.
  • The adenocarcinoma and squamous carcinomas induced in F344 rat lung can occur in the alveoli.
  • The further study on whether type II alveolar epithelial cells are the origin cells of adenocarcinoma and some peripheral squamous lung carcinomas is worthwhile.
  • [MeSH-major] Lung Neoplasms / pathology. Tin / adverse effects
  • [MeSH-minor] Animals. Disease Models, Animal. Dust. Female. Lung / drug effects. Lung / pathology. Male. Rats. Rats, Inbred F344

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  • (PMID = 17723188.001).
  • [ISSN] 1001-9391
  • [Journal-full-title] Zhonghua lao dong wei sheng zhi ye bing za zhi = Zhonghua laodong weisheng zhiyebing zazhi = Chinese journal of industrial hygiene and occupational diseases
  • [ISO-abbreviation] Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Dust; 7440-31-5 / Tin
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62. Huo Z, Liu HR, Wan JW: [Atypical adenomatous hyperplasia of lung: clinicopathologic study of 8 cases and review of literature]. Zhonghua Bing Li Xue Za Zhi; 2007 May;36(5):292-6
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  • [Title] [Atypical adenomatous hyperplasia of lung: clinicopathologic study of 8 cases and review of literature].
  • OBJECTIVE: To study the clinicopathologic and immunohistochemical features of atypical adenomatous hyperplasia (AAH) of lung.
  • METHODS: Eight cases of AAH of lung were studied by light microscopy and immunohistochemical staining for p16, thyroid transcription factor-1 (TTF-1), Ki-67, p53, epidermal growth factor receptor (EGFR) and c-erbB-2.
  • Three patients had past history of non-pulmonary tumors, while 4 patients had lung adenocarcinoma.
  • CONCLUSIONS: AAH of lung is associated with pulmonary adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Adenomatosis, Pulmonary / pathology. Lung Neoplasms / pathology. Neoplasms, Multiple Primary / pathology
  • [MeSH-minor] Adult. DNA-Binding Proteins / metabolism. Female. Follow-Up Studies. Humans. Hyperplasia / metabolism. Hyperplasia / pathology. Hyperplasia / surgery. Ki-67 Antigen / metabolism. Male. Middle Aged. Neoplasm Proteins / metabolism. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. Precancerous Conditions / surgery

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  • (PMID = 17706134.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Ki-67 Antigen; 0 / Neoplasm Proteins; 0 / P16 protein, human; 0 / TTF1 protein, human
  • [Number-of-references] 18
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63. 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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4. Sano T, Kitayama Y, Igarashi H, Suzuki M, Tanioka F, Chida K, Okudela K, Sugimura H: Chromosomal numerical abnormalities in early stage lung adenocarcinoma. Pathol Int; 2006 Mar;56(3):117-25
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  • [Title] Chromosomal numerical abnormalities in early stage lung adenocarcinoma.
  • Recent radiological scrutiny has enabled the identification of small peripheral lesions in the lung.
  • A chromosome-wide investigation encompassing almost all the chromosomal centromeres was performed using modified fluorescence in situ hybridization on the archived pathological samples of 16 atypical adenomatous hyperplasia (AAH) and 30 lung adenocarcioma (AdCa) specimens including those smaller than 1 cm in size.
  • The prevalence of the gain differed significantly between AAH and bronchioloalveolar carcinoma (BAC) </= 1 cm, but not between BAC < 1 cm and well-differentiated AdCa > 1 cm.
  • It is proposed that the CNA is a distinct phenomenon occurring in the early or premalignant stage of lung AdCa, and that the CNA itself may not be a sequel in the carcinogenetic process, but a driving factor in carcinogenesis.
  • [MeSH-major] Adenocarcinoma / genetics. Chromosome Aberrations. Lung Neoplasms / genetics

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  • (PMID = 16497244.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
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65. Mascaux C: [Etiology, epidemiology, biology. Lung carcinogenesis]. Rev Mal Respir; 2008 Oct;25(8 Pt 2):3S32-9
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  • [Title] [Etiology, epidemiology, biology. Lung carcinogenesis].
  • Lung cancer is a complex disease involving various oncogenic pathways.
  • Pre-invasive stages exist for different forms of lung cancer and some of them are recognized as being preneoplastic: dysplasias and in situ carcinoma, atypical adenomatous hyperplasia and diffuse idiopathic pulmonary neuroendocrine cell hyperplasia are supposed to be precursors of squamous cell carcinomas, adenocarcinomas and carcinoid tumors, respectively.
  • The sequence of histological modifications of bronchial mucosa preceding the development of a squamous cell carcinoma are well documented while those preceding other histological types are less known.
  • It also discusses arguments for their preneoplastic nature, their evolution and risk of progression risk, molecular abnormalities involved in lung carcinogenesis and clinical relevance of these lesions.
  • [MeSH-major] Lung Neoplasms / pathology. Precancerous Conditions
  • [MeSH-minor] Humans. Hyperplasia. Lung / pathology

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  • (PMID = 18971824.001).
  • [ISSN] 0761-8425
  • [Journal-full-title] Revue des maladies respiratoires
  • [ISO-abbreviation] Rev Mal Respir
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
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66. Seki M, Akasaka Y: Multiple lung adenocarcinomas and AAH treated by surgical resection. Lung Cancer; 2007 Feb;55(2):237-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Multiple lung adenocarcinomas and AAH treated by surgical resection.
  • Atypical adenomatous hyperplasia (AAH) is often found in the lungs of patients with multiple primary lung adenocarcinoma; however, treatment for such patients has not been clearly defined.
  • This report presents a case of multiple primary lung adenocarcinoma with multiple AAH treated by surgery.
  • Thirteen tumorous lesions were resected; 10 lesions were diagnosed as primary lung adenocarcinoma and the others as AAH.
  • The clinical course indicates that surgery can be a treatment strategy for synchronous or metachronous lung carcinoma with AAH.
  • [MeSH-major] Adenocarcinoma / surgery. Lung Neoplasms / surgery
  • [MeSH-minor] Humans. Hyperplasia / pathology. Hyperplasia / surgery. Male. Middle Aged. Neoplasms, Second Primary / pathology. Neoplasms, Second Primary / surgery. Tomography, X-Ray Computed

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  • (PMID = 17118487.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Ireland
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67. 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.
  • [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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68. Tsushima Y, Suzuki K, Watanabe S, Kusumoto M, Tsuta K, Matsuno Y, Asamura H: Multiple lung adenocarcinomas showing ground-glass opacities on thoracic computed tomography. Ann Thorac Surg; 2006 Oct;82(4):1508-10
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  • [Title] Multiple lung adenocarcinomas showing ground-glass opacities on thoracic computed tomography.
  • It is difficult to distinguish multiple primary lung cancers from pulmonary metastasis.
  • We experienced a case of surgically resected lung tumors that showed multiple ground-glass opacities on thoracic computed tomographic scan.
  • Surgical resection was performed because all tumors had a ground-glass opacity appearance on computed tomographic scan, which is compatible with a finding of primary lung adenocarcinoma.
  • The postoperative pathologic diagnoses were two cases of invasive adenocarcinoma, six cases of bronchioloalveolar carcinoma, and eight cases of atypical adenomatous hyperplasia.
  • A ground-glass opacity appearance on computed tomographic scan could be interpreted as supportive evidence for multiple primary lung adenocarcinoma rather than pulmonary metastases.
  • [MeSH-major] Adenocarcinoma / radiography. Lung Neoplasms / radiography
  • [MeSH-minor] Adenocarcinoma, Bronchiolo-Alveolar / pathology. Adenocarcinoma, Bronchiolo-Alveolar / radiography. Adenocarcinoma, Bronchiolo-Alveolar / surgery. Female. Humans. Hyperplasia / pathology. Hyperplasia / radiography. Hyperplasia / surgery. Lung Diseases / pathology. Lung Diseases / radiography. Lung Diseases / surgery. Middle Aged. Pneumonectomy. Tomography, X-Ray Computed

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  • (PMID = 16996967.001).
  • [ISSN] 1552-6259
  • [Journal-full-title] The Annals of thoracic surgery
  • [ISO-abbreviation] Ann. Thorac. Surg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
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69. Hanaoka T, Sone S, Takayama F, Hayano T, Yamaguchi S, Okada M: Presence of local pleural adhesion in CT screening-detected small nodule in the lung periphery suggests noncancerous, inflammatory nature of the lesion. Clin Imaging; 2007 Nov-Dec;31(6):385-9
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  • [Title] Presence of local pleural adhesion in CT screening-detected small nodule in the lung periphery suggests noncancerous, inflammatory nature of the lesion.
  • PURPOSE: Differential diagnosis of small nodules in the lung periphery detected by low-dose chest CT screening is important before surgery.
  • MATERIALS AND METHODS: This study is based on 106 patients (46 men and 60 women, median age: 61.5 years) with 123 CT screening-detected and histologically confirmed nodules smaller than 30 mm in the lung periphery identified between 2002 and 2005 at Azumi General Hospital, Japan.
  • Lesions were classified into three groups according to histological findings: adenocarcinoma, atypical adenomatous hyperplasia (AAH) and inflammatory focal lesions.
  • We examined the visceral pleura during surgery at a location close to lung nodules.
  • RESULTS: The median diameter of resected lung nodules on high-resolution CT (HRCT) was 9.0 mm.
  • Histopathological diagnosis was lung cancer in 69, AAH in 21, other noninflammatory tumours in 6 and inflammatory lesions in 27.
  • [MeSH-major] Adenocarcinoma / radiography. Lung Neoplasms / radiography. Pleural Diseases / radiography. Tissue Adhesions / radiography. Tomography, X-Ray Computed
  • [MeSH-minor] Adult. Aged. Chi-Square Distribution. Diagnosis, Differential. Female. Humans. Hyperplasia. Inflammation / pathology. Inflammation / radiography. Male. Middle Aged


70. Park CM, Goo JM, Lee HJ, Lee CH, Chun EJ, Im JG: Nodular ground-glass opacity at thin-section CT: histologic correlation and evaluation of change at follow-up. Radiographics; 2007 Mar-Apr;27(2):391-408
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  • The popularization of computed tomography (CT) in clinical practice and the introduction of mass screening for early lung cancer with the use of CT have increased the frequency of findings of subtle nodules or nodular ground-glass opacity.
  • Nodular ground-glass opacity may be observed in malignancies such as bronchioloalveolar carcinoma and adenocarcinoma, as well as in their putative precursors, such as atypical adenomatous hyperplasia.
  • [MeSH-minor] Humans. Lung Neoplasms / radiography. Practice Guidelines as Topic. Practice Patterns, Physicians'. Prognosis. Statistics as Topic

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  • [Copyright] (c) RSNA, 2007.
  • (PMID = 17374860.001).
  • [ISSN] 1527-1323
  • [Journal-full-title] Radiographics : a review publication of the Radiological Society of North America, Inc
  • [ISO-abbreviation] Radiographics
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 57
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71. Ferretti G, Félix L, Serra-Tosio G, Brambilla C, Moro-Sibilot D, Brichon PY, Coulomb M, Lantuejoul S: [Non-solid and part-solid pulmonary nodules on CT scanning]. Rev Mal Respir; 2007 Dec;24(10):1265-76
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  • STATE OF ART: Nonsolid and part-solid pulmonary nodules account for between 2.9 and 19% of all pulmonary nodules detected in high-risk patients included in CT screening series for lung cancer.
  • Radio-pathological correlations have shown that the aetiology could be either benign (chronic pneumonia, atypical adenomatous hyperplasia, localized fibrosis) or malignant (broncholoalveolar cell carcinoma, adenocarcinoma, more rarely metastasis).
  • [MeSH-minor] Algorithms. Humans. Lung / pathology. Lung Neoplasms / pathology. Precancerous Conditions / radiography. Prevalence

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  • (PMID = 18216747.001).
  • [ISSN] 0761-8425
  • [Journal-full-title] Revue des maladies respiratoires
  • [ISO-abbreviation] Rev Mal Respir
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 51
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72. Zhang Y, Lai B, Chen H, Yue W, Yang F, Xia D, Xiao J, Ye B, Liu M: [Induction of pulmonary precancerous lesions by tobacco-specific NNK in Wistar rats]. Zhongguo Fei Ai Za Zhi; 2006 Apr 20;9(2):152-6
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  • All of rats in trial group (15/15) displayed atypical hyperplasia in alveolar region, showing single or multiple layers of proliferative epithelial cells along intact alveolar septa with irregular and non-discrete margins of lesion, but continuous alveolar spaces were not obliterated by proliferative epithelial cells.
  • Ten of 15 rats in trial group showed severe atypical hyperplasia of glandular epithelium with occasional infiltrating to muscular layer.
  • All of those atypical hyperplasia cells showed positive AE1/AE3 expression.
  • CONCLUSIONS: Transbronchial instillation of iodized oil including tobacco-specific NNK can induce pulmonary lesions as atypical hyperplasia of alveolar cell and glandular epithelium in Wistar rats.
  • This model can be used in experimental studies about tobacco-related lung cancer.

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  • (PMID = 21144301.001).
  • [ISSN] 1009-3419
  • [Journal-full-title] Zhongguo fei ai za zhi = Chinese journal of lung cancer
  • [ISO-abbreviation] Zhongguo Fei Ai Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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73. Ohtsuka T, Watanabe K, Kaji M, Naruke T, Suemasu K: A clinicopathological study of resected pulmonary nodules with focal pure ground-glass opacity. Eur J Cardiothorac Surg; 2006 Jul;30(1):160-3
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  • RESULTS: The histological diagnosis was bronchioloalveolar carcinoma (BAC) in 10 patients (12 lesions), atypical adenomatous hyperplasia (AAH) in 15 patients (22 lesions), and focal scar in 1 patient (1 lesion).
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / pathology. Adenomatosis, Pulmonary / pathology. Lung Neoplasms / pathology

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  • (PMID = 16723239.001).
  • [ISSN] 1010-7940
  • [Journal-full-title] European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery
  • [ISO-abbreviation] Eur J Cardiothorac Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Carcinoembryonic Antigen
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74. Kawai T, Hiroi S, Nakanishi K, Meeker AK: Telomere length and telomerase expression in atypical adenomatous hyperplasia and small bronchioloalveolar carcinoma of the lung. Am J Clin Pathol; 2007 Feb;127(2):254-62
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  • [Title] Telomere length and telomerase expression in atypical adenomatous hyperplasia and small bronchioloalveolar carcinoma of the lung.
  • Telomeres are located at the ends of every human chromosome and are subject to shortening at each cycle of cell division in cell senescence and early carcinogenesis.
  • We examined the expression of telomeric DNA in 21 atypical adenomatous hyperplasias (AAHs) and 40 bronchioloalveolar carcinomas (BACs) measuring 2 cm or less in greatest diameter using fluorescent in situ hybridization and the expression of human telomerase reverse transcriptase (hTERT) messenger RNA (mRNA) in 35 AAHs and 37 BACs.
  • In "benign" lung samples, the pattern of expression of hTERT mRNA was barely detected in the nonciliated cells of the bronchioles and alveolar type II cells.
  • Telomere length and telomerase may be involved in carcinogenesis in the lung.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenocarcinoma, Bronchiolo-Alveolar / metabolism. Lung Neoplasms / metabolism. Telomerase / biosynthesis. Telomere / physiology
  • [MeSH-minor] Humans. Hyperplasia. In Situ Hybridization, Fluorescence

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  • (PMID = 17210516.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.7.49 / Telomerase
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75. Lantuejoul S, Raynaud C, Salameire D, Gazzeri S, Moro-Sibilot D, Soria JC, Brambilla C, Brambilla E: Telomere maintenance and DNA damage responses during lung carcinogenesis. Clin Cancer Res; 2010 Jun 1;16(11):2979-88
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  • [Title] Telomere maintenance and DNA damage responses during lung carcinogenesis.
  • EXPERIMENTAL DESIGN: We have evaluated telomere length by fluorescence in situ hybridization and analyzed DDR proteins p-CHK2, p-ATM, and p-H2AX, and telomeric maintenance proteins TRF1 and TRF2 expression by immunohistochemistry in normal bronchial/bronchiolar epithelium, and in 109 bronchial preneoplastic lesions, in comparison with 32 squamous invasive carcinoma (SCC), and in 27 atypical alveolar hyperplasia (AAH) in comparison with 6 adenocarcinoma in situ (AIS; formerly bronchiolo-alveolar carcinoma) and 24 invasive adenocarcinoma (ADC).
  • RESULTS: Telomere length critically shortened at bronchial metaplasia stage to increase gradually from dysplasia to invasive SCC; in bronchiolo-alveolar lesions, telomere length decreased from normal to AIS and increased from stage I to II to stage III to IV ADC.
  • CONCLUSION: Telomere attrition occurs at the earliest stage of lung carcinogenesis as an initiating event, preceding TRF1 and TRF2 overexpression for telomere stabilization.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma, Bronchiolo-Alveolar / genetics. DNA Damage. Lung Neoplasms / genetics. Precancerous Conditions / genetics. Telomere / ultrastructure
  • [MeSH-minor] Ataxia Telangiectasia Mutated Proteins. Carcinoma, Squamous Cell / genetics. Cell Cycle Proteins / metabolism. Checkpoint Kinase 2. DNA-Binding Proteins / metabolism. Disease Progression. Histones / metabolism. Hyperplasia / pathology. Immunohistochemistry. Lung / metabolism. Lung / pathology. Protein-Serine-Threonine Kinases / metabolism. Telomeric Repeat Binding Protein 1 / metabolism. Telomeric Repeat Binding Protein 2 / metabolism. Tumor Suppressor Proteins / metabolism

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  • [Copyright] Copyright 2010 AACR.
  • (PMID = 20404006.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / H2AFX protein, human; 0 / Histones; 0 / TERF2 protein, human; 0 / Telomeric Repeat Binding Protein 1; 0 / Telomeric Repeat Binding Protein 2; 0 / Tumor Suppressor Proteins; EC 2.7.1.11 / Checkpoint Kinase 2; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / CHEK2 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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76. Ikeda K, Awai K, Mori T, Kawanaka K, Yamashita Y, Nomori H: Differential diagnosis of ground-glass opacity nodules: CT number analysis by three-dimensional computerized quantification. Chest; 2007 Sep;132(3):984-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVES: To differentiate among atypical adenomatous hyperplasia (AAH), bronchioloalveolar carcinoma (BAC), and adenocarcinoma showing ground-glass opacity (GGO) on CT scans, we conducted a study to determine the optimal parameter on CT number analysis using three-dimensional (3D) computerized quantification.
  • [MeSH-major] Carcinoma / diagnosis. Imaging, Three-Dimensional. Lung / pathology. Lung Neoplasms / diagnosis. Solitary Pulmonary Nodule / diagnosis. Tomography, X-Ray Computed
  • [MeSH-minor] Aged. Diagnosis, Differential. Female. Humans. Hyperplasia. Male. Middle Aged

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  • [CommentIn] Chest. 2008 Mar;133(3):827-8; author reply 827-8 [18321915.001]
  • (PMID = 17573486.001).
  • [ISSN] 0012-3692
  • [Journal-full-title] Chest
  • [ISO-abbreviation] Chest
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
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77. Park CM, Goo JM, Lee HJ, Lee CH, Kim HC, Chung DH, Im JG: CT findings of atypical adenomatous hyperplasia in the lung. Korean J Radiol; 2006 Apr-Jun;7(2):80-6
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  • [Title] CT findings of atypical adenomatous hyperplasia in the lung.
  • OBJECTIVE: The aim of this study was to analyze the computed tomographic (CT) findings of atypical adenomatous hyperplasia (AAH) in the lung.
  • The CT findings of each AAH lesion were evaluated for multiplicity, location, shape, size and internal density of the lesion, the interface between the normal lung and the lesion, the internal features within the lesion and any change of the lesion on the follow-up CT scans (range: 33 to 540 days; average: 145.3 days).
  • Four of them (50%) had synchronous malignancies in the lung: adenocarcinoma of the lung (n = 3), and metastatic squamous cell carcinoma from the uterus (n = 1).
  • CONCLUSION: Atypical adenomatous hyperplasia is often associated with malignancy.
  • [MeSH-major] Lung / pathology. Lung / radiography. Precancerous Conditions / radiography. Tomography, X-Ray Computed
  • [MeSH-minor] Adenocarcinoma / pathology. Adenocarcinoma / radiography. Adult. Aged. Epithelial Cells / pathology. Female. Humans. Hyperplasia. Lung Neoplasms / epidemiology. Lung Neoplasms / radiography. Male. Middle Aged. Pulmonary Alveoli / pathology. Retrospective Studies

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  • (PMID = 16799268.001).
  • [ISSN] 1229-6929
  • [Journal-full-title] Korean journal of radiology
  • [ISO-abbreviation] Korean J Radiol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
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78. Gradowski JF, Mantha GS, Hunt JL, Dacic S: Molecular alterations in atypical adenomatous hyperplasia occurring in benign and cancer-bearing lungs. Diagn Mol Pathol; 2007 Jun;16(2):87-90
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  • [Title] Molecular alterations in atypical adenomatous hyperplasia occurring in benign and cancer-bearing lungs.
  • Atypical adenomatous hyperplasia (AAH) is considered to be a precursor lesion of the lung adenocarcinoma.
  • Several genetic abnormalities have been reported in AAH associated with adenocarcinoma, but little is known about AAH associated with benign lung lesions.
  • Seven cases of AAH from resected non-neoplastic lungs (AAH-B) and 12 cases from lungs resected for primary lung carcinoma (AAH-M) were analyzed for loss of heterozygosity (LOH) using 21 polymorphic microsatellite markers situated in proximity to known tumor suppressor genes on chromosomes 3p, 5q, 7p, 9p, 10q, and 17p.
  • Our results showed a significant overlap in LOH patterns between AAH with or without coexistent lung malignancy.
  • Therefore, AAH may represent a smoking induced low-grade neoplastic lesion that may be a precursor lesion of only a subset of invasive lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Adenomatosis, Pulmonary / genetics. Loss of Heterozygosity. Lung / pathology. Lung Neoplasms / genetics. Precancerous Conditions / genetics

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  • (PMID = 17525677.001).
  • [ISSN] 1052-9551
  • [Journal-full-title] Diagnostic molecular pathology : the American journal of surgical pathology, part B
  • [ISO-abbreviation] Diagn. Mol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Genetic Markers
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79. Yuan P, Kadara H, Behrens C, Tang X, Woods D, Solis LM, Huang J, Spinola M, Dong W, Yin G, Fujimoto J, Kim E, Xie Y, Girard L, Moran C, Hong WK, Minna JD, Wistuba II: Sex determining region Y-Box 2 (SOX2) is a potential cell-lineage gene highly expressed in the pathogenesis of squamous cell carcinomas of the lung. PLoS One; 2010 Feb 09;5(2):e9112
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  • [Title] Sex determining region Y-Box 2 (SOX2) is a potential cell-lineage gene highly expressed in the pathogenesis of squamous cell carcinomas of the lung.
  • BACKGROUND: Non-small cell lung cancer (NSCLC) represents the majority (85%) of lung cancers and is comprised mainly of adenocarcinomas and squamous cell carcinomas (SCCs).
  • The sequential pathogenesis of lung adenocarcinomas and SCCs occurs through dissimilar phases as the former tumors typically arise in the lung periphery whereas the latter normally arise near the central airway.
  • METHODOLOGY/PRINCIPAL FINDINGS: We assessed the expression of SOX2, an embryonic stem cell transcriptional factor that also plays important roles in the proliferation of basal tracheal cells and whose expression is restricted to the main and central airways and bronchioles of the developing and adult mouse lung, in NSCLC by various methodologies.
  • Here, we found that SOX2 mRNA levels, from various published datasets, were significantly elevated in lung SCCs compared to adenocarcinomas (all p<0.001).
  • Moreover, a previously characterized OCT4/SOX2/NANOG signature effectively separated lung SCCs from adenocarcinomas in two independent publicly available datasets which correlated with increased SOX2 mRNA in SCCs.
  • Immunohistochemical analysis of various histological lung tissue specimens demonstrated marked nuclear SOX2 protein expression in all normal bronchial epithelia, alveolar bronchiolization structures and premalignant lesions in SCC development (hyperplasia, dysplasia and carcinoma in situ) and absence of expression in all normal alveoli and atypical adenomatous hyperplasias.
  • Moreover, SOX2 protein expression was greatly higher in lung SCCs compared to adenocarcinomas following analyses in two independent large TMA sets (TMA set I, n = 287; TMA set II, n = 511 both p<0.001).
  • Furthermore, amplification of SOX2 DNA was detected in 20% of lung SCCs tested (n = 40) and in none of the adenocarcinomas (n = 17).
  • CONCLUSIONS/SIGNIFICANCE: Our findings highlight a cell-lineage gene expression pattern for the stem cell transcriptional factor SOX2 in the pathogenesis of lung SCCs and suggest a differential activation of stem cell-related pathways between squamous cell carcinomas and adenocarcinomas of the lung.

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  • (PMID = 20161759.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P50 CA070907; United States / NCI NIH HHS / CA / CA-16672; United States / NCI NIH HHS / CA / P50CA70907
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / NANOG protein, human; 0 / Octamer Transcription Factor-3; 0 / POU5F1 protein, human; 0 / SOX2 protein, human; 0 / SOXB1 Transcription Factors
  • [Other-IDs] NLM/ PMC2817751
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80. Kim Y, Liu XS, Liu C, Smith DE, Russell RM, Wang XD: Induction of pulmonary neoplasia in the smoke-exposed ferret by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK): a model for human lung cancer. Cancer Lett; 2006 Mar 28;234(2):209-19
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  • [Title] Induction of pulmonary neoplasia in the smoke-exposed ferret by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK): a model for human lung cancer.
  • Research into dietary chemoprevention against lung carcinogenesis has been limited by the lack of appropriate animal models that closely mimic smoking-related human lung cancer.
  • Ferrets (Mustela putorius furo) have been used to study the biologic activities of carotenoids against smoke-induced lung lesions, but this model has yet to be thoroughly established and validated.
  • To determine the appropriateness of the ferret as a model for human lung cancer, we have performed a 6-month in vivo study in ferrets exposed to both tobacco smoke and a carcinogen (4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone, NNK) found in cigarette smoke.
  • Results showed that six out 12 ferrets exposed to both NNK injection and cigarette smoke developed grossly identifiable lung tumors whereas none of nine ferrets from the sham treatment group developed any lung lesions.
  • The histopathological types of these tumors (squamous cell carcinoma, adenosquamous carcinoma and adenocarcinoma) in ferret lungs are very similar to those in humans.
  • In addition, 10 out of 12 ferrets exposed to both NNK and cigarette smoke developed preneoplastic lesions (squamous metaplasia, dysplasia, and atypical adenomatous hyperplasia) with complex growth patterns whereas the sham group did not show any of these lesions.
  • In summary, the development of both preneoplastic lesions and gross lung tumors in ferrets provides an excellent and unique model for studying lung cancer chemoprevention with agents such as carotenoids, and for studying the molecular mechanism of carcinogenesis in the earlier stages of smoke-related lung cancer.
  • [MeSH-major] Carcinogens / toxicity. Disease Models, Animal. Ferrets. Lung Neoplasms / etiology. Nitrosamines / toxicity. Smoking / adverse effects
  • [MeSH-minor] Adenocarcinoma / etiology. Adenocarcinoma / pathology. Animals. Carcinoma, Squamous Cell / etiology. Carcinoma, Squamous Cell / pathology. Humans. Immunohistochemistry. Male. Precancerous Conditions / etiology. Precancerous Conditions / pathology

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  • (PMID = 15894421.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / T32 DK062032
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Nitrosamines; 64091-91-4 / 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone
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81. Sakamoto H, Shimizu J, Horio Y, Ueda R, Takahashi T, Mitsudomi T, Yatabe Y: Disproportionate representation of KRAS gene mutation in atypical adenomatous hyperplasia, but even distribution of EGFR gene mutation from preinvasive to invasive adenocarcinomas. J Pathol; 2007 Jul;212(3):287-94
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  • [Title] Disproportionate representation of KRAS gene mutation in atypical adenomatous hyperplasia, but even distribution of EGFR gene mutation from preinvasive to invasive adenocarcinomas.
  • In the resected lung, additional small lesions are occasionally found incidentally, and include the full spectrum of preinvasive to invasive lesions under the current putative schema of the sequential development of lung cancer.
  • In this study, we examined EGFR and KRAS gene mutations in 119 synchronous pulmonary lesions, including 40 precursor lesions (atypical adenomatous hyperplasia, AAH), 26 carcinomas in situ (non-mucinous bronchioloalveolar carcinoma, BAC), 14 minimally invasive adenocarcinomas, 34 overt invasive adenocarcinomas, and five of other subtypes of cancer.
  • [MeSH-major] Adenocarcinoma / genetics. Lung Neoplasms / genetics. Mutation. Neoplasms, Multiple Primary / genetics. Precancerous Conditions / genetics. Proto-Oncogene Proteins / genetics. Receptor, Epidermal Growth Factor / genetics. ras Proteins / genetics
  • [MeSH-minor] DNA Mutational Analysis. Disease Progression. Humans. Hyperplasia / genetics. Smoking / genetics

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  • [Copyright] Copyright (c) 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • (PMID = 17534846.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [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
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82. Maeshima AM, Tochigi N, Yoshida A, Asamura H, Tsuta K, Tsuda H: Clinicopathologic analysis of multiple (five or more) atypical adenomatous hyperplasias (AAHs) of the lung: evidence for the AAH-adenocarcinoma sequence. J Thorac Oncol; 2010 Apr;5(4):466-71
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  • [Title] Clinicopathologic analysis of multiple (five or more) atypical adenomatous hyperplasias (AAHs) of the lung: evidence for the AAH-adenocarcinoma sequence.
  • OBJECTIVE: Clarification of the clinicopathologic characteristics of patients with multiple atypical adenomatous hyperplasias (AAHs).
  • MATERIALS AND METHODS: The subjects were 1,639 patients who underwent lobectomy or pneumonectomy for lung tumors.
  • The clinicopathologic features of the AAHs in the lung background and the main tumors were examined with regard to the number and the size of the AAHs, the incidence and histology of adenocarcinomas (ADs), and the outcome.
  • CONCLUSION: Five or more AAHs were seen in the background in 2.0% of lung tumors.
  • [MeSH-major] Adenocarcinoma / pathology. Adenoma / pathology. Carcinoma, Large Cell / pathology. Carcinoma, Squamous Cell / pathology. Lung Neoplasms / pathology
  • [MeSH-minor] Aged. Female. Follow-Up Studies. Humans. Hyperplasia. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Staging. Prognosis. Survival Rate

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  • (PMID = 20357616.001).
  • [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
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83. Kobashi Y, Sugiu T, Mouri K, Irei T, Nakata M, Oka M: Clinicopathological analysis of multifocal micronodular pneumocyte hyperplasia associated with tuberous sclerosis in Japan. Respirology; 2008 Nov;13(7):1076-81
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  • [Title] Clinicopathological analysis of multifocal micronodular pneumocyte hyperplasia associated with tuberous sclerosis in Japan.
  • BACKGROUND AND OBJECTIVE: This study investigated the clinical and pathological findings of lung disease in tuberous sclerosis complex (TSC) as previously reported in Japan.
  • METHODS: The clinical and pathological findings in 15 patients diagnosed as having multifocal micronodular pneumocyte hyperplasia (MMPH) with TSC were analysed.
  • The radiological findings were small multiple nodular shadows with ground-glass opacity randomly distributed in the bilateral whole-lung fields in most patients.
  • Differentiation from multiple atypical adenomatous hyperplasia or metastatic lung cancer was necessary in most patients.
  • The histological findings were papillary or tubular proliferation of type II pneumocytes without nuclear atypia lining the thickened alveolar septa and lymphocyte infiltration.
  • Immunohistochemical staining for cytokeratin, and surfactant proteins A and B was positive in alveolar lining cells of all MMPH lesions.
  • [MeSH-major] Lung / pathology. Multiple Pulmonary Nodules / pathology. Tuberous Sclerosis / pathology
  • [MeSH-minor] Adult. Diagnosis, Differential. Disease Progression. Female. Humans. Hyperplasia / pathology. Immunohistochemistry. Incidence. Japan / epidemiology. Keratins. Male. Middle Aged. Retrospective Studies. Young Adult

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  • (PMID = 18699800.001).
  • [ISSN] 1440-1843
  • [Journal-full-title] Respirology (Carlton, Vic.)
  • [ISO-abbreviation] Respirology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 68238-35-7 / Keratins
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84. Wistuba II, Gazdar AF: Lung cancer preneoplasia. Annu Rev Pathol; 2006;1:331-48
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  • [Title] Lung cancer preneoplasia.
  • From histological and biological perspectives, lung cancer is a complex neoplasm.
  • Although the sequential preneoplastic changes have been defined for centrally arising squamous carcinomas of the lung, they have been poorly documented for the other major forms of lung cancers, including small cell lung carcinoma and adenocarcinomas.
  • There are three main morphologic forms of preneoplastic lesions recognized in the lung: squamous dysplasias, atypical adenomatous hyperplasia, and diffuse idiopathic pulmonary neuroendocrine cell hyperplasia.
  • However, these lesions account for the development of only a subset of lung cancers.
  • Several studies have provided information regarding the molecular characterization of lung preneoplastic changes, especially for squamous cell carcinoma.
  • Two different molecular pathways have been detected in lung adenocarcinoma pathogenesis: smoking-associated activation of RAS signaling, and nonsmoking-associated activation of EGFR signaling; the latter is detected in histologically normal respiratory epithelium.
  • [MeSH-major] Adenocarcinoma / pathology. Lung Neoplasms / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Adenoma / pathology. Bronchi / pathology. Carcinoid Tumor / genetics. Carcinoid Tumor / pathology. Carcinoma in Situ / genetics. Carcinoma in Situ / pathology. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / pathology. Gene Expression Regulation, Neoplastic. Genes, erbB-1. Genetic Predisposition to Disease. Humans. Hyperplasia. Mutation. Signal Transduction. Smoking / adverse effects

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  • (PMID = 18039118.001).
  • [ISSN] 1553-4006
  • [Journal-full-title] Annual review of pathology
  • [ISO-abbreviation] Annu Rev Pathol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50CA70907; United States / NCI NIH HHS / CA / U01CA8497102
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] United States
  • [Number-of-references] 95
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85. 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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86. Tsutsui S, Ashizawa K, Minami K, Tagawa T, Nagayasu T, Hayashi T, Uetani M: Multiple focal pure ground-glass opacities on high-resolution CT images: Clinical significance in patients with lung cancer. AJR Am J Roentgenol; 2010 Aug;195(2):W131-8
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  • [Title] Multiple focal pure ground-glass opacities on high-resolution CT images: Clinical significance in patients with lung cancer.
  • OBJECTIVE: The purpose of this study was to evaluate the clinical significance of multiple focal pure ground-glass opacities (GGOs) on high-resolution CT images of patients with lung cancer.
  • MATERIALS AND METHODS: The cases of 23 patients with proven lung cancer and associated multiple focal pure GGOs on high-resolution CT images were retrospectively reviewed.
  • Lung cancer and focal pure GGOs were seen in the same lobe and/or in the other lobes.
  • Histologic findings were obtained for 15 lesions representing 74 focal pure GGOs that were surgically resected: 11 atypical adenomatous hyperplasia lesions, three bronchioloalveolar carcinomas, and one lesion of focal fibrosis.
  • CONCLUSION: The size of most focal pure GGOs associated with lung cancer did not change during the follow-up period.
  • Most of the small number of lesions histologically diagnosed were atypical adenomatous hyperplasia or bronchioloalveolar carcinoma.
  • [MeSH-major] Algorithms. Lung Neoplasms / radiography. Radiographic Image Enhancement / methods. Radiographic Image Interpretation, Computer-Assisted / methods. Tomography, X-Ray Computed / methods

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  • (PMID = 20651172.001).
  • [ISSN] 1546-3141
  • [Journal-full-title] AJR. American journal of roentgenology
  • [ISO-abbreviation] AJR Am J Roentgenol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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87. Sartori G, Cavazza A, Bertolini F, Longo L, Marchioni A, Costantini M, Barbieri F, Migaldi M, Rossi G: A subset of lung adenocarcinomas and atypical adenomatous hyperplasia-associated foci are genotypically related: an EGFR, HER2, and K-ras mutational analysis. Am J Clin Pathol; 2008 Feb;129(2):202-10
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  • [Title] A subset of lung adenocarcinomas and atypical adenomatous hyperplasia-associated foci are genotypically related: an EGFR, HER2, and K-ras mutational analysis.
  • Atypical adenomatous hyperplasia (AAH) is considered the preinvasive lesion of pulmonary adenocarcinoma, and mutations of EGFR, HER2, and K-ras are involved in the early stage of lung adenocarcinoma carcinogenesis, also predicting clinical response to anti-EGFR small molecule inhibitors.
  • We analyzed 18 cases of primary lung adenocarcinoma with concomitant AAH foci from 13 patients for mutations of EGFR (exons 18-21), HER2 (exons 19-20), and K-ras (exon 2) by direct sequencing polymerase chain reaction.
  • Mutations of EGFR and K-ras genes represent an early event in lung adenocarcinomagenesis, and AAH convincingly seems to be a precursor lesion in a subset of cases of adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Genes, erbB-2. Genes, ras. Hyperplasia / genetics. Lung Neoplasms / genetics. Precancerous Conditions / genetics. Receptor, Epidermal Growth Factor / genetics


88. Min JH, Lee HY, Lee KS, Han J, Park K, Ahn MJ, Lee SJ: Stepwise evolution from a focal pure pulmonary ground-glass opacity nodule into an invasive lung adenocarcinoma: an observation for more than 10 years. Lung Cancer; 2010 Jul;69(1):123-6
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  • [Title] Stepwise evolution from a focal pure pulmonary ground-glass opacity nodule into an invasive lung adenocarcinoma: an observation for more than 10 years.
  • The natural chronologic evolution of a lung cancer manifesting as a pure ground-glass opacity (GGO) nodule on CT scans still remains to be elucidated.
  • In the current case, we demonstrate serial morphologic (CT) and metabolic ((18)F-FDG PET) imaging findings in a case of adenocarcinoma, where stepwise progression from a focal pure GGO nodule (presumed atypical adenomatous hyperplasia [AAH] or bronchioloalveolar carcinoma [BAC]) eventually to an invasive adenocarcinoma was clearly depicted for more than 10-year follow-up period.
  • [MeSH-major] Adenocarcinoma / diagnosis. Carcinoma, Squamous Cell / diagnosis. Cell Transformation, Neoplastic / pathology. Lung Neoplasms / diagnosis. Solitary Pulmonary Nodule / diagnosis
  • [MeSH-minor] Biopsy, Fine-Needle. Diagnosis, Differential. Humans. Lung / pathology. Lung / radiography. Male. Middle Aged. Neoplasm Invasiveness. Positron-Emission Tomography. Time Factors. Tomography, X-Ray Computed

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  • [Copyright] Copyright 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20478641.001).
  • [ISSN] 1872-8332
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Ireland
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89. Sakuma Y, Matsukuma S, Yoshihara M, Nakamura Y, Nakayama H, Kameda Y, Tsuchiya E, Miyagi Y: Epidermal growth factor receptor gene mutations in atypical adenomatous hyperplasias of the lung. Mod Pathol; 2007 Sep;20(9):967-73
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  • [Title] Epidermal growth factor receptor gene mutations in atypical adenomatous hyperplasias of the lung.
  • Activating epidermal growth factor receptor (EGFR) gene mutations are frequently detected in lung adenocarcinomas, especially adenocarcinomas with a nonmucinous bronchioloalveolar carcinoma component.
  • EGFR-mutated lung adenocarcinomas respond well to EGFR tyrosine kinase inhibitors.
  • We previously found that most (88%) pure nonmucinous bronchioloalveolar carcinomas (adenocarcinoma in situ) already harbor EGFR mutations, indicating that the mutations are an early genetic event in the pathogenesis.
  • We examined 54 atypical adenomatous hyperplasias, precursor lesions of lung adenocarcinomas, obtained from 28 Japanese patients for the hotspot mutations of EGFR exons 19 and 21 and K-ras codon 12.
  • EGFR mutations were observed in 17 of the 54 (32%) atypical adenomatous hyperplasias examined: Ten and seven atypical adenomatous hyperplasias had deletion mutations at exon 19 or point mutations (L858R) at exon 21, respectively.
  • We did not observe apparent histological differences between atypical adenomatous hyperplasias with and without EGFR mutations.
  • K-ras mutation (G12S) was detected in only one atypical adenomatous hyperplasia.
  • As EGFR mutational frequency of atypical adenomatous hyperplasias was much lower than that of nonmucinous bronchioloalveolar carcinomas, we surmise that EGFR-mutated atypical adenomatous hyperplasias, but not atypical adenomatous hyperplasias with wild-type EGFR, are likely to progress to nonmucinous bronchioloalveolar carcinomas.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / genetics. Adenomatosis, Pulmonary / genetics. Gene Expression Regulation, Neoplastic. Lung Neoplasms / genetics. Mutation. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Adult. Aged. Asian Continental Ancestry Group / genetics. Codon. DNA Mutational Analysis. Disease Progression. Exons. Female. Genes, ras. Humans. Hyperplasia. Japan. Male. Middle Aged

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  • (PMID = 17618248.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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90. Shintani Y, Ohta M, Iwasaki T, Ikeda N, Tomita E, Nagano T, Kawahara K: A case of micronodular pneumocyte hyperplasia diagnosed through surgical resection. Ann Thorac Cardiovasc Surg; 2010 Aug;16(1):45-7
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  • [Title] A case of micronodular pneumocyte hyperplasia diagnosed through surgical resection.
  • Micronodular pneumocyte hyperplasia (MNPH) is often associated with tuberous sclerosis complex and/or lymphangioleiomyomatosis.
  • A preoperative high-resolution chest computed topographic scan demonstrated a ground-glass opacity 8 mm in diameter that revealed the possibility of atypical adenomatous hyperplasia (AAH) or bronchioloalveolar carcinoma (BAC).
  • Therefore an S3 segmentectomy of the right lung was performed, and the specimens revealed the characteristic histological and immunohistological features of MNPH.
  • [MeSH-minor] Biopsy. Diagnosis, Differential. Female. Humans. Hyperplasia. Immunohistochemistry. Middle Aged. Predictive Value of Tests. Tomography, X-Ray Computed

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  • (PMID = 20190710.001).
  • [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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91. Yee H, Yie TA, Goldberg J, Wong KM, Rom WN: Immunohistochemical study of fibrosis and adenocarcinoma in dominant-negative p53 transgenic mice exposed to chrysotile asbestos and benzo(a)pyrene. J Environ Pathol Toxicol Oncol; 2008;27(4):267-76
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  • We evaluated the mechanisms using immunohistochemistry whereby chrysotile asbestos and benzo(a)pyrene (BaP) instilled intratracheally into lung-specific dominant-negative p53 (dnp53) mice might interact in causing lung carcinomas and fibrosis.
  • Chrysotile asbestos and benzo(a)pyrene (BaP) were instilled intratracheally into lung-specific dominant-negative p53 (dnp53) and control mice.
  • The mice were sacrificed at 12 months and their lungs examined for lung carcinomas and fibrosis.
  • The dnp53 mice had increased numbers of lung adenocarcinomas with BaP alone and the combination of chrysotile and BaP (the latter was additive but not significant).
  • Several atypical adenomatous hyperplasia lesions were found in the combined treatment group. dnp53 and FVBN control mice developed nodular buds of fibrotic lung tissue after chrysotile asbestos exposure that were localized in respiratory bronchioles; these lesions had significant increases in immunohistochemical staining for TGF-beta, MMP-7 and -9, MIG-1, and SDF-1.
  • [MeSH-major] Adenocarcinoma. Asbestos, Serpentine / toxicity. Benzo(a)pyrene / toxicity. Lung Neoplasms. Pulmonary Fibrosis. Tumor Suppressor Protein p53 / biosynthesis

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  • (PMID = 19105532.001).
  • [ISSN] 0731-8898
  • [Journal-full-title] Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer
  • [ISO-abbreviation] J. Environ. Pathol. Toxicol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Asbestos, Serpentine; 0 / Cytokines; 0 / Tumor Suppressor Protein p53; 3417WMA06D / Benzo(a)pyrene; EC 3.4.22.- / Caspase 3; EC 3.4.24.- / Matrix Metalloproteinases
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92. Nakashima Y, Yamada T, Tanahashi M, Hikosaka Y, Yoshitomi H, Niwa H: [A study of high-resolution computed tomography (HRCT) findings of resected small pulmonary nodules 2 cm or less in diameter with reference to the malignant nature]. Kyobu Geka; 2006 Sep;59(10):917-22
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  • To identify the characteristics of peripheral small lung mass lesions on high-resolution computed tomography (HRCT) and discriminate between malignant and benign, 223 mass lesions 2 cm or less resected surgically were evaluated about following points.
  • Pure GGO lesions without scale-down between several months were all adenocarcinomas or atypical adenomatous hyperplasia (AAH).
  • 2) Spicular or pleural indentation :75.2% (88 of 117 cases) of adenocarcinomas and all squamous cell carcinomas (18 cases) showed these findings, but 26.6% (41 of 154 cases) of positive cases were benign lesion (non-specific inflammation, mycobacterisis, and so on).
  • [MeSH-major] Lung / pathology. Lung Diseases / radiography. Lung Neoplasms / radiography. Solitary Pulmonary Nodule / radiography. Tomography, X-Ray Computed / methods
  • [MeSH-minor] Adenocarcinoma / pathology. Adenocarcinoma / radiography. Adult. Aged. Aged, 80 and over. Carcinoma, Small Cell / pathology. Carcinoma, Small Cell / radiography. Carcinoma, Squamous Cell / pathology. Carcinoma, Squamous Cell / radiography. Diagnosis, Computer-Assisted. Diagnosis, Differential. Female. Humans. Hyperplasia. Male. Middle Aged. Retrospective Studies

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  • (PMID = 16986688.001).
  • [ISSN] 0021-5252
  • [Journal-full-title] Kyobu geka. The Japanese journal of thoracic surgery
  • [ISO-abbreviation] Kyobu Geka
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
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93. 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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94. Kozuki T, Hisamoto A, Tabata M, Takigawa N, Kiura K, Segawa Y, Nakata M, Mandai K, Eguchi K, Ueoka H, Tanimoto M: Mutation of the epidermal growth factor receptor gene in the development of adenocarcinoma of the lung. Lung Cancer; 2007 Oct;58(1):30-5
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  • [Title] Mutation of the epidermal growth factor receptor gene in the development of adenocarcinoma of the lung.
  • However, the involvement of the mutation in atypical adenomatous hyperplasia (AAH) and multiple adenocarcinomas still remains unclear.
  • [MeSH-major] Adenocarcinoma / genetics. Adenomatosis, Pulmonary / genetics. Genes, erbB-1. Lung Neoplasms / genetics. Mutation. Neoplasms, Multiple Primary / genetics. Receptor, Epidermal Growth Factor / genetics

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  • (PMID = 17561305.001).
  • [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
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Quinazolines; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
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95. 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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96. Xu X, Chung JH, Jheon S, Sung SW, Lee CT, Lee JH, Choe G: The accuracy of frozen section diagnosis of pulmonary nodules: evaluation of inflation method during intraoperative pathology consultation with cryosection. J Thorac Oncol; 2010 Jan;5(1):39-44
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  • The frozen section quality of lung tissue was excellent after inflation with diluted embedding medium.
  • Inflated lung specimens harboring minute lesion displayed distinct gross appearance, which could not be palpated.
  • Minute precancerous foci such as atypical adenomatous hyperplasia and bronchioloalveolar carcinoma could be readily identified.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / diagnosis. Frozen Sections / methods. Hyperplasia / diagnosis. Lung Neoplasms / diagnosis. Precancerous Conditions / diagnosis. Solitary Pulmonary Nodule / diagnosis

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  • (PMID = 19934776.001).
  • [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] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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97. Ishihara T, Takeuchi T, Nishimori I, Adachi Y, Minakuchi T, Fujita J, Sonobe H, Ohtsuki Y, Onishi S: Carbonic anhydrase-related protein VIII increases invasiveness of non-small cell lung adenocarcinoma. Virchows Arch; 2006 Jun;448(6):830-7
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  • [Title] Carbonic anhydrase-related protein VIII increases invasiveness of non-small cell lung adenocarcinoma.
  • Carbonic anhydrase-related protein VIII (CA-RP VIII) is believed to be an oncofetal antigen and is overexpressed in colorectal and non-small cell lung cancer.
  • However, the pathobiological properties of CA-RP VIII in lung cancer remain unclear.
  • In the present study, we examined ultrastructural changes caused by exogenous CA-RP VIII expression in a well-differentiated lung adenocarcinoma cell line, PC-9.
  • We subsequently examined CA-RP VIII expression in atypical adenomatous hyperplasia and early-stage lung adenocarcinoma (Stage Ia).
  • Significant expression of CA-RP VIII was observed in invasive lung adenocarcinoma but not in noninvasive adenocarcinoma.
  • Interestingly, CA-RP VIII was strongly expressed in signet-ring cell cancer and invasive mucinous adenocarcinoma components.
  • The present findings suggest that CA-RP VIII expression in lung adenocarcinoma is related to cancer cell invasion.
  • [MeSH-major] Carbonic Anhydrases / genetics. Carcinoma, Non-Small-Cell Lung / ultrastructure. Gene Expression Regulation, Neoplastic. Lung Neoplasms / ultrastructure. Nerve Tissue Proteins / genetics
  • [MeSH-minor] Adenoma / genetics. Adenoma / ultrastructure. Biomarkers, Tumor. Cell Line, Tumor. Cell Movement. Gene Expression. Humans. Hyperplasia. Immunohistochemistry. Microscopy, Electron, Transmission. Mucins / metabolism. Neoplasm Invasiveness. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction. Vacuoles / ultrastructure

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  • (PMID = 16609906.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CA8 protein, human; 0 / Car8 protein, mouse; 0 / Mucins; 0 / Nerve Tissue Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 4.2.1.1 / Carbonic Anhydrases
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98. Sakuma T, Iwata Y, Ueda Y, Gu X, Sugita M, Sagawa M: Annual periodic increases in serum carcinoembryonic antigen concurrent with ground-glass opacity in the lung: report of a case. Surg Today; 2005;35(10):883-5
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  • [Title] Annual periodic increases in serum carcinoembryonic antigen concurrent with ground-glass opacity in the lung: report of a case.
  • A 63-year-old woman underwent a video-assisted thoracoscopic lobectomy for cancer of the right lung in 1999.
  • The following year, a lesion with ground-glass opacity was found in the left lung, and pathological examination after a partial lung resection revealed atypical adenomatous hyperplasia with expression of carcinoembryonic antigen (CEA).
  • Clinical evaluations, including laboratory tests, radiographic imaging, and endoscopy examinations, showed no evidence of a CEA-producing tumor, except for a new ground-glass opacity in the left lung.
  • To our knowledge, this is the first report of periodic increases in serum CEA levels in a patient with ground-glass opacity in the lung, not reflecting recurrence of the lung tumor.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / surgery. Biomarkers, Tumor / blood. Carcinoembryonic Antigen / blood. Lung Neoplasms / surgery. Neoplasm Recurrence, Local / pathology

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  • (PMID = 16175472.001).
  • [ISSN] 0941-1291
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Carcinoembryonic Antigen
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99. Yatabe Y, Kosaka T, Takahashi T, Mitsudomi T: EGFR mutation is specific for terminal respiratory unit type adenocarcinoma. Am J Surg Pathol; 2005 May;29(5):633-9
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  • We have previously reported that terminal-respiratory-unit (TRU) type adenocarcinoma is a distinct subset of lung adenocarcinoma in terms of molecular pathway for carcinogenesis and phenotypic profiles.
  • The clinicopathologic features of gefitinib responders overlap with those of TRU-type adenocarcinoma, and the characteristics of TRU are likely to correspond to the bronchioloalveolar features reported as a predictor of gefitinib response.
  • In addition, EGFR mutation was detected in some cases of atypical adenomatous hyperplasia, a preinvasive lesion of TRU-type adenocarcinoma.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / genetics. Glycoproteins / genetics. Lung Neoplasms / genetics. Mutation. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] DNA Mutational Analysis. DNA, Neoplasm / analysis. Humans. Hyperplasia / genetics. Hyperplasia / metabolism. Hyperplasia / pathology. Immunoenzyme Techniques. Protein Array Analysis

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  • (PMID = 15832087.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Glycoproteins; 0 / epidermal growth factor receptor related protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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100. Pankiewicz W, Minarowski L, Niklińska W, Naumnik W, Nikliński J, Chyczewski L: Immunohistochemical markers of cancerogenesis in the lung. Folia Histochem Cytobiol; 2007;45(2):65-74
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  • [Title] Immunohistochemical markers of cancerogenesis in the lung.
  • Lung cancer is the leading cause of cancer deaths for people of both sexes worldwide.
  • Early diagnosis of precancer lesions may be of crucial significance to lowering lung cancer mortality.
  • The World Health Organization has defined three preneoplastic lesions of the bronchial epithelium: squamous dysplasia and carcinoma in situ, atypical adenomatous hyperplasia and diffuse idiopathic pulmonary neuroendocrine cell hyperplasia.
  • These lesions are believed to progress to squamous cell carcinoma, adenocarcinoma and carcinoid tumors, respectively.
  • Apart from WHO classification, two other lesions such as bronchiolization and bronchiolar columnar cell dysplasia (BCCD) can be observed and thought to be preneoplastic lesions leading to adenocarcinoma.
  • In this review we summarize the data of morphological and cell cycle related proteins changes in both central and peripheral compartments of lung.

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  • (PMID = 17597018.001).
  • [ISSN] 0239-8508
  • [Journal-full-title] Folia histochemica et cytobiologica
  • [ISO-abbreviation] Folia Histochem. Cytobiol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 67
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