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

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  • (PMID = 15833854.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P50 CA070907; United States / NCI NIH HHS / CA / R01 CA105155
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins; 624KN6GM2T / temsirolimus; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / Ribosomal Protein S6 Kinases; W36ZG6FT64 / Sirolimus
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2. Félix L, Lantuejoul S, Jankowski A, Ferretti G: [Localized pure or mixed ground-glass lung opacities]. J Radiol; 2009 Nov;90(11 Pt 2):1869-92
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  • [Title] [Localized pure or mixed ground-glass lung opacities].
  • Localized ground-glass opacities (GGOs) have been recently individualized and account for between 2.9% and 19% of all pulmonary nodules detected in high-risk patients included in CT screening series for lung cancer.
  • These opacities, nodular, lobular or flat, correspond to benign lesions (localised infectious and inflammatory diseases, focal interstitial fibrosis, and atypical alveolar hyperplasia) or malignant lesions (bronchioloalveolar carcinoma, early-stage adenocarcinoma and sometimes metastases).
  • [MeSH-major] Adenocarcinoma / radiography. Adenocarcinoma, Bronchiolo-Alveolar / radiography. Lung Neoplasms / radiography. Radiography, Thoracic / methods. Solitary Pulmonary Nodule / radiography. Tomography, X-Ray Computed / methods
  • [MeSH-minor] Algorithms. Biopsy. Clinical Trials as Topic. Diagnosis, Differential. Female. Humans. Hyperplasia. Lung / pathology. Middle Aged. Neoplasm Staging. Prognosis. Pulmonary Alveoli / pathology. Risk Factors. Smoking / adverse effects

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  • (PMID = 19953078.001).
  • [ISSN] 0221-0363
  • [Journal-full-title] Journal de radiologie
  • [ISO-abbreviation] J Radiol
  • [Language] fre
  • [Publication-type] Case Reports; Comparative Study; English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 101
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3. 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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4. Wu M, Orta L, Gil J, Li G, Hu A, Burstein DE: Immunohistochemical detection of XIAP and p63 in adenomatous hyperplasia, atypical adenomatous hyperplasia, bronchioloalveolar carcinoma and well-differentiated adenocarcinoma. Mod Pathol; 2008 May;21(5):553-8
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  • [Title] Immunohistochemical detection of XIAP and p63 in adenomatous hyperplasia, atypical adenomatous hyperplasia, bronchioloalveolar carcinoma and well-differentiated adenocarcinoma.
  • The critical distinction of bronchioloalveolar carcinoma (BAC), well-differentiated adenocarcinoma (WDAC) of lung, adenomatous hyperplasia (AH) and atypical adenomatous hyperplasia (AAH), is based on morphological criteria alone, and is therefore potentially subjective.
  • Neither XIAP nor p63 were detected in normal lung alveolar cells.
  • In contrast, diffuse p63 staining may facilitate the identification of rare cases that may have been misclassified as alveolar in origin based on morphology but may be of BRC origin.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma, Bronchiolo-Alveolar / diagnosis. Lung Neoplasms / diagnosis. Membrane Proteins / biosynthesis. Precancerous Conditions / diagnosis. X-Linked Inhibitor of Apoptosis Protein / biosynthesis
  • [MeSH-minor] Biomarkers, Tumor / analysis. Diagnosis, Differential. Humans. Hyperplasia / pathology. Immunohistochemistry. Lung / pathology

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  • (PMID = 18432259.001).
  • [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] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CKAP4 protein, human; 0 / Membrane Proteins; 0 / X-Linked Inhibitor of Apoptosis Protein; 0 / XIAP protein, human
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5. Pastorino U, Calabrò E, Tamborini E, Marchianò A, Orsenigo M, Fabbri A, Sozzi G, Novello S, De Marinis F: Prolonged remission of disseminated atypical adenomatous hyperplasia under gefitinib. J Thorac Oncol; 2009 Feb;4(2):266-7
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  • [Title] Prolonged remission of disseminated atypical adenomatous hyperplasia under gefitinib.
  • Atypical adenomatous hyperplasia (AAH) is a putative precursor of bronchioloalveolar carcinoma (BAC) and adenocarcinoma of the lung, developing from terminal respiratory unit cells.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / drug therapy. Antineoplastic Agents / therapeutic use. Lung / pathology. Lung Neoplasms / drug therapy. Quinazolines / therapeutic use
  • [MeSH-minor] Female. Humans. Hyperplasia. Middle Aged. Mutation / genetics. Polymerase Chain Reaction. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / genetics. Remission Induction. Tomography, X-Ray Computed

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  • (PMID = 19179908.001).
  • [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] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Quinazolines; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
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6. 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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7. Nakanishi K, Matsuo H, Kanai Y, Endou H, Hiroi S, Tominaga S, Mukai M, Ikeda E, Ozeki Y, Aida S, Kawai T: LAT1 expression in normal lung and in atypical adenomatous hyperplasia and adenocarcinoma of the lung. Virchows Arch; 2006 Feb;448(2):142-50
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  • [Title] LAT1 expression in normal lung and in atypical adenomatous hyperplasia and adenocarcinoma of the lung.
  • No previous study has investigated neutral large amino acid transporter type 1 (LAT1) in normal lung cells, or in atypical adenomatous hyperplasia(s) (AAH) and nonmucinous bronchioloalveolar carcinoma(s) (NMBAC) of the lung.
  • (1) the levels of LAT1 mRNA/glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNA in 41 normal lung tissues and 34 NMBAC using semiquantitative reverse transcription-polymerase chain reaction;.
  • (2) LAT1 mRNA and protein expressions in 35 normal lung tissues, 34 AAH (11 lesions were interpreted as low-grade AAH and 23 as high-grade AAH), and 43 NMBAC using in situ hybridization and immunohistochemistry; and (2) the association of the incidences of LAT1 mRNA and protein expressions with cell proliferation in these lesions.
  • The level of LAT1 mRNA/GAPDH mRNA (1) tended to be higher in NMBAC (12.0+/-8.1) than in normal lung tissues (1.0+/-0.2), and (2) covered a much wider range (from 0 to 276) in NMBAC than in normal lung tissues (from 0 to 5.8), with six NMBAC having values higher than 7.0, while 5.8 was the highest value detected in normal lung tissues.
  • In peripheral normal lung tissues, LAT1 mRNA and protein were detected in bronchial surface epithelial cells and alveolar macrophages (but not in nonciliated bronchiolar epithelial cells, or in alveolar type I or type II cells).
  • The Ki-67 labeling index (a cell proliferation score) was significantly higher in those AAH and NMBAC that were LTA1-protein-positive than in their LAT1-protein-negative counterparts.
  • In conclusion, LAT1 expression may increase with the upregulation of metabolic activity and cell proliferation in high-grade AAH and NMBAC.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / pathology. Adenomatosis, Pulmonary / pathology. Large Neutral Amino Acid-Transporter 1 / genetics. Lung / metabolism. Lung Neoplasms / pathology
  • [MeSH-minor] Gene Expression. Humans. Hyperplasia. Immunohistochemistry. In Situ Hybridization. Ki-67 Antigen / analysis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16175382.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Large Neutral Amino Acid-Transporter 1; 0 / RNA, Messenger
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8. Kobashi Y, Sugiu T, Mouri K, Irei T, Nakata M, Oka M: Multifocal micronodular pneumocyte hyperplasia associated with tuberous sclerosis: differentiation from multiple atypical adenomatous hyperplasia. Jpn J Clin Oncol; 2008 Jun;38(6):451-4
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  • [Title] Multifocal micronodular pneumocyte hyperplasia associated with tuberous sclerosis: differentiation from multiple atypical adenomatous hyperplasia.
  • We report a peculiar case of multifocal micronodular pneumocyte hyperplasia (MMPH) in a 54-year-old woman with tuberous sclerosis complex (TSC) diagnosed during antituberculous treatment.
  • Chest CT demonstrated multiple small nodules with ground-glass opacity, measuring up to 5 mm diameter, presenting in the bilateral lung fields, without cystic change.
  • Because the differentiation from multiple atypical adenomatous hyperplasia (AAH) was necessary, we finally performed a diagnosis of MMPH based on specimens obtained by video-assisted thoracoscopic surgery.
  • Histologically, type II pneumocytes without nuclear atypia lined the thickened alveolar septa and proliferated papillary structures.
  • Although immunohistochemical stains for cytokeratin and surfactant apoprotein A and B were positive for alveolar lining cells in each MMPH lesion, those for HMB-45, alpha-smooth muscle actin, p53 and carcinoembryonic antigen were negative.
  • [MeSH-major] Lung / pathology. Lung Diseases / diagnosis. Tuberous Sclerosis / complications. Tuberous Sclerosis / diagnosis
  • [MeSH-minor] Adenoma / diagnosis. Diagnosis, Differential. Female. Humans. Hyperplasia / diagnosis. Lung Neoplasms / diagnosis. Middle Aged. Thoracic Surgery, Video-Assisted. Tomography, X-Ray Computed. Tuberculosis, Lymph Node / drug therapy


9. 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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10. 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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11. Kohno T, Kakinuma R, Iwasaki M, Yamaji T, Kunitoh H, Suzuki K, Shimada Y, Shiraishi K, Kasuga Y, Hamada GS, Furuta K, Tsuta K, Sakamoto H, Kuchiba A, Yamamoto S, Kanai Y, Tsugane S, Yokota J: Association of CYP19A1 polymorphisms with risks for atypical adenomatous hyperplasia and bronchioloalveolar carcinoma in the lungs. Carcinogenesis; 2010 Oct;31(10):1794-9
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  • [Title] Association of CYP19A1 polymorphisms with risks for atypical adenomatous hyperplasia and bronchioloalveolar carcinoma in the lungs.
  • Estrogen has been indicated to play an etiological role in the development of lung adenocarcinoma (ADC), particularly bronchioloalveolar carcinoma (BAC), a type of ADC that develops from a benign adenomatous lesion, atypical adenomatous hyperplasia (AAH).
  • Here, 13 CYP19A1 single-nucleotide polymorphisms (SNPs) were examined for associations with lung AAH risk.
  • Associations of this SNP with risks for lung AAH and BAC in the lungs were next examined using 359 ADC cases whose resected lung lobes were subjected to a histological examination for AAH accompaniment and the presence of BAC components and 330 controls without cancer.
  • The ORs were also increased for lung ADC accompanied by AAH (OR = 1.74, P = 0.029) as well as lung ADC with BAC components (OR = 1.41, P = 0.091).
  • These results indicate that CYP19A1 polymorphisms are involved in the risk for lung AAH and BAC in the lungs by causing differences in estrogen levels.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / genetics. Aromatase / genetics. Lung / pathology. Lung Neoplasms / genetics. Polymorphism, Single Nucleotide. Precancerous Conditions / genetics
  • [MeSH-minor] Adult. Aged. Estrogens / blood. Female. Humans. Hyperplasia. Male. Middle Aged. Risk Factors. Smoking / adverse effects

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  • (PMID = 20688833.001).
  • [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 / Estrogens; EC 1.14.14.1 / Aromatase
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12. Oda S, Awai K, Liu D, Nakaura T, Yanaga Y, Nomori H, Yamashita Y: Ground-glass opacities on thin-section helical CT: differentiation between bronchioloalveolar carcinoma and atypical adenomatous hyperplasia. AJR Am J Roentgenol; 2008 May;190(5):1363-8
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  • [Title] Ground-glass opacities on thin-section helical CT: differentiation between bronchioloalveolar carcinoma and atypical adenomatous hyperplasia.
  • OBJECTIVE: The purpose of our study was to investigate the differentiation between bronchioloalveolar carcinoma and atypical adenomatous hyperplasia manifesting pure ground-glass opacity (GGO) based on selected features on thin-section helical CT scans.
  • MATERIALS AND METHODS: We evaluated 35 bronchioloalveolar carcinomas and 17 atypical adenomatous hyperplasias that were histologically confirmed and that manifested pure GGO on thin-section helical CT scans.
  • CT findings of atypical adenomatous hyperplasia and bronchioloalveolar carcinoma were compared using univariate and multivariate logistic regression analysis; the odds ratio was computed using the atypical adenomatous hyperplasia group as the reference group.
  • RESULTS: By univariate analysis, the patient age, nodular maximum diameter, mean attenuation value, and findings of an internal air bronchogram were statistically significantly associated with bronchioloalveolar carcinoma (odds ratio [OR] = 1.10 [p = 0.012], OR = 1.27 [p < 0.01], OR = 1.01 [p = 0.023], and OR = 25.30 [p < 0.001], respectively), and sphericity was significantly associated with atypical adenomatous hyperplasia (OR = 0.059, p < 0.001).
  • By multivariate analysis, sphericity was significantly associated with atypical adenomatous hyperplasia (OR = 0.125, p = 0.042) and findings of an internal air bronchogram were associated with bronchioloalveolar carcinoma (OR = 16.10, p = 0.007).
  • CONCLUSION: Nodular sphericity and an internal air bronchogram were useful at thin-section helical CT performed to differentiate between bronchioloalveolar carcinoma and atypical adenomatous hyperplasia.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / radiography. Lung Neoplasms / radiography. Solitary Pulmonary Nodule / radiography. Tomography, Spiral Computed
  • [MeSH-minor] Aged. Diagnosis, Differential. Female. Humans. Hyperplasia / radiography. Male. Middle Aged. Observer Variation. Retrospective Studies

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  • (PMID = 18430856.001).
  • [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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13. Licchesi JD, Westra WH, Hooker CM, Herman JG: Promoter hypermethylation of hallmark cancer genes in atypical adenomatous hyperplasia of the lung. Clin Cancer Res; 2008 May 1;14(9):2570-8
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  • [Title] Promoter hypermethylation of hallmark cancer genes in atypical adenomatous hyperplasia of the lung.
  • The recognition of an early form of glandular neoplasia termed atypical adenomatous hyperplasia (AAH), a precursor lesion from which lung adenocarcinomas arise, provides an opportunity for characterizing early epigenetic alterations involved in lung tumorigenesis.
  • EXPERIMENTAL DESIGN: We evaluated AAHs, adjacent normal lung tissue, and synchronous lung adenocarcinomas for promoter hypermethylation of genes implicated in lung tumorigenesis (p16, TIMP3, DAPK, MGMT, RARbeta, RASSF1A, and hTERT).
  • CONCLUSION: This study shows epigenetic progression in the earliest stages of glandular neoplasia of the lung and has implications for early lung cancer detection.
  • [MeSH-major] Adenocarcinoma / genetics. Adenoma / genetics. DNA Methylation. Genes, Neoplasm. Lung Neoplasms / genetics. Precancerous Conditions / genetics. Promoter Regions, Genetic
  • [MeSH-minor] Epigenesis, Genetic. Humans. Hyperplasia. Lung / metabolism. Lung / pathology

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  • (PMID = 18451218.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / CA058184
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
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14. 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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15. Yoshida Y, Shibata T, Kokubu A, Tsuta K, Matsuno Y, Kanai Y, Asamura H, Tsuchiya R, Hirohashi S: Mutations of the epidermal growth factor receptor gene in atypical adenomatous hyperplasia and bronchioloalveolar carcinoma of the lung. Lung Cancer; 2005 Oct;50(1):1-8
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  • [Title] Mutations of the epidermal growth factor receptor gene in atypical adenomatous hyperplasia and bronchioloalveolar carcinoma of the lung.
  • A hypothesis of multistep carcinogenesis of lung adenocarcinoma from atypical adenomatous hyperplasia (AAH) to invasive adenocarcinoma through bronchioloalveolar carcinoma (BAC) has been proposed.
  • Recently, somatic mutations of the epidermal growth factor receptor (EGFR) gene were found in lung adenocarcinoma.
  • We examined the status of EGFR mutations in AAH and BAC to elucidate the role they play during multistage of lung adenocarcinoma.
  • We analyzed 24 patients with multiple lung lesions and 13 patients had at least one lesion that had either an EGFR or K-ras mutation.
  • This finding suggests that the genetic alterations responsible for the development of lung adenocarcinoma occur randomly even under exposure to the same carcinogen.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma, Bronchiolo-Alveolar / genetics. Cell Transformation, Neoplastic / genetics. Lung Neoplasms / genetics. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Carcinogens. DNA Mutational Analysis. Female. Humans. Hyperplasia / genetics. Hyperplasia / physiopathology. Lung / pathology. Male. Middle Aged. Polymerase Chain Reaction

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  • (PMID = 15950315.001).
  • [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 / Carcinogens; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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16. McIntire MG, Santagata S, Ligon K, Chirieac LR: Epidermal growth factor receptor gene amplification in atypical adenomatous hyperplasia of the lung. Am J Transl Res; 2010 May 16;2(3):309-15
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  • [Title] Epidermal growth factor receptor gene amplification in atypical adenomatous hyperplasia of the lung.
  • Atypical adenomatous hyperplasia (AAH) is postulated to be the earliest morphologic precursor lesion in lung carcinogenesis.
  • The epidermal growth factor receptor (EGFR), one of the members of the Erb-2 family of receptors, is commonly expressed in non-small cell lung carcinoma (NSCLC).
  • Recent reports show that EGFR mutations are rare or absent in AAH and are rare in bronchioloalveolar carcinoma (BAC).
  • In this study, we examined the EGFR gene copy number status in lung adenocarcinomas, synchronous AAH, and BAC in surgical pathology resection specimens.
  • In our cohort, the rate of EGFR gene copy abnormalities in AAH appears similar to BAC and lower than in lung adenocarcinomas.
  • These findings suggest that although EGFR gene copy abnormalities may be an early event in lung carcinogenesis, they are associated with tumor progression to invasive cancer and highlight the complexity of tumor morphogenesis.

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  • (PMID = 20589169.001).
  • [ISSN] 1943-8141
  • [Journal-full-title] American journal of translational research
  • [ISO-abbreviation] Am J Transl Res
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P20 CA090578; United States / NCI NIH HHS / CA / P50 CA090578
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2892406
  • [Keywords] NOTNLM ; EGFR / chromogenic in situ hybridization / copy number / lung cancer
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17. 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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18. Wang GF, Lai MD, Chen PH: [Correlation of multiple primary lung cancer with bronchial and alveolar epithelial dysplasia]. Zhejiang Da Xue Xue Bao Yi Xue Ban; 2005 Sep;34(5):427-31
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  • [Title] [Correlation of multiple primary lung cancer with bronchial and alveolar epithelial dysplasia].
  • OBJECTIVE: To investigate the correlation of multiple primary lung cancer with bronchial epithelial dysplasia and atypical adenomatous hyperplasia of bronchiolo-alveolar epithelium.
  • METHODS: Careful pathological examinations were performed on 114 surgical specimens of primary lung carcinoma.
  • The correlation of multiple primary lung cancer with bronchial epithelial dysplasia and atypical adenomatous hyperplasia of bronchiolo-alveolar epithelium was analyzed.
  • RESULTS: Of 114 cases of primary lung cancer,13 cases of multiple primary lung cancer (11.4 %) was identifiedìwhich consisted of 6 cases containing two primary bronchogenic carcinoma and 7 containing one bronchogenic carcinoma and one bronchiolo-alveolar carcinoma.
  • The rate of multiple primary lung cancers was significantly higher in individuals with high grade bronchial epithelial dysplasia than in those with low grade dysplasia (r=0.238, P<0.05).
  • CONCLUSION: Bronchial and alveolar epithelial cells may develop malignancy synchronously or metachronously.
  • The probability of developing multiple primary lung cancer will increase in the lungs with extensive and severe bronchial epithelial dysplasia.
  • [MeSH-major] Bronchi / pathology. Carcinoma, Squamous Cell / pathology. Lung Neoplasms / pathology. Neoplasms, Multiple Primary / pathology. Pulmonary Alveoli / pathology
  • [MeSH-minor] Adenocarcinoma / pathology. Adult. Aged. Carcinoma, Small Cell / pathology. Cell Proliferation. Female. Humans. Hyperplasia. Male. Middle Aged. Precancerous Conditions / pathology. Respiratory Mucosa / pathology

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  • (PMID = 16216054.001).
  • [ISSN] 1008-9292
  • [Journal-full-title] Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences
  • [ISO-abbreviation] Zhejiang Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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19. 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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20. Ikeda K, Nomori H, Ohba Y, Shibata H, Mori T, Honda Y, Iyama K, Kobayashi T: Epidermal growth factor receptor mutations in multicentric lung adenocarcinomas and atypical adenomatous hyperplasias. J Thorac Oncol; 2008 May;3(5):467-71
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  • [Title] Epidermal growth factor receptor mutations in multicentric lung adenocarcinomas and atypical adenomatous hyperplasias.
  • BACKGROUND: The mechanisms of generation and progression of multicentric lung adenocarcinoma (AD), bronchioloalveolar carcinoma (BAC), and atypical adenomatous hyperplasia (AAH) in the peripheral lung is not well known.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma, Bronchiolo-Alveolar / genetics. Lung Neoplasms / genetics. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Aged. Cell Transformation, Neoplastic / genetics. DNA Mutational Analysis. Female. Humans. Hyperplasia / genetics. Hyperplasia / surgery. Male. Middle Aged. Polymerase Chain Reaction

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  • (PMID = 18448997.001).
  • [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] EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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21. Sak SD, Koseoglu RD, Demirag F, Akbulut H, Gungor A: Alveolar adenoma of the lung. Immunohistochemical and flow cytometric characteristics of two new cases and a review of the literature. APMIS; 2007 Dec;115(12):1443-9
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  • [Title] Alveolar adenoma of the lung. Immunohistochemical and flow cytometric characteristics of two new cases and a review of the literature.
  • Alveolar adenoma is a rare and benign tumour of the lung that usually presents in asymptomatic patients as a coin lesion on chest radiography.
  • Alveolar adenoma has a characteristic multicystic histology and often resembles the normal lung parenchyma.
  • Immunohistochemical analysis may aid in the characterization of alveolar adenoma and discriminate this condition from other types of benign lesions of the lung.
  • An indolent clinical progression and absence of recurrence and metastasis after complete resection are the most important characteristics indicative of the benign nature of alveolar adenoma.
  • Few studies have been conducted at the molecular level, such as by flow cytometry, with the objective of characterizing the biological nature of alveolar adenoma.
  • Differential diagnoses include sclerosing hemangioma, papillary adenoma, lymphangioma, atypical adenomatous hyperplasia and bronchioloalveolar carcinoma.
  • [MeSH-major] Adenoma / pathology. Pulmonary Alveoli / pathology. Solitary Pulmonary Nodule / pathology
  • [MeSH-minor] Biomarkers, Tumor / analysis. Cell Proliferation. Flow Cytometry. Humans. Immunohistochemistry. Lung Neoplasms / genetics. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Male. Middle Aged. Tumor Suppressor Protein p53 / biosynthesis

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  • (PMID = 18184418.001).
  • [ISSN] 0903-4641
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Tumor Suppressor Protein p53
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22. 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
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2667592
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23. 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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24. 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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25. Shiraishi K, Mori T, Ohba Y, Iwatani K, Yoshimoto K, Iyama K: Three young osteosarcoma patients with small adenocarcinoma or atypical adenomatous hyperplasia of the lung. Ann Thorac Cardiovasc Surg; 2010 Oct;16(5):358-61
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  • [Title] Three young osteosarcoma patients with small adenocarcinoma or atypical adenomatous hyperplasia of the lung.
  • Three young osteosarcoma patients with adenocarcinoma (AD) or atypical adenomatous hyperplasia (AAH) of the lung are reported.
  • A 14-year-old male patient with femoral osteosarcoma had solitary AD (case 1); a 23-year-old female patient with femoral osteosarcoma had AAH and lung metastasis (case 2); and a 17-year-old male patient with humeral osteosarcoma had AD and lung metastasis of osteosarcoma (case 3).
  • They have been the youngest patients with lung cancer or AAH in our hospital.
  • The maximum diameter of each lung tumor on computed tomography (CT) was 0.5, 0.6, and 0.5 cm, respectively.
  • Advances in CT and its applications to osteosarcoma patients as a method of assessing lung metastasis might contribute in large part to the detection of AD/AAH in patients younger than 30.
  • [MeSH-major] Adenocarcinoma / complications. Bone Neoplasms / complications. Lung Neoplasms / complications. Osteosarcoma / complications. Precancerous Conditions / complications
  • [MeSH-minor] Adolescent. Female. Femur. Humans. Humerus. Hyperplasia / complications. Male. Young Adult


26. 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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27. Nakamura H, Hirata T, Taguchi M, Kitamura H: Ground-glass opacities showing an adenoma-to-carcinoma sequence in the lung. Gen Thorac Cardiovasc Surg; 2008 Aug;56(8):421-3
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  • [Title] Ground-glass opacities showing an adenoma-to-carcinoma sequence in the lung.
  • Pathological diagnoses of the resected lesions included a focus of atypical adenomatous hyperplasia (AAH) and two localized noninvasive bronchioloalveolar carcinomas (BACs) of types A and C according to Noguchi's classification.
  • This case supports the hypothesis of an adenoma-to-carcinoma sequence in the lung, as the coexisting lesions represented sequential adenocarcinoma progression from a precancerous lesion, AAH, to very early-stage adenocarcinoma, noninvasive BAC.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / pathology. Cell Transformation, Neoplastic / pathology. Lung Neoplasms / pathology
  • [MeSH-minor] Adenoma / pathology. Adenoma / radiography. Aged. Female. Humans. Hyperplasia / pathology. Hyperplasia / radiography. Precancerous Conditions / pathology. Precancerous Conditions / radiography. Tomography, X-Ray Computed

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  • (PMID = 18696210.001).
  • [ISSN] 1863-6705
  • [Journal-full-title] General thoracic and cardiovascular surgery
  • [ISO-abbreviation] Gen Thorac Cardiovasc Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
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28. 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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29. 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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30. 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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31. Diederich S: Pulmonary nodules: do we need a separate algorithm for non-solid lesions? Cancer Imaging; 2009;9 Spec No A:S126-8
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  • If malignant, they are mostly due to atypical adenomatous hyperplasia and bronchioloalveolar carcinoma.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / diagnosis. Algorithms. Lung Neoplasms / diagnosis. Solitary Pulmonary Nodule / diagnosis. Tomography, X-Ray Computed / methods
  • [MeSH-minor] Adenoma / radiography. Adult. Aged. Follow-Up Studies. Humans. Hyperplasia. Incidental Findings. Mass Screening. Middle Aged. Positron-Emission Tomography. Precancerous Conditions / diagnosis. Precancerous Conditions / radiography

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  • (PMID = 19965304.001).
  • [ISSN] 1470-7330
  • [Journal-full-title] Cancer imaging : the official publication of the International Cancer Imaging Society
  • [ISO-abbreviation] Cancer Imaging
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 14
  • [Other-IDs] NLM/ PMC2797465
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32. 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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33. Chandan VS, Truong LD, Khurana KK: The utility of B72.3, carcinoembryonic antigen, and Leu M-1 in cell blocks: an adjunct to fine-needle aspiration diagnosis of bronchioloalveolar carcinoma of the lung. Cancer; 2005 Aug 25;105(4):246-52
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  • [Title] The utility of B72.3, carcinoembryonic antigen, and Leu M-1 in cell blocks: an adjunct to fine-needle aspiration diagnosis of bronchioloalveolar carcinoma of the lung.
  • BACKGROUND: The distinction of bronchioloalveolar carcinoma (BAC) from atypical adenomatous hyperplasia (AAH) or reactive alveolar cell hyperplasia (RAH) can be difficult on aspiration cytology, even when cell block preparations are available.
  • METHODS: Immunostains for B72.3, CEA, and Leu M-1 were performed on cell block sections from 11 lung lesions that were diagnosed cytologically as BAC (6 lesions) and "atypical cells, cannot exclude BAC" (5 lesions).
  • Among the five lesions that were diagnosed as "atypical cells, cannot exclude BAC," four lesions were positive for two of three immunostains, and one lesion was negative for all three immunostains.
  • Follow-up histology of the wedge resection on the lesion in the atypical category that was negative for B72.3, CEA, and Leu M-1 showed only AAH.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / diagnosis. Antibodies, Neoplasm / metabolism. Antigens, CD15 / metabolism. Biomarkers, Tumor / metabolism. Carcinoembryonic Antigen / metabolism. Lung Neoplasms / diagnosis

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  • [Copyright] Copyright (c) 2005 American Cancer Society.
  • (PMID = 15971208.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Neoplasm; 0 / Antigens, CD15; 0 / B72.3 antibody; 0 / Biomarkers, Tumor; 0 / Carcinoembryonic Antigen
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34. 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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35. 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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36. Kim HY, Shim YM, Lee KS, Han J, Yi CA, Kim YK: Persistent pulmonary nodular ground-glass opacity at thin-section CT: histopathologic comparisons. Radiology; 2007 Oct;245(1):267-75
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  • RESULTS: Of 53 nodules in 49 patients (20 men, 29 women; mean age, 54 years; range, 29-78 years), 40 (75%) proved to be broncholoalveolar cell carcinoma (BAC) (n=36) or adenocarcinoma with predominant BAC component (n=4), three (6%) atypical adenomatous hyperplasia, and 10 (19%) nonspecific fibrosis or organizing pneumonia.
  • [MeSH-major] Lung / pathology. Lung / radiography. Lung Neoplasms / radiography. Tomography, X-Ray Computed / methods
  • [MeSH-minor] Adenocarcinoma / pathology. Adenocarcinoma / radiography. Adenocarcinoma, Bronchiolo-Alveolar / pathology. Adenocarcinoma, Bronchiolo-Alveolar / radiography. Adult. Aged. Female. Humans. Hyperplasia. Male. Middle Aged. Pneumonia / pathology. Pneumonia / radiography. Pulmonary Fibrosis / pathology. Pulmonary Fibrosis / radiography. Retrospective Studies

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  • [Copyright] Copyright (c) RSNA, 2007.
  • [CommentIn] Radiology. 2008 Apr;247(1):296; author reply 296 [18372478.001]
  • [ErratumIn] Radiology. 2008 Apr;247(1):297
  • (PMID = 17885195.001).
  • [ISSN] 0033-8419
  • [Journal-full-title] Radiology
  • [ISO-abbreviation] Radiology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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37. Solano-Lopez C, Zeidler-Erdely PC, Hubbs AF, Reynolds SH, Roberts JR, Taylor MD, Young SH, Castranova V, Antonini JM: Welding fume exposure and associated inflammatory and hyperplastic changes in the lungs of tumor susceptible a/j mice. Toxicol Pathol; 2006;34(4):364-72
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  • It has been suggested that welding fume (WF) exposure increases lung cancer risk in welders.
  • Epidemiology studies have failed to conclude that WF alone causes lung cancer and animal studies are lacking.
  • We examined the course of inflammation, damage, and repair in the lungs of A/J mice, a lung tumor susceptible strain, caused by stainless steel WF.
  • Bronchoalveolar lavage (BAL) was performed 24 hours, 1 and 16 weeks to assess lung injury and inflammation and histopathology was done 1, 8, 16, 24, and 48 weeks postexposure.
  • Histopathologic evaluation at 1 week indicated that WF induced bronchiolar epithelial hyperplasia with associated cellular atypia, alveolar bronchiolo-alveolar hyperplasia (BAH) in peribronchiolar alveoli, and peribronchiolar lymphogranulomatous inflammation.
  • Persistent changes included foci of histiocytic inflammation, fibrosis, atypical bronchiolar epithelial cells, and bronchiolar BAH.
  • The principle changes in silica-exposed mice were histiocytic and suppurative inflammation, fibrosis, and alveolar BAH.
  • [MeSH-major] Genetic Predisposition to Disease. Inhalation Exposure. Lung / drug effects. Lung Neoplasms / genetics. Welding
  • [MeSH-minor] Animals. Bronchoalveolar Lavage Fluid / chemistry. Bronchoalveolar Lavage Fluid / cytology. Gases / chemistry. Gases / toxicity. Hyperplasia / chemically induced. Hyperplasia / pathology. Male. Mice. Mice, Inbred A. Particle Size. Pulmonary Fibrosis / chemically induced. Pulmonary Fibrosis / pathology. Silicon Dioxide / toxicity. Specific Pathogen-Free Organisms. Stainless Steel / toxicity. Time Factors

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  • (PMID = 16844664.001).
  • [ISSN] 0192-6233
  • [Journal-full-title] Toxicologic pathology
  • [ISO-abbreviation] Toxicol Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gases; 12597-68-1 / Stainless Steel; 7631-86-9 / Silicon Dioxide
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38. Marciniak-Czochra A, Kimmel M: Reaction-diffusion approach to modeling of the spread of early tumors along linear or tubular structures. J Theor Biol; 2007 Feb 7;244(3):375-87
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  • A biomedical example of such process might be the atypical adenomatous hyperplasia in the lung.
  • Equation for the cell number follows from an accepted model of cell cycle.
  • [MeSH-minor] Animals. Cell Division. Cell Movement. Diffusion. Humans. Intercellular Signaling Peptides and Proteins / metabolism. Lung / pathology. Lung Neoplasms / pathology. Models, Biological

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  • (PMID = 17046022.001).
  • [ISSN] 0022-5193
  • [Journal-full-title] Journal of theoretical biology
  • [ISO-abbreviation] J. Theor. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Intercellular Signaling Peptides and Proteins
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39. Garfield DH, Cadranel JL, Wislez M, Franklin WA, Hirsch FR: The bronchioloalveolar carcinoma and peripheral adenocarcinoma spectrum of diseases. J Thorac Oncol; 2006 May;1(4):344-59
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  • [Title] The bronchioloalveolar carcinoma and peripheral adenocarcinoma spectrum of diseases.
  • Bronchioloalveolar carcinoma (BAC) develops from terminal bronchiolar and acinar epithelia, growing along alveolar septa but without evidence of vascular or pleural involvement.
  • BAC, in turn, appears to arise from smaller peripheral nodules, called atypical adenomatous hyperplasia.
  • Clinical characteristics often differ from other types of non-small cell lung cancers.
  • Because of frequent lung-only recurrences, lung transplantation, although performed rarely, may hold promise.
  • [MeSH-major] Adenocarcinoma / therapy. Adenocarcinoma, Bronchiolo-Alveolar / therapy. Lung Neoplasms / therapy
  • [MeSH-minor] Female. Humans. Lung Transplantation. Male. Neoplasm Invasiveness. Neoplasm Staging. Positron-Emission Tomography. Prognosis. Tomography, X-Ray Computed

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  • [ErratumIn] J Thorac Oncol. 2006 Jun;1(5):405
  • (PMID = 17409882.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / P50 CA 058187
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 207
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40. Soh J, Toyooka S, Ichihara S, Asano H, Kobayashi N, Suehisa H, Otani H, Yamamoto H, Ichimura K, Kiura K, Gazdar AF, Date H: Sequential molecular changes during multistage pathogenesis of small peripheral adenocarcinomas of the lung. J Thorac Oncol; 2008 Apr;3(4):340-7
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  • [Title] Sequential molecular changes during multistage pathogenesis of small peripheral adenocarcinomas of the lung.
  • INTRODUCTION: We investigated EGFR and KRAS alterations among atypical adenomatous hyperplasia and small lung adenocarcinomas with bronchioloalveolar features to understand their role during multistage pathogenesis.
  • METHODS: Sixty lesions measuring 2 cm or less were studied, including 38 noninvasive lesions (4 atypical adenomatous hyperplasias, 19 Noguchi type A and 15 type B) and 22 invasive lesions (type C) based on the World Health Organization classification and Noguchi's criteria.
  • CONCLUSIONS: EGFR and KRAS mutations occur early during the multistage pathogenesis of peripheral lung adenocarcinomas.
  • By contrast, increased EGFR copy number is a late event during tumor development and plays a role in the progression of lung adenocarcinoma independent of the initiating molecular events.

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  • (PMID = 18379350.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / U01 CA084971-09; United States / NCI NIH HHS / CA / CA084971-09; United States / NCI NIH HHS / CA / P50CA70907; United States / NCI NIH HHS / CA / U01 CA084971; United States / NCI NIH HHS / CA / P50 CA070907-05S30003; United States / NCI NIH HHS / CA / P50 CA070907; United States / NCI NIH HHS / CA / CA070907-05S30003
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ NIHMS137273; NLM/ PMC2758162
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41. Nakano H, Soda H, Takasu M, Tomonaga N, Yamaguchi H, Nakatomi K, Fujino S, Hayashi T, Nakamura Y, Tsukamoto K, Kohno S: Heterogeneity of epidermal growth factor receptor mutations within a mixed adenocarcinoma lung nodule. Lung Cancer; 2008 Apr;60(1):136-40
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  • [Title] Heterogeneity of epidermal growth factor receptor mutations within a mixed adenocarcinoma lung nodule.
  • It has been proposed that stepwise progression occurs from atypical adenomatous hyperplasia (AAH) through bronchioloalveolar carcinoma (BAC) to invasive lung adenocarcinoma.
  • We report a patient with a mixed adenocarcinoma of the lung that had different EGFR mutations in the papillary subtype, the acinar subtype, and the surrounding AAH and BAC areas.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma, Bronchiolo-Alveolar / genetics. Lung Neoplasms / genetics. Mutation. Receptor, Epidermal Growth Factor / genetics. Solitary Pulmonary Nodule / genetics

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  • (PMID = 17889960.001).
  • [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
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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42. Cheng YS, Kessler H, Rees TD, Philofsky D, Pontikas A: Gingival swelling in a 13-year-old girl with multiple recurrences. Oral Surg Oral Med Oral Pathol Oral Radiol Endod; 2007 Jan;103(1):85-91
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  • With the tissue specimens from subsequent multiple excisions and several immunohistochemical studies, the diagnoses evolved to benign cellular infiltrate of undetermined origin, epithelioid hemangioma, proliferating endothelial cell neoplasm of uncertain biologic potential, atypical vascular tumor, epithelioid hemangioendothelioma, and kaposiform hemangioendothelioma.
  • [MeSH-major] Alveolar Process / surgery. Gingiva / pathology. Gingival Neoplasms / pathology. Hemangioendothelioma, Epithelioid / pathology. Neoplasm Recurrence, Local / pathology
  • [MeSH-minor] Adolescent. Angiolymphoid Hyperplasia with Eosinophilia / pathology. Biomarkers / analysis. Biopsy. Diagnosis, Differential. Epithelioid Cells / pathology. Female. Humans. Reoperation

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  • (PMID = 17178499.001).
  • [ISSN] 1528-395X
  • [Journal-full-title] Oral surgery, oral medicine, oral pathology, oral radiology, and endodontics
  • [ISO-abbreviation] Oral Surg Oral Med Oral Pathol Oral Radiol Endod
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers
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43. Ide F, Kikuchi K, Kusama K, Kanazawa H: Sialadenoma papilliferum with potentially malignant features. J Clin Pathol; 2010 Apr;63(4):362-4

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  • Histological features were also atypical: surface verrucous hyperplasia and deeper florid cystic-duct adenoma.
  • [MeSH-major] Adenoma / diagnosis. Mandibular Neoplasms / diagnosis. Papilloma / diagnosis
  • [MeSH-minor] Aged. Alveolar Process. Carcinoma, Verrucous / diagnosis. Diagnosis, Differential. Humans. Male. Tomography, X-Ray Computed

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  • (PMID = 20354209.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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44. Syrjä P, Saari S, Rajamäki M, Saario E, Järvinen AK: Pulmonary histopathology in dalmatians with familial acute respiratory distress syndrome (ARDS). J Comp Pathol; 2009 Nov;141(4):254-9
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  • Affected dogs had multiple foci of marked atypical hyperplasia and squamous metaplasia of the bronchiolar epithelium, patchy ongoing fibrosis with myofibroblastic metaplasia, smooth muscle hyperplasia and occasional honeycombing of alveolar walls, and hyperplasia of atypical type II pneumocytes.
  • There was an abrupt transition between these proliferative lesions and areas of acute alveolar oedema with hyaline membranes in partially normal lung.
  • Immunohistochemical labelling for cytokeratin expression indicated that the metaplastic epithelium was of bronchiolar origin and that it extended into peribronchiolar alveolar spaces.
  • The observed lesions in the Dalmatians are distinct from the diffuse alveolar damage that characterizes AIP, but show some histological similarities to the usual interstitial pneumonia (UIP) that occurs in IPF with acute exacerbation in man.
  • [MeSH-major] Dog Diseases / pathology. Lung / pathology. Pneumocytes / pathology. Respiratory Distress Syndrome, Adult / veterinary

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  • (PMID = 19628215.001).
  • [ISSN] 1532-3129
  • [Journal-full-title] Journal of comparative pathology
  • [ISO-abbreviation] J. Comp. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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45. 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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46. Mun M, Kohno T: Efficacy of thoracoscopic resection for multifocal bronchioloalveolar carcinoma showing pure ground-glass opacities of 20 mm or less in diameter. J Thorac Cardiovasc Surg; 2007 Oct;134(4):877-82
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  • [Title] Efficacy of thoracoscopic resection for multifocal bronchioloalveolar carcinoma showing pure ground-glass opacities of 20 mm or less in diameter.
  • OBJECTIVE: Small bronchioloalveolar carcinoma showing pure ground-glass opacity on high-resolution computed tomographic scans is commonly multifocal.
  • We discuss the efficacy of video-assisted thoracic surgery for multifocal bronchioloalveolar carcinoma in patients at our institution.
  • METHODS: Twenty-seven patients with multifocal bronchioloalveolar carcinoma lesions less than or equal to 20 mm in diameter (105 lesions) underwent video-assisted thoracic surgery pulmonary resection between 2000 and 2006.
  • The distribution of bronchioloalveolar carcinoma lesions was unilateral in 14 patients and bilateral in 13 patients.
  • Histologic diagnoses showed 62 bronchioloalveolar carcinoma type A lesions, 28 type B lesions, and 15 type C lesions according to Noguchi's classification, and atypical adenomatous hyperplasia in 43 lesions (13 patients).
  • Patients with new lesions had a higher incidence of bronchioloalveolar carcinoma lesions of 3 mm or less in diameter (P = .0254) and atypical adenomatous hyperplasia (P = .011).
  • CONCLUSION: Video-assisted thoracic surgery management of multifocal bronchioloalveolar carcinoma yielded satisfactory results.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / radiography. Adenocarcinoma, Bronchiolo-Alveolar / surgery. Lung Neoplasms / radiography. Lung Neoplasms / surgery. Thoracic Surgery, Video-Assisted. Thoracoscopy / methods. Tomography, X-Ray Computed
  • [MeSH-minor] Adenoma / pathology. Adenoma / radiography. Adenoma / surgery. Adult. Aged. Female. Humans. Male. Middle Aged. Retrospective Studies. Survival Rate. Treatment Outcome

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  • (PMID = 17903500.001).
  • [ISSN] 1097-685X
  • [Journal-full-title] The Journal of thoracic and cardiovascular surgery
  • [ISO-abbreviation] J. Thorac. Cardiovasc. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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47. 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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48. Ioachimescu OC, Mehta AC: From cystic pulmonary airway malformation, to bronchioloalveolar carcinoma and adenocarcinoma of the lung. Eur Respir J; 2005 Dec;26(6):1181-7
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  • [Title] From cystic pulmonary airway malformation, to bronchioloalveolar carcinoma and adenocarcinoma of the lung.
  • Bronchioloalveolar carcinoma (BAC) of the lungs is a known morphological subtype of nonsmall cell cancer.
  • The current study presents several carcinogenetic theories of BAC and the possible relationship with atypical adenomatous hyperplasia and congenital pulmonary airway malformation (CPAM).
  • The case is unique due to the combination of: early age of presentation; neoplastic transformation of a CPAM; unaltered course over 15 yrs; and its particular pattern of slow morphogenesis and degeneration into an invasive AC of the lung.
  • In conclusion, clinicians and pathologists need to be aware of the fact that congenital pulmonary airway malformation so far represents the only known pre-invasive lesion for mucinous bronchioloalveolar carcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma, Bronchiolo-Alveolar / pathology. Cell Transformation, Neoplastic / pathology. Cystic Adenomatoid Malformation of Lung, Congenital / pathology. Lung Neoplasms / pathology

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  • (PMID = 16319347.001).
  • [ISSN] 0903-1936
  • [Journal-full-title] The European respiratory journal
  • [ISO-abbreviation] Eur. Respir. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
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49. 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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50. Chhieng DC: Cytology of bronchial associated lymphoid tissue lymphoma. Diagn Cytopathol; 2008 Oct;36(10):723-8
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  • Fine needle aspiration biopsy (FNA) of the right lower lobe mass was performed and revealed atypical alveolar cells in a lymphoid background.
  • The initial cytologic interpretation was "atypical alveolar cells, probably reactive."
  • Intraoperative touch preparation revealed an atypical lymphoid proliferation.
  • Histologic findings revealed multiple nodules of small and medium-sized lymphocytes replacing the lung parenchyma; lymphoepithelial lesions, and type II pneumocytes hyperplasia were also noted.
  • Flow cytometry demonstrated the presence of a monoclonal B-cell population.
  • [MeSH-major] Lung Neoplasms / pathology. Lymphoma, B-Cell / pathology. Pulmonary Alveoli / pathology
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / pathology. Aged. Biopsy, Fine-Needle. Cell Proliferation. Diagnosis, Differential. Humans. Male

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  • (PMID = 18773446.001).
  • [ISSN] 1097-0339
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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51. Myung JK, Choe G, Chung DH, Seo JW, Jheon S, Lee CT, Chung JH: A simple inflation method for frozen section diagnosis of minute precancerous lesions of the lung. Lung Cancer; 2008 Feb;59(2):198-202
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  • [Title] A simple inflation method for frozen section diagnosis of minute precancerous lesions of the lung.
  • Evaluation of minute precancerous lesions of the lung by frozen section is very difficult for the pathologist as uninflated lung tissue usually shows severe atelectasis and frozen artifact.
  • We tried to inflate lung tissue with the embedding medium used for frozen section and to determine the appropriate dilution ratio of the embedding medium for optimization of frozen section morphology.
  • METHODS: The lung specimens were derived from 10 patients who underwent video-assisted thoracoscopic surgery (VATS) due to pneumothorax (four patients) and GGO (six patients) detected on high-resolution computed tomography (HRCT) at Seoul National University Bundang Hospital.
  • Lung specimens obtained from the six people with GGO detected on HRCT were submitted for intraoperative pathology consultation.
  • RESULTS: The frozen section quality of lung tissue was excellent after simple inflation with diluted embedding medium (2:3).
  • Minute precancerous foci such as atypical adenomatous hyperplasia (AAH) and bronchioloalveolar carcinoma (BAC) could be readily identified in frozen sections using this method.
  • CONCLUSIONS: An inflation procedure using diluted embedding medium can make lung tissue expand well during frozen section.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / pathology. Frozen Sections / methods. Lung Neoplasms / pathology. Precancerous Conditions / pathology. Solitary Pulmonary Nodule / pathology. Tissue Embedding / methods

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  • (PMID = 17905468.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Ireland
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52. Mucenski ML, Nation JM, Thitoff AR, Besnard V, Xu Y, Wert SE, Harada N, Taketo MM, Stahlman MT, Whitsett JA: Beta-catenin regulates differentiation of respiratory epithelial cells in vivo. Am J Physiol Lung Cell Mol Physiol; 2005 Dec;289(6):L971-9
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  • An activated form of beta-catenin [Catnb(Delta(ex3))] was expressed in respiratory epithelial cells of the developing lung.
  • Although morphogenesis was not altered at birth, air space enlargement and epithelial cell dysplasia were observed in the early postnatal period and persisted into adulthood.
  • The Catnb(Delta(ex3)) protein caused squamous, cuboidal, and goblet cell dysplasia in intrapulmonary conducting airways.
  • Atypical epithelial cells that stained for surfactant pro protein C (pro-SP-C) and had morphological characteristics of alveolar type II cells were observed in bronchioles of the transgenic mice.
  • Catnb(Delta(ex3)) inhibited expression of Foxa2 and caused goblet cell hyperplasia associated with increased staining for mucins and the MUC5A/C protein.
  • Activation of beta-catenin caused ectopic differentiation of alveolar type II-like cells in conducting airways, goblet cell hyperplasia, and air space enlargement, demonstrating a critical role for the Wnt/beta-catenin signal transduction pathway in the differentiation of the respiratory epithelium in the postnatal lung.
  • [MeSH-major] Cell Differentiation. Epithelial Cells / metabolism. Lung / embryology. Morphogenesis. beta Catenin / metabolism

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  • (PMID = 16040629.001).
  • [ISSN] 1040-0605
  • [Journal-full-title] American journal of physiology. Lung cellular and molecular physiology
  • [ISO-abbreviation] Am. J. Physiol. Lung Cell Mol. Physiol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL 56387; United States / NHLBI NIH HHS / HL / HL 75770
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Foxa2 protein, mouse; 0 / Muc5ac protein, mouse; 0 / Mucin 5AC; 0 / Mucins; 0 / Peptides; 0 / Protein Precursors; 0 / Sftpc protein, mouse; 0 / Wnt Proteins; 0 / beta Catenin; 135845-92-0 / Hepatocyte Nuclear Factor 3-beta
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53. Gandara DR, Aberle D, Lau D, Jett J, Akhurst T, Heelan R, Mulshine J, Berg C, Patz EF Jr: Radiographic imaging of bronchioloalveolar carcinoma: screening, patterns of presentation and response assessment. J Thorac Oncol; 2006 Nov;1(9 Suppl):S20-6
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  • [Title] Radiographic imaging of bronchioloalveolar carcinoma: screening, patterns of presentation and response assessment.
  • Bronchioloalveolar carcinoma (BAC) is a previously uncommon subset of adenocarcinoma with unique epidemiology, pathology, radiographic presentation, clinical features, and natural history compared with other non-small cell lung cancer (NSCLC) subtypes.
  • The rising incidence of BAC is also reflected in recent lung cancer screening studies employing helical computed tomography (CT), where the differential diagnosis of GGOs includes not only BAC and overt adenocarcinoma, but inflammatory disease, focal fibrosis, and atypical adenomatous hyperplasia.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / radiography. Carcinoma, Non-Small-Cell Lung / radiography. Lung Neoplasms / radiography. Neoplasm Recurrence, Local / radiography. Tomography, Spiral Computed

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  • [ErratumIn] J Thorac Oncol. 2007 Jan;2(1):11. Heelan, Robert [added]
  • (PMID = 17409997.001).
  • [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] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 65
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54. Haneda H, Sasaki H, Shimizu S, Endo K, Suzuki E, Yukiue H, Kobayashi Y, Yano M, Fujii Y: Epidermal growth factor receptor gene mutation defines distinct subsets among small adenocarcinomas of the lung. Lung Cancer; 2006 Apr;52(1):47-52
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  • [Title] Epidermal growth factor receptor gene mutation defines distinct subsets among small adenocarcinomas of the lung.
  • Epidermal growth factor receptor (EGFR) gene mutations are frequently detected in lung cancer, especially in adenocarcinoma, in females, and non-smoking patients.
  • Bronchioloalveolar carcinoma (BAC) appearance is a good predictor of response to this agent.
  • Noguchi et al. subdivided small peripheral adenocarcinoma of the lung into two groups.
  • One group was characterized with tumor cell growth replacing the normal alveolar cells with varying degree of fibrosis (types A-C), and the other shows non-replacing and destructive growth (types D-F).
  • Using probes for the 13 mutations which have been previously described, we have genotyped the EGFR gene status in surgically resected atypical adenomatous hyperplasias (AAH) and small peripheral adenocarcinomas up to 2 cm in diameter using TaqMan PCR assay.
  • [MeSH-major] Adenocarcinoma / genetics. Cell Transformation, Neoplastic / genetics. Lung Neoplasms / genetics. Mutation / genetics. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Hyperplasia / genetics. Male. Middle Aged

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  • [CommentIn] Lung Cancer. 2007 Jan;55(1):129-30 [17156891.001]
  • (PMID = 16503085.001).
  • [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] EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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55. Kovalchuk O, Tryndyak VP, Montgomery B, Boyko A, Kutanzi K, Zemp F, Warbritton AR, Latendresse JR, Kovalchuk I, Beland FA, Pogribny IP: Estrogen-induced rat breast carcinogenesis is characterized by alterations in DNA methylation, histone modifications and aberrant microRNA expression. Cell Cycle; 2007 Aug 15;6(16):2010-8
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  • Breast cancer emerges through a multi-step process, encompassing progressive changes from a normal cell to hyperplasia (with and without atypia), carcinoma in situ, invasive carcinoma, and metastasis.
  • The pattern of morphological changes in mammary glands during E(2)-induced carcinogenesis was characterized by transition from normal appearing alveolar and ductular hyperplasia to focal hyperplastic areas of atypical glands and ducts accompanied by a rapid and sustained loss of global DNA methylation, LINE-1 hypomethylation, loss of histone H3 lysine 9 and histone H4 lysine 20 trimethylation, and altered microRNAs expression.
  • More importantly, these alterations in the mammary tissue occurred after six weeks of E(2)-treatment, whereas the atypical hyperplasia, which represents a putative precursor lesion to mammary carcinoma in this model, was detected only after twelve weeks of exposure, demonstrating clearly that these events are directly associated with the effects of E(2) and are not a consequence of the preexisting preneoplastic lesions.
  • [MeSH-minor] Animals. Blotting, Western. Cell Transformation, Neoplastic / chemically induced. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. DNA (Cytosine-5-)-Methyltransferase / metabolism. Electrophoresis, Polyacrylamide Gel. Estradiol / toxicity. Female. Gene Expression Regulation / drug effects. Methylation / drug effects. Rats

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  • (PMID = 17700064.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Estrogens; 0 / Histones; 0 / MicroRNAs; 4TI98Z838E / Estradiol; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase
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56. Yoo SB, Chung JH, Lee HJ, Lee CT, Jheon S, Sung SW: Epidermal growth factor receptor mutation and p53 overexpression during the multistage progression of small adenocarcinoma of the lung. J Thorac Oncol; 2010 Jul;5(7):964-9
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  • [Title] Epidermal growth factor receptor mutation and p53 overexpression during the multistage progression of small adenocarcinoma of the lung.
  • INTRODUCTION: A progression model of atypical adenomatous hyperplasia (AAH) to bronchioloalveolar carcinoma (BAC) to invasive adenocarcinoma (ADC) has been proposed.
  • CONCLUSIONS: High frequency and similar incidence of EGFR mutation in AAH, BAC, and ADC support that EGFR gene mutation occurs in the early stage of pulmonary ADC development and tumor initiation from the preneoplastic lung parenchyma to neoplastic conditions.
  • [MeSH-major] Lung Neoplasms / genetics. Lung Neoplasms / metabolism. Mutation / genetics. Receptor, Epidermal Growth Factor / genetics. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adenocarcinoma, Bronchiolo-Alveolar / genetics. Adenocarcinoma, Bronchiolo-Alveolar / metabolism. Adenocarcinoma, Bronchiolo-Alveolar / pathology. Adenomatosis, Pulmonary / genetics. Adenomatosis, Pulmonary / metabolism. Adenomatosis, Pulmonary / pathology. Adult. Aged. Aged, 80 and over. Disease Progression. Female. Humans. Immunoenzyme Techniques. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging. Polymerase Chain Reaction. Precancerous Conditions / genetics. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. Prognosis

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  • (PMID = 20512074.001).
  • [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 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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57. 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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58. Tsubura A, Yoshizawa K, Uehara N, Yuri T, Matsuoka Y: Multistep mouse mammary tumorigenesis through pre-neoplasia to neoplasia and acquisition of metastatic potential. Med Mol Morphol; 2007 Mar;40(1):9-17
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  • Human breast tissue can give rise to hyperplasias, atypical hyperplasias, and in situ carcinomas originating in a terminal duct-lobular unit (TDLU).
  • Mouse mammary tissue can give rise to several characteristic types of premalignant hyperplasia and tumor, originating in a duct or acinus, that progress to carcinoma.
  • Three specific types of mouse mammary lesion with premalignant potential have been identified: hyperplastic alveolar nodule (HAN), plaque (PLQ), and ductal hyperplasia (DH).

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  • (PMID = 17384984.001).
  • [ISSN] 1860-1480
  • [Journal-full-title] Medical molecular morphology
  • [ISO-abbreviation] Med Mol Morphol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Japan
  • [Number-of-references] 51
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59. Sheehan M, Cassidy JP, Brady J, Ball H, Doherty ML, Quinn PJ, Nicholas RA, Markey BK: An aetiopathological study of chronic bronchopneumonia in lambs in Ireland. Vet J; 2007 May;173(3):630-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Chronic bronchopneumonia in lambs, also known as 'atypical' or 'chronic, non-progressive' pneumonia is a common, frequently sub-clinical disease affecting animals under 12-months-old in intensive production systems.
  • In this study, detailed laboratory examination of 30 abattoir-derived lungs with the characteristic gross features of atypical pneumonia (AP) was carried out with a view to refining and correlating the histopathological and microbiological criteria required for the diagnosis of this disease.
  • Furthermore, peri-airway lymphoid hyperplasia, intra-alveolar exudation and nodular 'hyaline scars', which are all previously reported microscopic lesions of AP, were not identified in 12 (40%) of the cases and isolation of M. haemolytica was over-represented in lungs exhibiting suppurative lesions.
  • [MeSH-major] Bronchopneumonia / veterinary. Lung. Mannheimia haemolytica / isolation & purification. Mycoplasma ovipneumoniae / isolation & purification. Sheep Diseases / microbiology. Sheep Diseases / pathology

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  • (PMID = 16632391.001).
  • [ISSN] 1090-0233
  • [Journal-full-title] Veterinary journal (London, England : 1997)
  • [ISO-abbreviation] Vet. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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60. 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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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. Lucattelli M, Fineschi S, Geppetti P, Gerard NP, Lungarella G: Neurokinin-1 receptor blockade and murine lung tumorigenesis. Am J Respir Crit Care Med; 2006 Sep 15;174(6):674-83
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  • [Title] Neurokinin-1 receptor blockade and murine lung tumorigenesis.
  • RATIONALE: Analogous to the adenoma-carcinoma sequence in the colon, it has been proposed that adenocarcinoma (AC) in the lung arises from adenomatous hyperplasia that progresses through atypical adenomatous hyperplasia to AC.
  • We also demonstrate that a series of alterations in gene expression of proliferation markers (i.e., PCNA and Ki-67) and cell cycle regulators (i.e., FHIT, p53, and p21) characterizes the sequence of the precursor lesions.
  • The loss of function of the NK-1R results in changes of the apoptotic rate and in a delay of DNA break recovery of alveolar epithelial cells following bleomycin treatment.
  • CONCLUSIONS: To our knowledge, this is the first model to demonstrate a role for NK-1R in lung epithelial cell death and tumorigenesis.
  • [MeSH-major] Adenocarcinoma / metabolism. Antibiotics, Antineoplastic / toxicity. Lung Neoplasms / metabolism. Neurokinin-1 Receptor Antagonists
  • [MeSH-minor] Animals. Apoptosis. Bleomycin / toxicity. DNA, Neoplasm / genetics. Gene Expression Regulation, Neoplastic / drug effects. Genes, p53 / genetics. Immunohistochemistry. Ki-67 Antigen / genetics. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Mice, Knockout. Proliferating Cell Nuclear Antigen / genetics. Protein-Tyrosine Kinases / metabolism. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins c-bcl-2. Receptors, Neurokinin-1 / metabolism

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  • (PMID = 16799078.001).
  • [ISSN] 1073-449X
  • [Journal-full-title] American journal of respiratory and critical care medicine
  • [ISO-abbreviation] Am. J. Respir. Crit. Care Med.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / DNA, Neoplasm; 0 / Ki-67 Antigen; 0 / Neurokinin-1 Receptor Antagonists; 0 / Proliferating Cell Nuclear Antigen; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Receptors, Neurokinin-1; 11056-06-7 / Bleomycin; 114100-40-2 / Bcl2 protein, mouse; EC 2.7.10.1 / Protein-Tyrosine Kinases
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63. 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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64. Jin Z, Liu B, Feng D, Chen C, Li X, Hu Y, Peng J, Liu Y, Du J, Fu C, Wen J: Identification of differentially expressed genes in rat silicosis model by suppression subtractive hybridization analysis. Acta Biochim Biophys Sin (Shanghai); 2008 Aug;40(8):740-6
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  • Radiographs of chests showed that some scattered high-density shadows appeared in the lung field.
  • Typical microscopic fibrosing silicotic nodules formed in the lung, alveolar epithelial cells and bronchial epithelial cells, particularly around the partial fibrosing silicotic nodules; some of them showed atypical hyperplasia that suggested a correlation between silicosis and lung cancer.
  • Suppression subtractive hybridization analysis was performed to compare gene expression in lung tissue with silicosis and normal lung tissue.
  • Reverse transcription-polymerase chain reaction showed that the expressions of seven novel cDNA sequences identified by suppression subtractive hybridization in lung tissue with silicosis differed from normal lung tissue.
  • [MeSH-minor] Animals. DNA Primers / genetics. DNA, Complementary / genetics. Disease Models, Animal. Female. Gene Expression. Humans. Lung / metabolism. Lung / pathology. Nucleic Acid Hybridization. Pulmonary Fibrosis / genetics. Rats. Rats, Sprague-Dawley. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 18685790.001).
  • [ISSN] 1745-7270
  • [Journal-full-title] Acta biochimica et biophysica Sinica
  • [ISO-abbreviation] Acta Biochim. Biophys. Sin. (Shanghai)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA, Complementary
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65. Echiburú-Chau C, Calaf GM: Rat lung cancer induced by malathion and estrogen. Int J Oncol; 2008 Sep;33(3):603-11
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  • [Title] Rat lung cancer induced by malathion and estrogen.
  • Lung cancer can originate from exposure to exogenous and endogenous environmental carcinogens.
  • There is evidence that estrogen can increase lung cancer risk in women.
  • The aim of the present study was to analyze morphological and molecular alterations induced by malathion (M) and 17beta-estradiol (E2) in rat lung tissues.
  • The animals were injected over a 5-day period and sacrificed 240 days after treatments and lung tissues were excised and analyzed for morphological alterations.
  • Morphometric analysis indicated that M plus E2-treated animals showed a significantly (P<0.05) higher incidence of parenchyma with alveolar proliferative lesions (PAPL), preneoplastic lesions in bronchiolar epithelium (hyperplasia, metaplasia, carcinoma in situ and invasive carcinoma) and atypical lymphatic morphology (lymphatic cell aggregates;.
  • In summary, the combination of M and E2 sharply induced pathological lesions in lung alveolar parenchyma, bronchiolar epithelia and lymphatic tissues, in comparison to control animals or in animals treated with either substance alone.
  • These results indicated an increase in risk of rodent lung tumor formation by environmental and endogenous substances.
  • [MeSH-major] Estradiol / toxicity. Estrogens / toxicity. Insecticides / toxicity. Lung Neoplasms / chemically induced. Lung Neoplasms / pathology. Malathion / toxicity
  • [MeSH-minor] Animals. Female. Immunohistochemistry. Lung / drug effects. Lung / pathology. Rats. Rats, Sprague-Dawley. Receptor, ErbB-2 / biosynthesis. Receptor, ErbB-2 / drug effects. rhoA GTP-Binding Protein / biosynthesis. rhoA GTP-Binding Protein / drug effects

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  • (PMID = 18695892.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Estrogens; 0 / Insecticides; 4TI98Z838E / Estradiol; EC 2.7.10.1 / Receptor, ErbB-2; EC 3.6.5.2 / rhoA GTP-Binding Protein; U5N7SU872W / Malathion
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66. 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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  • [Cites] Proc Natl Acad Sci U S A. 2001 Nov 20;98(24):13790-5 [11707567.001]
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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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67. National Toxicology Program: Toxicology and carcinogenesis studies of divinylbenzene-HP (Cas No. 1321-74-0) in F344/N rats and B6C3F1 mice (inhalation studies). Natl Toxicol Program Tech Rep Ser; 2006 Nov;(534):1-290
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  • Incidences of degeneration of the olfactory epithelium in 200 and 400 ppm rats and basal cell hyperplasia of the olfactory epithelium in rats exposed to 100 ppm or greater were significantly increased.
  • In 400 ppm males, the incidence of renal tubule hyperplasia was increased, and the incidence of nephropathy was significantly increased.
  • Following combined analysis of single and step-section data, the incidences of renal tubule adenoma and adenoma or carcinoma (combined) were marginally higher in 200 and 400 ppm males, and the incidence of renal tubule hyperplasia was significantly increased in 400 ppm males.
  • The incidences of malignant glial cell tumors (malignant astrocytoma and oligodendroglioma) in the brain were slightly increased in 100 and 200 ppm males, and the incidence in the 200 ppm group exceeded the historical range for chamber controls.
  • The incidence of focal chronic inflammation in the lung of 400 ppm males was significantly greater than in the chamber control group.
  • The incidences of alveolar/bronchiolar adenoma and alveolar/bronchiolar adenoma or carcinoma (combined) in 100 ppm males were greater than chamber control incidences, but the incidences of adenoma or carcinoma (combined) were within the historical control range.
  • The incidences of alveolar/bronchiolar adenoma and alveolar/bronchiolar adenoma or carcinoma (combined) in all exposed groups of females were generally greater than those of the chamber controls; the incidences were at the upper end or exceeded the historical control ranges.
  • There was a greater incidence and severity of alveolar epithelial hyperplasia in 100 ppm females and a greater severity of this lesion in 30 ppm females, when compared to chamber controls.
  • The incidences and/or severities of atypical bronchiole hyperplasia were significantly increased in all exposed groups of mice.
  • There was equivocal evidence of carcinogenic activity of divinylbenzene-HP in female B6C3F1 mice based on the incidences of alveolar/bronchiolar adenoma or carcinoma (combined) in the lung.
  • Exposure to divinylbenzene-HP caused nonneoplastic lesions of the nasal cavity in male and female rats and of the lung and nasal cavity in male and female mice.

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  • (PMID = 17342197.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article; Technical Report
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Vinyl Compounds; IZ715T4SBU / divinyl benzene
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68. Garfield D: Can K-ras-mutated atypical adenomatous hyperplasia be another precursor lesion for mucinous bronchioloalveolar carcinoma? Am J Clin Pathol; 2008 Aug;130(2):315-6; author reply 316
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  • [Title] Can K-ras-mutated atypical adenomatous hyperplasia be another precursor lesion for mucinous bronchioloalveolar carcinoma?
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / pathology. Adenoma / genetics. Genes, ras. Lung Neoplasms / genetics
  • [MeSH-minor] Humans. Hyperplasia. Mutation. Precancerous Conditions / genetics

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  • [CommentOn] Am J Clin Pathol. 2008 Feb;129(2):202-10 [18208799.001]
  • (PMID = 18697292.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
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