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1. 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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2. 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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3. 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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4. 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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5. 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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6. 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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7. 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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8. 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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9. 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


10. 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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11. Nakanishi K, Kumaki F, Hiroi S, Mukai M, Ikeda E, Kawai T: Mre11 expression in atypical adenomatous hyperplasia and adenocarcinoma of the lung. Arch Pathol Lab Med; 2006 Sep;130(9):1330-4
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  • [Title] Mre11 expression in atypical adenomatous hyperplasia and adenocarcinoma of the lung.
  • OBJECTIVE: To investigate Mre11 in atypical adenomatous hyperplasia (AAH) and nonmucinous bronchioloalveolar carcinoma (NMBAC), an issue not previously explored.
  • CONCLUSIONS: On this basis, we suggest that the part played by Mre11 in telomere maintenance may not be important for the progression of the adenoma-carcinoma (AAH-NMBAC) sequence in the lung, although some role for it in carcinogenesis cannot be completely ruled out.
  • [MeSH-major] Adenocarcinoma / pathology. DNA-Binding Proteins / genetics. Lung Neoplasms / pathology
  • [MeSH-minor] Bronchial Neoplasms / genetics. Bronchial Neoplasms / pathology. Humans. Hyperplasia. Immunohistochemistry. Pulmonary Alveoli / pathology. RNA, Messenger / genetics. Retrospective Studies. Telomere / genetics

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  • (PMID = 16948520.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / MRE11A protein, human; 0 / RNA, Messenger
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12. 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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13. 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


14. Goto A, Nakajima J, Hara K, Niki T, Fukayama M: Lung adenocarcinoma associated with familial adenomatous polyposis. Clear cell carcinoma with beta-catenin accumulation accompanied by atypical adenomatous hyperplasia. Virchows Arch; 2005 Jan;446(1):73-7
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  • [Title] Lung adenocarcinoma associated with familial adenomatous polyposis. Clear cell carcinoma with beta-catenin accumulation accompanied by atypical adenomatous hyperplasia.
  • A 46-year-old man presented with a lung tumor 17 years after a subtotal colectomy and 13 years after a partial duodenectomy for familial adenomatous polyposis (FAP).
  • Pathological analysis of the lung tumor demonstrated adenocarcinoma with clear cells and a papillary structure, accompanied by tiny tumorous nodules in the background lung parenchyma.
  • Many of the nodules were multifocal adenocarcinoma; however, some of the nodules demonstrated atypical adenomatous hyperplasia (AAH).
  • This is the first case report of a lung adenocarcinoma accompanied by AAH in a FAP patient.
  • Immunohistochemical and loss of heterozygosity studies revealed unique features of the lesions reflecting a disruption of the adenomatous poliposis coli-beta-catenin pathway.
  • [MeSH-major] Adenocarcinoma / pathology. Adenomatous Polyposis Coli / complications. Cytoskeletal Proteins / metabolism. Lung Neoplasms / pathology. Trans-Activators / metabolism
  • [MeSH-minor] Genes, APC. Humans. Hyperplasia. Immunohistochemistry. Loss of Heterozygosity. Male. Middle Aged. beta Catenin

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  • (PMID = 15660284.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / Cytoskeletal Proteins; 0 / Trans-Activators; 0 / beta Catenin
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15. 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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16. 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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17. Gradowski JF, Mantha GS, Hunt JL, Dacic S: Molecular alterations in atypical adenomatous hyperplasia occurring in benign and cancer-bearing lungs. Diagn Mol Pathol; 2007 Jun;16(2):87-90
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  • [Title] Molecular alterations in atypical adenomatous hyperplasia occurring in benign and cancer-bearing lungs.
  • Atypical adenomatous hyperplasia (AAH) is considered to be a precursor lesion of the lung adenocarcinoma.
  • Several genetic abnormalities have been reported in AAH associated with adenocarcinoma, but little is known about AAH associated with benign lung lesions.
  • Seven cases of AAH from resected non-neoplastic lungs (AAH-B) and 12 cases from lungs resected for primary lung carcinoma (AAH-M) were analyzed for loss of heterozygosity (LOH) using 21 polymorphic microsatellite markers situated in proximity to known tumor suppressor genes on chromosomes 3p, 5q, 7p, 9p, 10q, and 17p.
  • Our results showed a significant overlap in LOH patterns between AAH with or without coexistent lung malignancy.
  • Therefore, AAH may represent a smoking induced low-grade neoplastic lesion that may be a precursor lesion of only a subset of invasive lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Adenomatosis, Pulmonary / genetics. Loss of Heterozygosity. Lung / pathology. Lung Neoplasms / genetics. Precancerous Conditions / genetics

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  • (PMID = 17525677.001).
  • [ISSN] 1052-9551
  • [Journal-full-title] Diagnostic molecular pathology : the American journal of surgical pathology, part B
  • [ISO-abbreviation] Diagn. Mol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Genetic Markers
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18. 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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19. 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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20. 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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21. Kohno T, Kunitoh H, Suzuki K, Yamamoto S, Kuchiba A, Matsuno Y, Yanagitani N, Yokota J: Association of KRAS polymorphisms with risk for lung adenocarcinoma accompanied by atypical adenomatous hyperplasias. Carcinogenesis; 2008 May;29(5):957-63
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  • [Title] Association of KRAS polymorphisms with risk for lung adenocarcinoma accompanied by atypical adenomatous hyperplasias.
  • The pulmonary adenoma susceptibility 1 (Pas1) gene affects susceptibility to the development of lung adenomas in mice with a subset of the adenomas progressing to adenocarcinoma (ADC).
  • In this study, genotype distributions for 10 polymorphisms in the human counterparts for three mouse candidate Pas1 genes, KRAS, CASC1/LAS1 and LRMP, were examined in a hospital-based case-control study consisting of 364 lung ADC cases and 253 controls.
  • All the ADC cases were subjected to lobectomy and subsequent pathological investigation of atypical adenomatous hyperplasia (AAH), a putative precursor for peripheral lung ADC, including bronchioloalveolar carcinoma, in the resected lobes.
  • None of the 10 polymorphisms examined showed significant associations with overall lung ADC risk (P > 0.05).
  • Minor haplotypes including the minor allele for the KRAS-6 polymorphism showed increased ORs for ADC accompanied by multiple AAHs, and KRAS transcripts from the minor allele for this polymorphism were more abundantly detected in lung tissues than those from the major allele.
  • [MeSH-major] Adenocarcinoma / genetics. Lung Neoplasms / genetics. Polymorphism, Genetic. Polymorphism, Single Nucleotide. Proto-Oncogene Proteins / genetics. ras Proteins / genetics
  • [MeSH-minor] Adenomatosis, Pulmonary / epidemiology. Adenomatosis, Pulmonary / genetics. Aged. Antigens, Neoplasm / genetics. Antigens, Nuclear / genetics. DNA, Neoplasm / blood. DNA, Neoplasm / genetics. DNA, Neoplasm / isolation & purification. Female. Humans. Hyperplasia / complications. Hyperplasia / epidemiology. Hyperplasia / genetics. Japan / epidemiology. Male. Middle Aged. Risk Factors. Smoking / epidemiology

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  • (PMID = 18299280.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Antigens, Nuclear; 0 / DNA, Neoplasm; 0 / KRAS protein, human; 0 / PASD1 protein, human; 0 / Proto-Oncogene Proteins; EC 3.6.5.2 / ras Proteins
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22. Sakamoto H, Shimizu J, Horio Y, Ueda R, Takahashi T, Mitsudomi T, Yatabe Y: Disproportionate representation of KRAS gene mutation in atypical adenomatous hyperplasia, but even distribution of EGFR gene mutation from preinvasive to invasive adenocarcinomas. J Pathol; 2007 Jul;212(3):287-94
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  • [Title] Disproportionate representation of KRAS gene mutation in atypical adenomatous hyperplasia, but even distribution of EGFR gene mutation from preinvasive to invasive adenocarcinomas.
  • In the resected lung, additional small lesions are occasionally found incidentally, and include the full spectrum of preinvasive to invasive lesions under the current putative schema of the sequential development of lung cancer.
  • In this study, we examined EGFR and KRAS gene mutations in 119 synchronous pulmonary lesions, including 40 precursor lesions (atypical adenomatous hyperplasia, AAH), 26 carcinomas in situ (non-mucinous bronchioloalveolar carcinoma, BAC), 14 minimally invasive adenocarcinomas, 34 overt invasive adenocarcinomas, and five of other subtypes of cancer.
  • [MeSH-major] Adenocarcinoma / genetics. Lung Neoplasms / genetics. Mutation. Neoplasms, Multiple Primary / genetics. Precancerous Conditions / genetics. Proto-Oncogene Proteins / genetics. Receptor, Epidermal Growth Factor / genetics. ras Proteins / genetics
  • [MeSH-minor] DNA Mutational Analysis. Disease Progression. Humans. Hyperplasia / genetics. Smoking / genetics

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  • [Copyright] Copyright (c) 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • (PMID = 17534846.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.6.5.2 / ras Proteins
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23. Sartori G, Cavazza A, Bertolini F, Longo L, Marchioni A, Costantini M, Barbieri F, Migaldi M, Rossi G: A subset of lung adenocarcinomas and atypical adenomatous hyperplasia-associated foci are genotypically related: an EGFR, HER2, and K-ras mutational analysis. Am J Clin Pathol; 2008 Feb;129(2):202-10
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  • [Title] A subset of lung adenocarcinomas and atypical adenomatous hyperplasia-associated foci are genotypically related: an EGFR, HER2, and K-ras mutational analysis.
  • Atypical adenomatous hyperplasia (AAH) is considered the preinvasive lesion of pulmonary adenocarcinoma, and mutations of EGFR, HER2, and K-ras are involved in the early stage of lung adenocarcinoma carcinogenesis, also predicting clinical response to anti-EGFR small molecule inhibitors.
  • We analyzed 18 cases of primary lung adenocarcinoma with concomitant AAH foci from 13 patients for mutations of EGFR (exons 18-21), HER2 (exons 19-20), and K-ras (exon 2) by direct sequencing polymerase chain reaction.
  • Mutations of EGFR and K-ras genes represent an early event in lung adenocarcinomagenesis, and AAH convincingly seems to be a precursor lesion in a subset of cases of adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Genes, erbB-2. Genes, ras. Hyperplasia / genetics. Lung Neoplasms / genetics. Precancerous Conditions / genetics. Receptor, Epidermal Growth Factor / genetics

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  • [CommentIn] Am J Clin Pathol. 2008 Aug;130(2):315-6; author reply 316 [18697292.001]
  • (PMID = 18208799.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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24. Maeshima AM, Tochigi N, Yoshida A, Asamura H, Tsuta K, Tsuda H: Clinicopathologic analysis of multiple (five or more) atypical adenomatous hyperplasias (AAHs) of the lung: evidence for the AAH-adenocarcinoma sequence. J Thorac Oncol; 2010 Apr;5(4):466-71
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  • [Title] Clinicopathologic analysis of multiple (five or more) atypical adenomatous hyperplasias (AAHs) of the lung: evidence for the AAH-adenocarcinoma sequence.
  • OBJECTIVE: Clarification of the clinicopathologic characteristics of patients with multiple atypical adenomatous hyperplasias (AAHs).
  • MATERIALS AND METHODS: The subjects were 1,639 patients who underwent lobectomy or pneumonectomy for lung tumors.
  • The clinicopathologic features of the AAHs in the lung background and the main tumors were examined with regard to the number and the size of the AAHs, the incidence and histology of adenocarcinomas (ADs), and the outcome.
  • CONCLUSION: Five or more AAHs were seen in the background in 2.0% of lung tumors.
  • [MeSH-major] Adenocarcinoma / pathology. Adenoma / pathology. Carcinoma, Large Cell / pathology. Carcinoma, Squamous Cell / pathology. Lung Neoplasms / pathology
  • [MeSH-minor] Aged. Female. Follow-Up Studies. Humans. Hyperplasia. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Staging. Prognosis. Survival Rate

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  • (PMID = 20357616.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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25. Awaya H, Takeshima Y, Furonaka O, Kohno N, Inai K: Gene amplification and protein expression of EGFR and HER2 by chromogenic in situ hybridisation and immunohistochemistry in atypical adenomatous hyperplasia and adenocarcinoma of the lung. J Clin Pathol; 2005 Oct;58(10):1076-80
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  • [Title] Gene amplification and protein expression of EGFR and HER2 by chromogenic in situ hybridisation and immunohistochemistry in atypical adenomatous hyperplasia and adenocarcinoma of the lung.
  • AIMS: To investigate the importance of gene amplification and EGFR (epidermal growth factor receptor) and HER2 protein expression during the progression of adenocarcinoma of the lung.
  • METHODS: EGFR and HER2 gene amplification was examined in atypical adenomatous hyperplasia (AAH), bronchioloalveolar carcinoma (BAC), and adenocarcinoma with mixed subtypes (MX) by chromogenic in situ hybridisation (CISH), and protein expression was examined by immunohistochemistry using paraffin wax embedded tissues.
  • CONCLUSIONS: EGFR and HER2 gene amplification may be a late event and EGFR and HER2 protein expression may be associated with the development of adenocarcinoma of the lung.
  • [MeSH-major] Adenocarcinoma / genetics. Genes, erbB-2. Lung Neoplasms / genetics. Precancerous Conditions / genetics. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Adenoma / genetics. Adenoma / metabolism. Adenoma / pathology. Adult. Aged. Aged, 80 and over. Chromogenic Compounds. Disease Progression. Female. Humans. Hyperplasia / genetics. Hyperplasia / metabolism. Hyperplasia / pathology. Immunoenzyme Techniques. In Situ Hybridization / methods. Male. Middle Aged. Neoplasm Invasiveness. Receptor, ErbB-2 / metabolism

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  • (PMID = 16189154.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chromogenic Compounds; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2
  • [Other-IDs] NLM/ PMC1770741
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26. 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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27. Hayashi T, Kumasaka T, Mitani K, Yao T, Suda K, Seyama K: Loss of heterozygosity on tuberous sclerosis complex genes in multifocal micronodular pneumocyte hyperplasia. Mod Pathol; 2010 Sep;23(9):1251-60
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  • [Title] Loss of heterozygosity on tuberous sclerosis complex genes in multifocal micronodular pneumocyte hyperplasia.
  • Multifocal micronodular pneumocyte hyperplasia is a rare pulmonary manifestation of tuberous sclerosis complex (TSC) that is a tumor suppressor gene disorder characterized by many hamartomas.
  • Although multifocal micronodular pneumocyte hyperplasia develops locally as self-limited, benign lesions, it is morphologically similar to the preinvasive lesion of pneumocytes that characterize atypical adenomatous hyperplasia or bronchioloalveolar carcinoma.
  • The goal of this study was to determine whether multifocal micronodular pneumocyte hyperplasia is neoplastic.
  • Loss of heterozygosity on TSC genes and immunohistochemistry for mTOR-related proteins (phospho-mTOR, phospho-p70S6K, phospho-S6, and phospho-Akt) were analyzed in 42 lesions: 16 multifocal micronodular pneumocyte hyperplasia (7 patients with TSC, 1 TSC not confirmed), 14 atypical adenomatous hyperplasia, and 12 bronchioloalveolar carcinoma (9 and 12 patients, respectively).
  • The results showed that at least one of two multifocal micronodular pneumocyte hyperplasia lesions from each patient had loss of heterozygosity on TSC1 or TSC2 (15 or 50%) and were frequently immunopositive for phospho-mTOR (88%), phospho-p70S6K (100%), and phospho-S6 (100%) but not phospho-Akt (14%), an upstream regulatory protein of mTOR.
  • Loss of heterozygosity of TSC was found in the preinvasive lesions of pneumocytes, equal to or less than multifocal micronodular pneumocyte hyperplasia.
  • In contrast, phospho-Akt was expressed in the preinvasive lesions of pneumocytes more frequently than multifocal micronodular pneumocyte hyperplasia, but the other mTOR-related proteins were less frequently expressed in the former than in the latter.
  • These outcomes suggest that functional loss of TSCs and consequent hyperphosphorylation of mTOR-related proteins in multifocal micronodular pneumocyte hyperplasia may cause its benign neoplastic proliferation of pneumocytes.
  • [MeSH-major] Lung Diseases / etiology. Lung Diseases / genetics. Pneumocytes / pathology. Tuberous Sclerosis / complications
  • [MeSH-minor] Adult. Female. Humans. Hyperplasia / etiology. Hyperplasia / genetics. Immunohistochemistry. Loss of Heterozygosity. Middle Aged. Polymerase Chain Reaction


28. 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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29. Shintani Y, Ohta M, Iwasaki T, Ikeda N, Tomita E, Nagano T, Kawahara K: A case of micronodular pneumocyte hyperplasia diagnosed through surgical resection. Ann Thorac Cardiovasc Surg; 2010 Aug;16(1):45-7

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  • [Title] A case of micronodular pneumocyte hyperplasia diagnosed through surgical resection.
  • Micronodular pneumocyte hyperplasia (MNPH) is often associated with tuberous sclerosis complex and/or lymphangioleiomyomatosis.
  • A preoperative high-resolution chest computed topographic scan demonstrated a ground-glass opacity 8 mm in diameter that revealed the possibility of atypical adenomatous hyperplasia (AAH) or bronchioloalveolar carcinoma (BAC).
  • Therefore an S3 segmentectomy of the right lung was performed, and the specimens revealed the characteristic histological and immunohistological features of MNPH.
  • [MeSH-minor] Biopsy. Diagnosis, Differential. Female. Humans. Hyperplasia. Immunohistochemistry. Middle Aged. Predictive Value of Tests. Tomography, X-Ray Computed

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  • (PMID = 20190710.001).
  • [ISSN] 2186-1005
  • [Journal-full-title] Annals of thoracic and cardiovascular surgery : official journal of the Association of Thoracic and Cardiovascular Surgeons of Asia
  • [ISO-abbreviation] Ann Thorac Cardiovasc Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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30. Pankiewicz W, Minarowski L, Niklińska W, Naumnik W, Nikliński J, Chyczewski L: Immunohistochemical markers of cancerogenesis in the lung. Folia Histochem Cytobiol; 2007;45(2):65-74
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  • [Title] Immunohistochemical markers of cancerogenesis in the lung.
  • Lung cancer is the leading cause of cancer deaths for people of both sexes worldwide.
  • Early diagnosis of precancer lesions may be of crucial significance to lowering lung cancer mortality.
  • The World Health Organization has defined three preneoplastic lesions of the bronchial epithelium: squamous dysplasia and carcinoma in situ, atypical adenomatous hyperplasia and diffuse idiopathic pulmonary neuroendocrine cell hyperplasia.
  • These lesions are believed to progress to squamous cell carcinoma, adenocarcinoma and carcinoid tumors, respectively.
  • Apart from WHO classification, two other lesions such as bronchiolization and bronchiolar columnar cell dysplasia (BCCD) can be observed and thought to be preneoplastic lesions leading to adenocarcinoma.
  • In this review we summarize the data of morphological and cell cycle related proteins changes in both central and peripheral compartments of lung.

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  • (PMID = 17597018.001).
  • [ISSN] 0239-8508
  • [Journal-full-title] Folia histochemica et cytobiologica
  • [ISO-abbreviation] Folia Histochem. Cytobiol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 67
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31. Wistuba II, Gazdar AF: Lung cancer preneoplasia. Annu Rev Pathol; 2006;1:331-48
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  • [Title] Lung cancer preneoplasia.
  • From histological and biological perspectives, lung cancer is a complex neoplasm.
  • Although the sequential preneoplastic changes have been defined for centrally arising squamous carcinomas of the lung, they have been poorly documented for the other major forms of lung cancers, including small cell lung carcinoma and adenocarcinomas.
  • There are three main morphologic forms of preneoplastic lesions recognized in the lung: squamous dysplasias, atypical adenomatous hyperplasia, and diffuse idiopathic pulmonary neuroendocrine cell hyperplasia.
  • However, these lesions account for the development of only a subset of lung cancers.
  • Several studies have provided information regarding the molecular characterization of lung preneoplastic changes, especially for squamous cell carcinoma.
  • Two different molecular pathways have been detected in lung adenocarcinoma pathogenesis: smoking-associated activation of RAS signaling, and nonsmoking-associated activation of EGFR signaling; the latter is detected in histologically normal respiratory epithelium.
  • [MeSH-major] Adenocarcinoma / pathology. Lung Neoplasms / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Adenoma / pathology. Bronchi / pathology. Carcinoid Tumor / genetics. Carcinoid Tumor / pathology. Carcinoma in Situ / genetics. Carcinoma in Situ / pathology. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / pathology. Gene Expression Regulation, Neoplastic. Genes, erbB-1. Genetic Predisposition to Disease. Humans. Hyperplasia. Mutation. Signal Transduction. Smoking / adverse effects

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  • (PMID = 18039118.001).
  • [ISSN] 1553-4006
  • [Journal-full-title] Annual review of pathology
  • [ISO-abbreviation] Annu Rev Pathol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50CA70907; United States / NCI NIH HHS / CA / U01CA8497102
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] United States
  • [Number-of-references] 95
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32. Mascaux C: [Etiology, epidemiology, biology. Lung carcinogenesis]. Rev Mal Respir; 2008 Oct;25(8 Pt 2):3S32-9
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  • [Title] [Etiology, epidemiology, biology. Lung carcinogenesis].
  • Lung cancer is a complex disease involving various oncogenic pathways.
  • Pre-invasive stages exist for different forms of lung cancer and some of them are recognized as being preneoplastic: dysplasias and in situ carcinoma, atypical adenomatous hyperplasia and diffuse idiopathic pulmonary neuroendocrine cell hyperplasia are supposed to be precursors of squamous cell carcinomas, adenocarcinomas and carcinoid tumors, respectively.
  • The sequence of histological modifications of bronchial mucosa preceding the development of a squamous cell carcinoma are well documented while those preceding other histological types are less known.
  • It also discusses arguments for their preneoplastic nature, their evolution and risk of progression risk, molecular abnormalities involved in lung carcinogenesis and clinical relevance of these lesions.
  • [MeSH-major] Lung Neoplasms / pathology. Precancerous Conditions
  • [MeSH-minor] Humans. Hyperplasia. Lung / pathology

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  • (PMID = 18971824.001).
  • [ISSN] 0761-8425
  • [Journal-full-title] Revue des maladies respiratoires
  • [ISO-abbreviation] Rev Mal Respir
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
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33. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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34. Chiosea S, Jelezcova E, Chandran U, Luo J, Mantha G, Sobol RW, Dacic S: Overexpression of Dicer in precursor lesions of lung adenocarcinoma. Cancer Res; 2007 Mar 1;67(5):2345-50
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  • [Title] Overexpression of Dicer in precursor lesions of lung adenocarcinoma.
  • Differential microRNA (miR) expression is described in non-small cell lung carcinoma. miR biogenesis requires a set of proteins collectively referred to as the miR machinery.
  • In the proposed multistep carcinogenesis model, peripheral adenocarcinoma of the lung develops from noninvasive precursor lesions known as atypical adenomatous hyperplasia (AAH) and bronchioloalveolar carcinoma (BAC).
  • Expanded immunohistochemical and Western blot analysis showed higher Dicer level in squamous cell carcinoma (SCC) of the lung when compared with adenocarcinoma.
  • Other proteins of the RNA-induced silencing complex (RISC; SND1, PACT, and FXR1) were also present at higher levels in a SCC cell line when compared with an adenocarcinoma cell line.
  • In conclusion, the stoichiometry of miR machinery and RISC depends on histologic subtype of lung carcinoma, varies along the AAH-BAC-adenocarcinoma sequence, and might explain the observed abnormal miR profile in lung cancer.
  • The status of the endogenous miR machinery in various histologic subtypes and stages of lung cancer may help to predict the toxicity of and susceptibility to future RNA interference-based therapy.

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  • (PMID = 17332367.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCATS NIH HHS / TR / UL1 TR000005; United States / NCI NIH HHS / CA / R01 CA 098249
  • [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 / FXR1 protein, human; 0 / PRKRA protein, human; 0 / RNA-Binding Proteins; EC 3.1.- / Endoribonucleases; EC 3.1.26.3 / DICER1 protein, human; EC 3.1.26.3 / Ribonuclease III; EC 3.6.4.13 / DEAD-box RNA Helicases
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35. 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 / diagnostic imaging. Adenoma / pathology. Aged. Female. Humans. Hyperplasia / diagnostic imaging. Hyperplasia / pathology. Precancerous Conditions / diagnostic imaging. Precancerous Conditions / pathology. Tomography, X-Ray Computed

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  • [Cites] Lung Cancer. 2004 Apr;44(1):61-8 [15013584.001]
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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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36. Seki M, Akasaka Y: Multiple lung adenocarcinomas and AAH treated by surgical resection. Lung Cancer; 2007 Feb;55(2):237-40
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  • [Title] Multiple lung adenocarcinomas and AAH treated by surgical resection.
  • Atypical adenomatous hyperplasia (AAH) is often found in the lungs of patients with multiple primary lung adenocarcinoma; however, treatment for such patients has not been clearly defined.
  • This report presents a case of multiple primary lung adenocarcinoma with multiple AAH treated by surgery.
  • Thirteen tumorous lesions were resected; 10 lesions were diagnosed as primary lung adenocarcinoma and the others as AAH.
  • The clinical course indicates that surgery can be a treatment strategy for synchronous or metachronous lung carcinoma with AAH.
  • [MeSH-major] Adenocarcinoma / surgery. Lung Neoplasms / surgery
  • [MeSH-minor] Humans. Hyperplasia / pathology. Hyperplasia / surgery. Male. Middle Aged. Neoplasms, Second Primary / pathology. Neoplasms, Second Primary / surgery. Tomography, X-Ray Computed

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  • (PMID = 17118487.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Ireland
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37. 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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38. 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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39. 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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40. Shimada A, Kano J, Ishiyama T, Okubo C, Iijima T, Morishita Y, Minami Y, Inadome Y, Shu Y, Sugita S, Takeuchi T, Noguchi M: Establishment of an immortalized cell line from a precancerous lesion of lung adenocarcinoma, and genes highly expressed in the early stages of lung adenocarcinoma development. Cancer Sci; 2005 Oct;96(10):668-75
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  • [Title] Establishment of an immortalized cell line from a precancerous lesion of lung adenocarcinoma, and genes highly expressed in the early stages of lung adenocarcinoma development.
  • Atypical adenomatous hyperplasia (AAH) is classified as a precancerous lesion of lung adenocarcinoma.
  • We established an immortalized AAH cell line (PL16T) and a human non-neoplastic bronchial epithelial cell line (PL16B) from the same patient by transfection with the gene for SV40 large T antigen.
  • In normal lung tissue, both TACSTD2 and S100A2 were expressed at very low levels, but seven and five of 14 AAH were positive for TACSTD2 and S100A2, respectively.
  • The frequency of TACSTD2 positivity was increased in 16 of 22 bronchioloalveolar carcinomas (BAC) and adenocarcinoma with mixed subtype with BAC component (mixed BAC).
  • The abnormal transcription of TACSTD2 and S100A2 are thought to be unique molecular markers of the preinvasive stage of lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Antigens, Neoplasm / biosynthesis. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / pathology. Cell Adhesion Molecules / biosynthesis. Chemotactic Factors / biosynthesis. Lung Neoplasms / genetics. Lung Neoplasms / pathology. Precancerous Conditions / genetics. Precancerous Conditions / pathology. S100 Proteins / biosynthesis
  • [MeSH-minor] Female. Gene Expression Profiling. Humans. Hyperplasia. Lung / pathology. Middle Aged. Neoplasm Staging. Nucleic Acid Hybridization. Tumor Cells, Cultured

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  • (PMID = 16232198.001).
  • [ISSN] 1347-9032
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cell Adhesion Molecules; 0 / Chemotactic Factors; 0 / S100 Proteins; 0 / S100A2 protein, human; 0 / TACSTD2 protein, human
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41. Orita H, Coulter J, Tully E, Kuhajda FP, Gabrielson E: Inhibiting fatty acid synthase for chemoprevention of chemically induced lung tumors. Clin Cancer Res; 2008 Apr 15;14(8):2458-64
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  • [Title] Inhibiting fatty acid synthase for chemoprevention of chemically induced lung tumors.
  • PURPOSE: Fatty acid synthase (FAS) is overexpressed in lung cancer, and we have investigated the potential use of FAS inhibitors for chemoprevention of lung cancer.
  • EXPERIMENTAL DESIGN: Expression of FAS was evaluated in preinvasive human lung lesions (bronchial squamous dysplasia and atypical adenomatous hyperplasia) and in murine models of lung tumorigenesis [4-(methylnitrosamino)-I-(3-pyridyl)-1-butanone-induced and urethane-induced lung tumors in A/J mice].
  • RESULTS: Immunohistochemical studies show that human bronchial dysplasia and atypical adenomatous hyperplasia express high levels of FAS compared with normal lung tissues, suggesting that FAS might be a target for intervention in lung carcinogenesis.
  • FAS is also expressed at high levels in chemically induced murine lung tumors, and the numbers and sizes of those murine tumors are significantly reduced by treating carcinogen-exposed mice with pharmacologic inhibitors of FAS, C75 and C93.
  • CONCLUSIONS: We conclude that increased levels of FAS are common in human preinvasive neoplasia of the lung.
  • Based on studies in mouse models, it seems that inhibiting FAS is an effective strategy in preventing and retarding growth of lung tumors that have high expression of this enzyme.
  • [MeSH-major] Anticarcinogenic Agents / therapeutic use. Enzyme Inhibitors / therapeutic use. Fatty Acid Synthases / antagonists & inhibitors. Lung Neoplasms / prevention & control


42. 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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43. Akyürek N, Memiş L, Ekinci O, Köktürk N, Oztürk C: Survivin expression in pre-invasive lesions and non-small cell lung carcinoma. Virchows Arch; 2006 Aug;449(2):164-70
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  • [Title] Survivin expression in pre-invasive lesions and non-small cell lung carcinoma.
  • Survivin is an inhibitor of apoptosis protein, which is overexpressed in many carcinomas, including lung carcinoma.
  • The aim of this immunohistochemical study was to investigate the role of survivin in the early steps of lung carcinogenesis and non-small cell lung carcinomas (NSCLC), and its relationship with expression of p53 protein, a tumor suppressor gene involved in cell cycle control.
  • In the normal bronchial epithelium, low-grade atypical adenomatous hyperplasia (AAH) and non-neoplastic lung parenchyma adjacent to tumor, survivin was found completely negative.
  • In conclusion, survivin expression might be an early step in lung carcinogenesis.
  • Survivin expression might also be used as a prognostic indicator predicting the worse outcome in NSCLC, and might be a novel target for the treatment of patients with preinvasive lesions of lung and NSCLC.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / chemistry. Lung Neoplasms / chemistry. Microtubule-Associated Proteins / analysis. Neoplasm Proteins / analysis
  • [MeSH-minor] Adult. Aged. Female. Humans. Hyperplasia. Immunohistochemistry. Inhibitor of Apoptosis Proteins. Lung / chemistry. Lung / pathology. Male. Middle Aged. Prognosis

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  • (PMID = 16810543.001).
  • [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 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins
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44. Licchesi JD, Westra WH, Hooker CM, Machida EO, Baylin SB, Herman JG: Epigenetic alteration of Wnt pathway antagonists in progressive glandular neoplasia of the lung. Carcinogenesis; 2008 May;29(5):895-904
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  • [Title] Epigenetic alteration of Wnt pathway antagonists in progressive glandular neoplasia of the lung.
  • BACKGROUND: Atypical adenomatous hyperplasia (AAH) is now recognized as a precursor lesion from which lung adenocarcinomas arise and thus represents an ideal target for studying the early genetic and epigenetic alterations associated with lung tumorigenesis such as alterations of the Wnt pathway.
  • METHODS: We assessed the level of Wnt signaling activity in lung cancer cell lines by determining the level of active beta-catenin and determined the level of expression of Wnt antagonists APC, DKK1, DKK3, LKB1, SFRP1, 2, 4, 5, WIF1 and RUNX3 using reverse transcription-polymerase chain reaction.
  • Using multiplex nested methylation-specific polymerase chain reaction, we analyzed promoter region methylation of these genes in resected lung tissue in the histopathologic sequence of glandular neoplasia (normal lung parenchyma, low-grade and high-grade AAH, adenocarcinoma).
  • RESULTS: The majority of non-small cell lung cancer cell lines (11 of 16, 69%) have evidence of active Wnt signaling and silencing of Wnt antagonists correlated with promoter hypermethylation.
  • Promoter region methylation of Wnt antagonists was common in primary lung adenocarcinoma and there was a significant increase in the frequency of methylation for Wnt antagonist genes and the number of genes methylated with each stage of tumorigenesis (test for rend P <or= 0.01).
  • CONCLUSION: These results show that gene silencing of Wnt antagonists by promoter hypermethylation occurs during the earliest stages of glandular neoplasia of the lung and accumulates with progression toward malignancy.

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  • (PMID = 18308762.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA058184
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 3 Subunit; 0 / DMAP1 protein, human; 0 / DNA, Neoplasm; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; 0 / RNA, Neoplasm; 0 / Repressor Proteins; 0 / Wnt Proteins; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ PMC3312609
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45. 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

  • Hazardous Substances Data Bank. 4-(N-Nitrosomethylamino)-1-(3-pyridyl)-1-butanone .
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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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46. 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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47. Ishihara T, Takeuchi T, Nishimori I, Adachi Y, Minakuchi T, Fujita J, Sonobe H, Ohtsuki Y, Onishi S: Carbonic anhydrase-related protein VIII increases invasiveness of non-small cell lung adenocarcinoma. Virchows Arch; 2006 Jun;448(6):830-7
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  • [Title] Carbonic anhydrase-related protein VIII increases invasiveness of non-small cell lung adenocarcinoma.
  • Carbonic anhydrase-related protein VIII (CA-RP VIII) is believed to be an oncofetal antigen and is overexpressed in colorectal and non-small cell lung cancer.
  • However, the pathobiological properties of CA-RP VIII in lung cancer remain unclear.
  • In the present study, we examined ultrastructural changes caused by exogenous CA-RP VIII expression in a well-differentiated lung adenocarcinoma cell line, PC-9.
  • We subsequently examined CA-RP VIII expression in atypical adenomatous hyperplasia and early-stage lung adenocarcinoma (Stage Ia).
  • Significant expression of CA-RP VIII was observed in invasive lung adenocarcinoma but not in noninvasive adenocarcinoma.
  • Interestingly, CA-RP VIII was strongly expressed in signet-ring cell cancer and invasive mucinous adenocarcinoma components.
  • The present findings suggest that CA-RP VIII expression in lung adenocarcinoma is related to cancer cell invasion.
  • [MeSH-major] Carbonic Anhydrases / genetics. Carcinoma, Non-Small-Cell Lung / ultrastructure. Gene Expression Regulation, Neoplastic. Lung Neoplasms / ultrastructure. Nerve Tissue Proteins / genetics
  • [MeSH-minor] Adenoma / genetics. Adenoma / ultrastructure. Biomarkers, Tumor. Cell Line, Tumor. Cell Movement. Gene Expression. Humans. Hyperplasia. Immunohistochemistry. Microscopy, Electron, Transmission. Mucins / metabolism. Neoplasm Invasiveness. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction. Vacuoles / ultrastructure

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  • (PMID = 16609906.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CA8 protein, human; 0 / Car8 protein, mouse; 0 / Mucins; 0 / Nerve Tissue Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 4.2.1.1 / Carbonic Anhydrases
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48. Sano T, Kitayama Y, Igarashi H, Suzuki M, Tanioka F, Chida K, Okudela K, Sugimura H: Chromosomal numerical abnormalities in early stage lung adenocarcinoma. Pathol Int; 2006 Mar;56(3):117-25
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  • [Title] Chromosomal numerical abnormalities in early stage lung adenocarcinoma.
  • Recent radiological scrutiny has enabled the identification of small peripheral lesions in the lung.
  • A chromosome-wide investigation encompassing almost all the chromosomal centromeres was performed using modified fluorescence in situ hybridization on the archived pathological samples of 16 atypical adenomatous hyperplasia (AAH) and 30 lung adenocarcioma (AdCa) specimens including those smaller than 1 cm in size.
  • The prevalence of the gain differed significantly between AAH and bronchioloalveolar carcinoma (BAC) </= 1 cm, but not between BAC < 1 cm and well-differentiated AdCa > 1 cm.
  • It is proposed that the CNA is a distinct phenomenon occurring in the early or premalignant stage of lung AdCa, and that the CNA itself may not be a sequel in the carcinogenetic process, but a driving factor in carcinogenesis.
  • [MeSH-major] Adenocarcinoma / genetics. Chromosome Aberrations. Lung Neoplasms / genetics

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  • (PMID = 16497244.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
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49. Shu Y, Iijima T, Sun W, Kano J, Ishiyama T, Okubo C, Anami Y, Tanaka R, Fukai S, Noguchi M: The ACIN1 gene is hypermethylated in early stage lung adenocarcinoma. J Thorac Oncol; 2006 Feb;1(2):160-7
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  • [Title] The ACIN1 gene is hypermethylated in early stage lung adenocarcinoma.
  • We hypothesized that characteristic aberrant hypermethylation of CpG islands of certain genes may exist in the early stages of lung adenocarcinoma and that such alterations may be useful in the detection and treatment of early lung adenocarcinoma.
  • METHODS: A pair of immortalized cell lines originating from atypical adenomatous hyperplasia (PL16T) and from the resected end of the bronchus of the same patient (PL16B) was searched for aberrantly and differentially hypermethylated DNA fragments by a combination of the methylated CpG island amplification and suppression subtractive hybridization methods.
  • A higher frequency of hypermethylation at a locus at the 5': end of the DNA fragment isolated from the ACIN1 gene was found in small-sized adenocarcinoma (2 cm or less) (30/37, 81%) compared with normal lung tissue (9/37, 24%, p < 0.05).
  • Interestingly, hypermethylation of ACIN1 was detected relatively frequently in the normal counterpart of adenocarcinoma without bronchioloalveolar carcinoma (BAC) component (7/16, 44%), but was rare in the normal counterpart of adenocarcinoma with BAC component (2/21, 10%, P < 0.05).
  • CONCLUSIONS: We found hypermethylation of the ACIN1 gene in early stage lung adenocarcinoma.
  • The role of methylation status in the development and malignant transformation of lung adenocarcinoma requires clarification.
  • [MeSH-major] Adenocarcinoma / genetics. Biomarkers, Tumor / genetics. DNA, Neoplasm / genetics. Lung Neoplasms / genetics. Nuclear Proteins / genetics
  • [MeSH-minor] Cell Line, Tumor. Disease Progression. Female. Follow-Up Studies. Humans. Male. Methylation. Middle Aged. Neoplasm Staging. Prognosis. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17409846.001).
  • [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 / ACIN1 protein, human; 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 0 / Nuclear Proteins
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50. Hanaoka T, Sone S, Takayama F, Hayano T, Yamaguchi S, Okada M: Presence of local pleural adhesion in CT screening-detected small nodule in the lung periphery suggests noncancerous, inflammatory nature of the lesion. Clin Imaging; 2007 Nov-Dec;31(6):385-9
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  • [Title] Presence of local pleural adhesion in CT screening-detected small nodule in the lung periphery suggests noncancerous, inflammatory nature of the lesion.
  • PURPOSE: Differential diagnosis of small nodules in the lung periphery detected by low-dose chest CT screening is important before surgery.
  • MATERIALS AND METHODS: This study is based on 106 patients (46 men and 60 women, median age: 61.5 years) with 123 CT screening-detected and histologically confirmed nodules smaller than 30 mm in the lung periphery identified between 2002 and 2005 at Azumi General Hospital, Japan.
  • Lesions were classified into three groups according to histological findings: adenocarcinoma, atypical adenomatous hyperplasia (AAH) and inflammatory focal lesions.
  • We examined the visceral pleura during surgery at a location close to lung nodules.
  • RESULTS: The median diameter of resected lung nodules on high-resolution CT (HRCT) was 9.0 mm.
  • Histopathological diagnosis was lung cancer in 69, AAH in 21, other noninflammatory tumours in 6 and inflammatory lesions in 27.
  • [MeSH-major] Adenocarcinoma / radiography. Lung Neoplasms / radiography. Pleural Diseases / radiography. Tissue Adhesions / radiography. Tomography, X-Ray Computed
  • [MeSH-minor] Adult. Aged. Chi-Square Distribution. Diagnosis, Differential. Female. Humans. Hyperplasia. Inflammation / pathology. Inflammation / radiography. Male. Middle Aged


51. 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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52. Okudela K, Woo T, Kitamura H: KRAS gene mutations in lung cancer: particulars established and issues unresolved. Pathol Int; 2010 Oct;60(10):651-60
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  • [Title] KRAS gene mutations in lung cancer: particulars established and issues unresolved.
  • Lung cancer, like other cancers, is considered to develop through the accumulation of genetic alterations.
  • Mutation of the KRAS gene is one of the most important events in carcinogenesis of the lung.
  • In lung cancers, the mutations concentrate at codon 12 and mostly affect adenocarcinomas (ADCs).
  • They also affect atypical adenomatous hyperplasia, the precursor of ADCs.
  • In this review, particulars that have been established are introduced, and important issues remaining to be resolved are discussed, with special reference to carcinogenesis of the lung.
  • [MeSH-major] Carcinoma / genetics. Lung Neoplasms / genetics. Proto-Oncogene Proteins / genetics. ras Proteins / genetics

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  • [Copyright] © 2010 The Authors. Pathology International © 2010 Japanese Society of Pathology and Blackwell Publishing Asia Pty Ltd.
  • [ErratumIn] Pathol Int. 2010 Dec;60(12):798
  • (PMID = 20846262.001).
  • [ISSN] 1440-1827
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 3.6.5.2 / ras Proteins
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53. Ohta Y, Shimizu Y, Kobayashi T, Matsui O, Minato H, Matsumoto I, Watanabe G: Pathologic and biological assessment of lung tumors showing ground-glass opacity. Ann Thorac Surg; 2006 Apr;81(4):1194-7
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  • [Title] Pathologic and biological assessment of lung tumors showing ground-glass opacity.
  • BACKGROUND: We evaluated the pathologic and biological aspects of lung tumors 3.0 cm or less in diameter with the appearance of ground-glass opacity (GGO).
  • METHODS: Of 988 patients with non-small cell lung cancer who underwent operations at our institute between January 1994 and December 2004, 87 resected lung tumor specimens that showed GGO appearance on helical computed tomography were obtained from 81 patients.
  • Although atypical adenomatous hyperplasia and localized bronchioloalveolar cell carcinoma of Noguchi's A and B were the predominant pathologic subtypes and nm23 negativity was rare in the pure GGO group, a high score for expression of MIB1 was often found in pure GGO tumors even though the tumors were less than 10 mm in diameter.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / pathology. Carcinoma, Non-Small-Cell Lung / radiography. Lung Neoplasms / pathology. Lung Neoplasms / radiography. Tomography, Spiral Computed

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  • [CommentIn] Ann Thorac Surg. 2006 Apr;81(4):1197-8 [16564242.001]
  • (PMID = 16564241.001).
  • [ISSN] 1552-6259
  • [Journal-full-title] The Annals of thoracic surgery
  • [ISO-abbreviation] Ann. Thorac. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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54. 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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55. Ikeda K, Nomori H, Mori T, Sasaki J, Kobayashi T: Novel germline mutation: EGFR V843I in patient with multiple lung adenocarcinomas and family members with lung cancer. Ann Thorac Surg; 2008 Apr;85(4):1430-2
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  • [Title] Novel germline mutation: EGFR V843I in patient with multiple lung adenocarcinomas and family members with lung cancer.
  • A novel germline transmission of the epidermal growth factor receptor (EGFR) mutation V843I in a family with multiple members with lung cancer is reported.
  • These observations suggest that the germline EGFR V843I mutation might have altered EGFR signaling in the multicentric development of adenocarcinoma, bronchoalveolar carcinoma, and atypical adenomatous hyperplasia and also might have had a role in the development of lung cancer in multiple members of her family.
  • [MeSH-major] Adenocarcinoma / genetics. Germ-Line Mutation. Lung Neoplasms / genetics. Neoplasm Invasiveness / pathology. Neoplasms, Multiple Primary / genetics. Receptor, Epidermal Growth Factor / genetics

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  • (PMID = 18355544.001).
  • [ISSN] 1552-6259
  • [Journal-full-title] The Annals of thoracic surgery
  • [ISO-abbreviation] Ann. Thorac. Surg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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56. Brannan JM, Sen B, Saigal B, Prudkin L, Behrens C, Solis L, Dong W, Bekele BN, Wistuba I, Johnson FM: EphA2 in the early pathogenesis and progression of non-small cell lung cancer. Cancer Prev Res (Phila); 2009 Dec;2(12):1039-49
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  • [Title] EphA2 in the early pathogenesis and progression of non-small cell lung cancer.
  • Overexpression of the receptor tyrosine kinase EphA2 occurs in non-small cell lung cancer (NSCLC) and a number of other human cancers.
  • To determine if EphA2 can promote NSCLC progression, we examined the relationship of EphA2 with proliferation and migration in cell lines and with metastases in patient tumors.
  • Knockdown of EphA2 in NSCLC cell lines decreased proliferation (colony size) by 20% to 70% in four of five cell lines (P < 0.
  • 04) and cell migration by 7% to 75% in five of six cell lines (P < 0. 03).
  • We also examined EphA2 expression in the putative premalignant lung lesion, atypical adenomatous hyperplasia, and the noninvasive bronchioloalveolar component of adenocarcinoma because K-Ras mutations occur in atypical adenomatous hyperplasia and are common in lung adenocarcinomas.
  • Both preinvasive lesion types expressed EphA2, showing its expression in the early pathogenesis of lung adenocarcinoma.


57. Flieder DB, Vazquez M, Carter D, Brambilla E, Gazdar A, Noguchi M, Travis WD, Kramer A, Yankelevitz DF, Henschke CI: Pathologic findings of lung tumors diagnosed on baseline CT screening. Am J Surg Pathol; 2006 May;30(5):606-13
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  • [Title] Pathologic findings of lung tumors diagnosed on baseline CT screening.
  • Sixty-five people had a resection of their baseline screen-diagnosed lung cancers in the Early Lung Cancer Action Program.
  • Eighteen cases were submitted by local pathologists as Bronchioloalveolar carcinomas but were found to be invasive adenocarcinomas according to the World Health Organization classification by the Pathology Review Panel.
  • Eighty-three percent (76/92) of the carcinomas invaded the stroma with destruction of normal lung, and 21% (19/92) also showed either pleural or angiolymphatic invasion, even though 88% (57/65) of the carcinomas were free of lymph node metastases.
  • Histopathologic distinctions among atypical adenomatous hyperplasia, bronchioloalveolar carcinomas, and invasive adenocarcinoma are described in detail.
  • [MeSH-major] Carcinoma / classification. Carcinoma / pathology. Lung Neoplasms / classification. Lung Neoplasms / pathology. Mass Screening. Tomography, X-Ray Computed

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  • (PMID = 16699315.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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58. Meng YH, Yu JY, Lu YL, Zhu YJ, Zhang JQ, Ning HY, Hu M, Liu X, Kang XL, Duan W: [Expression of PAR-1 in human lung carcinoma and its relationship with tumor metastatic potential]. Zhonghua Bing Li Xue Za Zhi; 2006 Jan;35(1):24-8
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  • [Title] [Expression of PAR-1 in human lung carcinoma and its relationship with tumor metastatic potential].
  • OBJECTIVE: To explore the correlation between expression of PAR-1 and metastasis of human lung carcinoma.
  • METHODS: Expression levels of PAR-1 were examined in surgically resected lung carcinoma specimens and corresponding lymph nodes by RT-PCR and immunohistochemistry, combined with morphometric methodology and clinicopathologic profiles.
  • RESULTS: Strong PAR-1 staining was detected in the periphery of carcinoma nests, adenocarcinomatous emboli, foci of atypical adenomatous hyperplasia adjacent to the adenocarcinoma and atypical proliferation of duct epithelium of bronchial mucous glands.
  • Morphometric study demonstrated that there were significant differences of PAR-1 protein expression levels between tumors with metastatic and those without, primary and metastatic carcinomas, primary carcinomas and benign lung tissues adjacent to the carcinoma.
  • CONCLUSION: PAR-1 expression may play an important role in determining the malignant phenotypes of lung cancers and significantly contribute to their initiation, progression and metastasis.
  • [MeSH-major] Adenocarcinoma / metabolism. Carcinoma, Squamous Cell / metabolism. Lung Neoplasms / metabolism. Receptor, PAR-1 / biosynthesis

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  • (PMID = 16608645.001).
  • [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
  • [Publication-country] China
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptor, PAR-1
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59. 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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60. 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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61. 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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62. 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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63. Al-Sarraf N, Aziz R, Doddakula K, Gately K, Wilson L, McGovern E, Young V: Factors causing inaccurate staging of mediastinal nodal involvement in non-small cell lung cancer patients staged by positron emission tomography. Interact Cardiovasc Thorac Surg; 2007 Jun;6(3):350-3
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  • [Title] Factors causing inaccurate staging of mediastinal nodal involvement in non-small cell lung cancer patients staged by positron emission tomography.
  • Despite documented superiority of positron emission tomography over other investigative modalities in the preoperative staging of non-small cell lung cancer, a proportion of patients will have an inaccurate staging of their mediastinal nodes.
  • A total of 100 consecutive patients with histologically proven non-small cell lung cancer underwent staging with PET-CT prior to lung resection.
  • In multivariate analysis, we have identified the following as independent factors in causing inaccurate staging of mediastinal lymph nodes: rheumatoid arthritis, non-insulin dependent diabetes, history of tuberculosis, presence of atypical adenomatous hyperplasia and pneumonia (P<0.05).
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / pathology. Carcinoma, Non-Small-Cell Lung / radionuclide imaging. Lung Neoplasms / pathology. Lung Neoplasms / radionuclide imaging. Lymphatic Metastasis / radionuclide imaging. Tomography, Emission-Computed

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  • (PMID = 17669863.001).
  • [ISSN] 1569-9285
  • [Journal-full-title] Interactive cardiovascular and thoracic surgery
  • [ISO-abbreviation] Interact Cardiovasc Thorac Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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64. 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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65. Ohashi K, Takigawa N, Osawa M, Ichihara E, Takeda H, Kubo T, Hirano S, Yoshino T, Takata M, Tanimoto M, Kiura K: Chemopreventive effects of gefitinib on nonsmoking-related lung tumorigenesis in activating epidermal growth factor receptor transgenic mice. Cancer Res; 2009 Sep 1;69(17):7088-95
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  • [Title] Chemopreventive effects of gefitinib on nonsmoking-related lung tumorigenesis in activating epidermal growth factor receptor transgenic mice.
  • Twenty-five percent of all lung cancer cases are not attributable to smoking.
  • Epidermal growth factor receptor (EGFR) mutations, which are involved in approximately 50% of nonsmoker lung cancer, are positively correlated with responsiveness to gefitinib, and inversely correlated with smoking history.
  • Activating EGFR mutations play a critical role in the carcinogenesis of nonsmoking-related lung cancer.
  • To investigate the chemopreventive effects of gefitinib on nonsmoking-related lung cancer, we generated transgenic mice expressing EGFR L858R in type II pneumocytes constitutively using the surfactant protein-C promoter.
  • The transgenic mice invariably developed atypical adenomatous hyperplasia at age 4 weeks and multifocal adenocarcinoma of varying sizes at age 7 weeks.
  • The numbers of lung tumors in the control and gefitinib-treated groups were 1.75, 5.8, 10.2, and 0 (P < 0.05), respectively.
  • These results suggest the utility of molecular targeted chemoprevention against nonsmoking-related lung cancer.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / prevention & control. Antineoplastic Agents / pharmacology. Disease Models, Animal. Lung Neoplasms / genetics. Lung Neoplasms / prevention & control. Quinazolines / pharmacology. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Animals. Cell Transformation, Neoplastic / drug effects. Gene Expression Regulation, Neoplastic. Genes, erbB-2. Humans. Mice. Mice, Transgenic. Mutation. Phosphorylation. Promoter Regions, Genetic. Pulmonary Surfactant-Associated Protein C. Receptor, ErbB-3 / genetics. Smoking


66. 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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67. 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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68. Novello S, Fava C, Borasio P, Dogliotti L, Cortese G, Crida B, Selvaggi G, Lausi P, Brizzi MP, Sperone P, Cardinale L, Ferraris F, Perotto F, Priola A, Scagliotti GV: Three-year findings of an early lung cancer detection feasibility study with low-dose spiral computed tomography in heavy smokers. Ann Oncol; 2005 Oct;16(10):1662-6
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  • [Title] Three-year findings of an early lung cancer detection feasibility study with low-dose spiral computed tomography in heavy smokers.
  • BACKGROUND: Low-dose spiral computed tomography (sCT) showed a four-fold increase in the detection rate in high-risk subjects and a higher percentage of stage I lung cancer in comparison with chest X-ray.
  • However, there is a considerable discrepancy among studies in the percentage of lung nodules, overall lung cancer and stage I detection rate.
  • At baseline, nodules >or=5 mm were detected in 114 (22%) undergoing sCT; the size of lung nodules ranged from 5 to 9.9 mm in 81.5% of the cases.
  • Five (1%) cases of lung cancer were detected.
  • In two additional cases a pathological diagnosis of atypical adenomatous hyperplasia was made.
  • Three new cases of lung cancer were detected in the second and third year of the study.
  • CONCLUSIONS: Despite some promising data, convincing evidence from ongoing randomized trials is needed to support the routine use of sCT as a recommended tool for screening of lung cancer.

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  • (PMID = 16006584.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
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69. Kim Y, Liu XS, Liu C, Smith DE, Russell RM, Wang XD: Induction of pulmonary neoplasia in the smoke-exposed ferret by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK): a model for human lung cancer. Cancer Lett; 2006 Mar 28;234(2):209-19
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  • [Title] Induction of pulmonary neoplasia in the smoke-exposed ferret by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK): a model for human lung cancer.
  • Research into dietary chemoprevention against lung carcinogenesis has been limited by the lack of appropriate animal models that closely mimic smoking-related human lung cancer.
  • Ferrets (Mustela putorius furo) have been used to study the biologic activities of carotenoids against smoke-induced lung lesions, but this model has yet to be thoroughly established and validated.
  • To determine the appropriateness of the ferret as a model for human lung cancer, we have performed a 6-month in vivo study in ferrets exposed to both tobacco smoke and a carcinogen (4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone, NNK) found in cigarette smoke.
  • Results showed that six out 12 ferrets exposed to both NNK injection and cigarette smoke developed grossly identifiable lung tumors whereas none of nine ferrets from the sham treatment group developed any lung lesions.
  • The histopathological types of these tumors (squamous cell carcinoma, adenosquamous carcinoma and adenocarcinoma) in ferret lungs are very similar to those in humans.
  • In addition, 10 out of 12 ferrets exposed to both NNK and cigarette smoke developed preneoplastic lesions (squamous metaplasia, dysplasia, and atypical adenomatous hyperplasia) with complex growth patterns whereas the sham group did not show any of these lesions.
  • In summary, the development of both preneoplastic lesions and gross lung tumors in ferrets provides an excellent and unique model for studying lung cancer chemoprevention with agents such as carotenoids, and for studying the molecular mechanism of carcinogenesis in the earlier stages of smoke-related lung cancer.
  • [MeSH-major] Carcinogens / toxicity. Disease Models, Animal. Ferrets. Lung Neoplasms / etiology. Nitrosamines / toxicity. Smoking / adverse effects
  • [MeSH-minor] Adenocarcinoma / etiology. Adenocarcinoma / pathology. Animals. Carcinoma, Squamous Cell / etiology. Carcinoma, Squamous Cell / pathology. Humans. Immunohistochemistry. Male. Precancerous Conditions / etiology. Precancerous Conditions / pathology

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  • (PMID = 15894421.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / T32 DK062032
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Nitrosamines; 64091-91-4 / 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone
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70. 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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71. Shen J, Behrens C, Wistuba II, Feng L, Lee JJ, Hong WK, Lotan R: Identification and validation of differences in protein levels in normal, premalignant, and malignant lung cells and tissues using high-throughput Western Array and immunohistochemistry. Cancer Res; 2006 Dec 1;66(23):11194-206
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  • [Title] Identification and validation of differences in protein levels in normal, premalignant, and malignant lung cells and tissues using high-throughput Western Array and immunohistochemistry.
  • The identification of proteins, which exhibit different levels in normal, premalignant, and malignant lung cells, could improve early diagnosis and intervention.
  • These proteins are involved in DNA synthesis and repair, cell cycle regulation, RNA transcription and degradation, translation, differentiation, angiogenesis, apoptosis, cell adhesion, cytoskeleton and cell motility, and the phosphatidylinositol 3-kinase signaling pathway.
  • Conventional Western blotting using lysates of normal, immortalized, transformed, and tumorigenic HBEs and non-small cell lung cancer cell lines confirmed some of these changes.
  • The expression of several of these proteins has been then analyzed by immunohistochemistry in tissue microarrays containing 323 samples, including normal bronchial epithelium, hyperplasia, squamous metaplasia, dysplasias, squamous cell carcinomas, atypical adenomatous hyperplasia, and adenocarcinomas from 144 patients.
  • These results indicate that the changes in proteins detected in this study may occur early in lung carcinogenesis and persist in lung cancer.
  • In addition, some of the proteins detected by this approach may be novel biomarkers for early detection of lung cancer and novel targets for chemoprevention or therapy.
  • [MeSH-major] Lung / metabolism. Lung Neoplasms / metabolism. Precancerous Conditions / metabolism. Proteins / analysis. Proteomics / methods
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Blotting, Western / methods. Cell Adhesion Molecules / analysis. Cell Cycle Proteins / analysis. Cell Line, Tumor. Cells, Cultured. Electrophoresis, Polyacrylamide Gel. Female. Humans. Immunohistochemistry. Male. Middle Aged. Reproducibility of Results

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  • (PMID = 17145864.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30CA-16672-30; United States / NCI NIH HHS / CA / U01 CA86390
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Validation Studies
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / Cell Cycle Proteins; 0 / Proteins
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72. 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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73. Tsutsui S, Ashizawa K, Minami K, Tagawa T, Nagayasu T, Hayashi T, Uetani M: Multiple focal pure ground-glass opacities on high-resolution CT images: Clinical significance in patients with lung cancer. AJR Am J Roentgenol; 2010 Aug;195(2):W131-8
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  • [Title] Multiple focal pure ground-glass opacities on high-resolution CT images: Clinical significance in patients with lung cancer.
  • OBJECTIVE: The purpose of this study was to evaluate the clinical significance of multiple focal pure ground-glass opacities (GGOs) on high-resolution CT images of patients with lung cancer.
  • MATERIALS AND METHODS: The cases of 23 patients with proven lung cancer and associated multiple focal pure GGOs on high-resolution CT images were retrospectively reviewed.
  • Lung cancer and focal pure GGOs were seen in the same lobe and/or in the other lobes.
  • Histologic findings were obtained for 15 lesions representing 74 focal pure GGOs that were surgically resected: 11 atypical adenomatous hyperplasia lesions, three bronchioloalveolar carcinomas, and one lesion of focal fibrosis.
  • CONCLUSION: The size of most focal pure GGOs associated with lung cancer did not change during the follow-up period.
  • Most of the small number of lesions histologically diagnosed were atypical adenomatous hyperplasia or bronchioloalveolar carcinoma.
  • [MeSH-major] Algorithms. Lung Neoplasms / radiography. Radiographic Image Enhancement / methods. Radiographic Image Interpretation, Computer-Assisted / methods. Tomography, X-Ray Computed / methods

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  • (PMID = 20651172.001).
  • [ISSN] 1546-3141
  • [Journal-full-title] AJR. American journal of roentgenology
  • [ISO-abbreviation] AJR Am J Roentgenol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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74. Min JH, Lee HY, Lee KS, Han J, Park K, Ahn MJ, Lee SJ: Stepwise evolution from a focal pure pulmonary ground-glass opacity nodule into an invasive lung adenocarcinoma: an observation for more than 10 years. Lung Cancer; 2010 Jul;69(1):123-6
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  • [Title] Stepwise evolution from a focal pure pulmonary ground-glass opacity nodule into an invasive lung adenocarcinoma: an observation for more than 10 years.
  • The natural chronologic evolution of a lung cancer manifesting as a pure ground-glass opacity (GGO) nodule on CT scans still remains to be elucidated.
  • In the current case, we demonstrate serial morphologic (CT) and metabolic ((18)F-FDG PET) imaging findings in a case of adenocarcinoma, where stepwise progression from a focal pure GGO nodule (presumed atypical adenomatous hyperplasia [AAH] or bronchioloalveolar carcinoma [BAC]) eventually to an invasive adenocarcinoma was clearly depicted for more than 10-year follow-up period.
  • [MeSH-major] Adenocarcinoma / diagnosis. Carcinoma, Squamous Cell / diagnosis. Cell Transformation, Neoplastic / pathology. Lung Neoplasms / diagnosis. Solitary Pulmonary Nodule / diagnosis
  • [MeSH-minor] Biopsy, Fine-Needle. Diagnosis, Differential. Humans. Lung / pathology. Lung / radiography. Male. Middle Aged. Neoplasm Invasiveness. Positron-Emission Tomography. Time Factors. Tomography, X-Ray Computed

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  • [Copyright] Copyright 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20478641.001).
  • [ISSN] 1872-8332
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Ireland
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75. 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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76. Yuan P, Kadara H, Behrens C, Tang X, Woods D, Solis LM, Huang J, Spinola M, Dong W, Yin G, Fujimoto J, Kim E, Xie Y, Girard L, Moran C, Hong WK, Minna JD, Wistuba II: Sex determining region Y-Box 2 (SOX2) is a potential cell-lineage gene highly expressed in the pathogenesis of squamous cell carcinomas of the lung. PLoS One; 2010 Feb 09;5(2):e9112
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  • [Title] Sex determining region Y-Box 2 (SOX2) is a potential cell-lineage gene highly expressed in the pathogenesis of squamous cell carcinomas of the lung.
  • BACKGROUND: Non-small cell lung cancer (NSCLC) represents the majority (85%) of lung cancers and is comprised mainly of adenocarcinomas and squamous cell carcinomas (SCCs).
  • The sequential pathogenesis of lung adenocarcinomas and SCCs occurs through dissimilar phases as the former tumors typically arise in the lung periphery whereas the latter normally arise near the central airway.
  • METHODOLOGY/PRINCIPAL FINDINGS: We assessed the expression of SOX2, an embryonic stem cell transcriptional factor that also plays important roles in the proliferation of basal tracheal cells and whose expression is restricted to the main and central airways and bronchioles of the developing and adult mouse lung, in NSCLC by various methodologies.
  • Here, we found that SOX2 mRNA levels, from various published datasets, were significantly elevated in lung SCCs compared to adenocarcinomas (all p<0.001).
  • Moreover, a previously characterized OCT4/SOX2/NANOG signature effectively separated lung SCCs from adenocarcinomas in two independent publicly available datasets which correlated with increased SOX2 mRNA in SCCs.
  • Immunohistochemical analysis of various histological lung tissue specimens demonstrated marked nuclear SOX2 protein expression in all normal bronchial epithelia, alveolar bronchiolization structures and premalignant lesions in SCC development (hyperplasia, dysplasia and carcinoma in situ) and absence of expression in all normal alveoli and atypical adenomatous hyperplasias.
  • Moreover, SOX2 protein expression was greatly higher in lung SCCs compared to adenocarcinomas following analyses in two independent large TMA sets (TMA set I, n = 287; TMA set II, n = 511 both p<0.001).
  • Furthermore, amplification of SOX2 DNA was detected in 20% of lung SCCs tested (n = 40) and in none of the adenocarcinomas (n = 17).
  • CONCLUSIONS/SIGNIFICANCE: Our findings highlight a cell-lineage gene expression pattern for the stem cell transcriptional factor SOX2 in the pathogenesis of lung SCCs and suggest a differential activation of stem cell-related pathways between squamous cell carcinomas and adenocarcinomas of the lung.

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  • (PMID = 20161759.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P50 CA070907; United States / NCI NIH HHS / CA / CA-16672; United States / NCI NIH HHS / CA / P50CA70907
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / NANOG protein, human; 0 / Octamer Transcription Factor-3; 0 / POU5F1 protein, human; 0 / SOX2 protein, human; 0 / SOXB1 Transcription Factors
  • [Other-IDs] NLM/ PMC2817751
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77. 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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78. Shikada Y, Yonemitsu Y, Koga T, Onimaru M, Nakano T, Okano S, Sata S, Nakagawa K, Yoshino I, Maehara Y, Sueishi K: Platelet-derived growth factor-AA is an essential and autocrine regulator of vascular endothelial growth factor expression in non-small cell lung carcinomas. Cancer Res; 2005 Aug 15;65(16):7241-8
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  • [Title] Platelet-derived growth factor-AA is an essential and autocrine regulator of vascular endothelial growth factor expression in non-small cell lung carcinomas.
  • Using cell lines and surgical specimens of human non-small cell lung cancers (NSCLCs), we here show that platelet-derived growth factor-AA (PDGF-AA) is an essential autocrine regulator for VEGF expression.
  • To directly assess the expression of PDGF-AA-dependent VEGF and its roles in tumorigenesis, we stably transfected established cell lines with their antisense genes.
  • PDGF-AA tightly regulated VEGF expression and had a greater effect on tumor size and patient prognosis than did VEGF in both cell lines and surgical sections.
  • PDGF-AA expression was not seen in the atypical adenomatous hyperplasia at all, whereas VEGF was occasionally seen.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / blood supply. Carcinoma, Non-Small-Cell Lung / metabolism. Lung Neoplasms / blood supply. Lung Neoplasms / metabolism. Platelet-Derived Growth Factor / metabolism. Vascular Endothelial Growth Factor A / biosynthesis
  • [MeSH-minor] Animals. Cell Line, Tumor. Humans. Immunohistochemistry. Male. Mice. Mice, Inbred BALB C. Neovascularization, Pathologic / metabolism. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Transfection. Transplantation, Heterologous

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  • (PMID = 16103075.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Platelet-Derived Growth Factor; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A; 0 / platelet-derived growth factor A
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79. Kozuki T, Hisamoto A, Tabata M, Takigawa N, Kiura K, Segawa Y, Nakata M, Mandai K, Eguchi K, Ueoka H, Tanimoto M: Mutation of the epidermal growth factor receptor gene in the development of adenocarcinoma of the lung. Lung Cancer; 2007 Oct;58(1):30-5
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  • [Title] Mutation of the epidermal growth factor receptor gene in the development of adenocarcinoma of the lung.
  • However, the involvement of the mutation in atypical adenomatous hyperplasia (AAH) and multiple adenocarcinomas still remains unclear.
  • [MeSH-major] Adenocarcinoma / genetics. Adenomatosis, Pulmonary / genetics. Genes, erbB-1. Lung Neoplasms / genetics. Mutation. Neoplasms, Multiple Primary / genetics. Receptor, Epidermal Growth Factor / genetics

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  • (PMID = 17561305.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Quinazolines; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
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80. Kamiya H, Shinoda K, Kobayashi N, Kudo K, Nomura T, Morita T, Fujii T: Tuberous sclerosis complex complicated by pulmonary multinodular shadows. Intern Med; 2006;45(5):275-8
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  • They were initially suspected of representing atypical adenomatous hyperplasia or well-differentiated adenocarcinoma.
  • Histological examination of a video-assisted thoracoscopic lung biopsy specimen disclosed multiple nodules of type II pneumocyte hyperplasia with septal thickening.
  • Based on all of these findings taken together, a diagnosis of tuberous sclerosis complex with multifocal micronodular pneumocyte hyperplasia (MMPH) was made.
  • [MeSH-major] Lung / pathology. Tuberous Sclerosis / complications
  • [MeSH-minor] Adult. Calcinosis / radiography. Female. Humans. Hyperplasia / pathology. Hyperplasia / radiography. Thoracic Surgery, Video-Assisted. Tomography, X-Ray Computed

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  • (PMID = 16595993.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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81. 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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82. Nakashima Y, Yamada T, Tanahashi M, Hikosaka Y, Yoshitomi H, Niwa H: [A study of high-resolution computed tomography (HRCT) findings of resected small pulmonary nodules 2 cm or less in diameter with reference to the malignant nature]. Kyobu Geka; 2006 Sep;59(10):917-22
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  • To identify the characteristics of peripheral small lung mass lesions on high-resolution computed tomography (HRCT) and discriminate between malignant and benign, 223 mass lesions 2 cm or less resected surgically were evaluated about following points.
  • Pure GGO lesions without scale-down between several months were all adenocarcinomas or atypical adenomatous hyperplasia (AAH).
  • 2) Spicular or pleural indentation :75.2% (88 of 117 cases) of adenocarcinomas and all squamous cell carcinomas (18 cases) showed these findings, but 26.6% (41 of 154 cases) of positive cases were benign lesion (non-specific inflammation, mycobacterisis, and so on).
  • [MeSH-major] Lung / pathology. Lung Diseases / radiography. Lung Neoplasms / radiography. Solitary Pulmonary Nodule / radiography. Tomography, X-Ray Computed / methods
  • [MeSH-minor] Adenocarcinoma / pathology. Adenocarcinoma / radiography. Adult. Aged. Aged, 80 and over. Carcinoma, Small Cell / pathology. Carcinoma, Small Cell / radiography. Carcinoma, Squamous Cell / pathology. Carcinoma, Squamous Cell / radiography. Diagnosis, Computer-Assisted. Diagnosis, Differential. Female. Humans. Hyperplasia. Male. Middle Aged. Retrospective Studies

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  • (PMID = 16986688.001).
  • [ISSN] 0021-5252
  • [Journal-full-title] Kyobu geka. The Japanese journal of thoracic surgery
  • [ISO-abbreviation] Kyobu Geka
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
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83. 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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84. 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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85. 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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  • [Cites] Am J Respir Crit Care Med. 2002 Feb 15;165(4):508-13 [11850344.001]
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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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86. Ikeda K, Awai K, Mori T, Kawanaka K, Yamashita Y, Nomori H: Differential diagnosis of ground-glass opacity nodules: CT number analysis by three-dimensional computerized quantification. Chest; 2007 Sep;132(3):984-90
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  • OBJECTIVES: To differentiate among atypical adenomatous hyperplasia (AAH), bronchioloalveolar carcinoma (BAC), and adenocarcinoma showing ground-glass opacity (GGO) on CT scans, we conducted a study to determine the optimal parameter on CT number analysis using three-dimensional (3D) computerized quantification.
  • [MeSH-major] Carcinoma / diagnosis. Imaging, Three-Dimensional. Lung / pathology. Lung Neoplasms / diagnosis. Solitary Pulmonary Nodule / diagnosis. Tomography, X-Ray Computed
  • [MeSH-minor] Aged. Diagnosis, Differential. Female. Humans. Hyperplasia. Male. Middle Aged

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  • [CommentIn] Chest. 2008 Mar;133(3):827-8; author reply 827-8 [18321915.001]
  • (PMID = 17573486.001).
  • [ISSN] 0012-3692
  • [Journal-full-title] Chest
  • [ISO-abbreviation] Chest
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
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87. Wang GF, Lai MD, Yang RR, Chen PH, Su YY, Lv BJ, Sun LP, Huang Q, Chen SZ: Histological types and significance of bronchial epithelial dysplasia. Mod Pathol; 2006 Mar;19(3):429-37
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  • Pulmonary epithelium is known to undergo a preneoplastic process prior to the development of lung carcinoma.
  • Squamous dysplasia and atypical adenomatous hyperplasia have been identified and classified as preinvasive lesions of squamous cell carcinoma and peripheral pulmonary adenocarcinoma, respectively.
  • However, these commonly recognized preinvasive lesions do not completely explain the development of all histological types of lung carcinoma.
  • By examining 114 resection lung specimens, we concluded that there are four histological patterns of bronchial epithelial dysplasia based on morphological features (basal cell dysplasia, columnar cell dysplasia, bronchial epithelial dysplasia with transitional differentiation, and squamous dysplasia).
  • Basal cell dysplasia was focally positive for cytokeratin (CK) 17 and 10/13; columnar cell dysplasia was generally positive for CK7, 8, and 18; bronchial epithelial dysplasia with transitional differentiation had a heterogeneous immunoprofile, while squamous dysplasia was positive for CK10/13 and focally positive for CK17.
  • By Crosstabs McNemar test, the Mann-Whitney U-test (for two independent groups), the Kruskal-Wallis one-way nonparametric ANOVA (for >2 independent groups) and Spearman correlation analysis, the degree and extent of bronchial epithelial dysplasia was shown to be positively correlated with the incidence of bronchogenic carcinoma and multifocal primary lung carcinoma (P<0.05).
  • (1) bronchial epithelium can develop various patterns of dysplasia with abnormal/ambiguous cell differentiation and abnormal expressions of p53 and Ki-67.
  • Thus, these bronchial epithelial dysplastic lesions may represent a preneoplastic process. (2) The degree of bronchial epithelial dysplasia may significantly predispose individuals to bronchogenic carcinoma and multifocal primary lung carcinoma.
  • [MeSH-major] Lung Neoplasms / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Adult. Aged. Bronchial Neoplasms / metabolism. Bronchial Neoplasms / pathology. Carcinoma, Bronchogenic / metabolism. Carcinoma, Bronchogenic / pathology. Cell Differentiation. Epithelial Cells / chemistry. Epithelial Cells / pathology. Female. Humans. Immunohistochemistry. Keratins / analysis. Ki-67 Antigen / analysis. Male. Middle Aged. Respiratory Mucosa / chemistry. Respiratory Mucosa / pathology. Tumor Suppressor Protein p53 / analysis

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  • (PMID = 16415791.001).
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53; 68238-35-7 / Keratins
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88. 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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89. Dacic S: Pulmonary preneoplasia. Arch Pathol Lab Med; 2008 Jul;132(7):1073-8
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  • CONTEXT: Improved screening techniques for lung cancer have resulted in detection of lesions that are considered to represent precursors of invasive lung carcinomas.
  • OBJECTIVE: To review currently proposed morphologic criteria for precursor lesions of non-small cell lung carcinomas including squamous dysplasias, atypical adenomatous hyperplasia, and diffuse idiopathic neuroendocrine cell hyperplasia.
  • DATA SOURCES: Published literature and recent World Health Organization classification of lung tumors.
  • Future understanding of underlying molecular abnormalities associated with progression of these lesions into invasive lung carcinoma may result in a development of molecular assays with potential diagnostic and prognostic importance.
  • [MeSH-major] Lung Neoplasms / pathology. Precancerous Conditions / pathology

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  • (PMID = 18605763.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 33
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90. Kishi K, Hara S, Kurosaki A, Fujii T, Yoshimura K: [The efficacy of low-dose helical CT screening as an option for health examination]. Nihon Kokyuki Gakkai Zasshi; 2007 Aug;45(8):593-7
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  • Of 14 patients with neoplastic lesions, 13 had lung cancer, 1 of whom had double primary lung cancer, and 1 had atypical adenomatous hyperplasia.
  • The mean diameter of the 14 lung cancers was 14.4 mm.
  • The histology of these lesions was adenocarcinoma in 13 and squamous cell carcinoma in 1.
  • CT screening is useful for detecting not only early lung cancer but also non-neoplastic lung diseases.
  • [MeSH-major] Lung Neoplasms / radiography. Multiphasic Screening / methods. Pulmonary Emphysema / radiography. Tomography, Spiral Computed

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  • (PMID = 17763686.001).
  • [ISSN] 1343-3490
  • [Journal-full-title] Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society
  • [ISO-abbreviation] Nihon Kokyuki Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
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91. Yee H, Yie TA, Goldberg J, Wong KM, Rom WN: Immunohistochemical study of fibrosis and adenocarcinoma in dominant-negative p53 transgenic mice exposed to chrysotile asbestos and benzo(a)pyrene. J Environ Pathol Toxicol Oncol; 2008;27(4):267-76
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  • We evaluated the mechanisms using immunohistochemistry whereby chrysotile asbestos and benzo(a)pyrene (BaP) instilled intratracheally into lung-specific dominant-negative p53 (dnp53) mice might interact in causing lung carcinomas and fibrosis.
  • Chrysotile asbestos and benzo(a)pyrene (BaP) were instilled intratracheally into lung-specific dominant-negative p53 (dnp53) and control mice.
  • The mice were sacrificed at 12 months and their lungs examined for lung carcinomas and fibrosis.
  • The dnp53 mice had increased numbers of lung adenocarcinomas with BaP alone and the combination of chrysotile and BaP (the latter was additive but not significant).
  • Several atypical adenomatous hyperplasia lesions were found in the combined treatment group. dnp53 and FVBN control mice developed nodular buds of fibrotic lung tissue after chrysotile asbestos exposure that were localized in respiratory bronchioles; these lesions had significant increases in immunohistochemical staining for TGF-beta, MMP-7 and -9, MIG-1, and SDF-1.
  • [MeSH-major] Adenocarcinoma. Asbestos, Serpentine / toxicity. Benzo(a)pyrene / toxicity. Lung Neoplasms. Pulmonary Fibrosis. Tumor Suppressor Protein p53 / biosynthesis

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  • (PMID = 19105532.001).
  • [ISSN] 0731-8898
  • [Journal-full-title] Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer
  • [ISO-abbreviation] J. Environ. Pathol. Toxicol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Asbestos, Serpentine; 0 / Cytokines; 0 / Tumor Suppressor Protein p53; 3417WMA06D / Benzo(a)pyrene; EC 3.4.22.- / Caspase 3; EC 3.4.24.- / Matrix Metalloproteinases
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92. 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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93. 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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94. Lantuéjoul S, Salameire D, Salon C, Brambilla E: Pulmonary preneoplasia--sequential molecular carcinogenetic events. Histopathology; 2009 Jan;54(1):43-54
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  • Bronchial and bronchioloalveolar carcinogenesis is a multicentric and multistep process, leading to a sequential accumulation of molecular and genetic abnormalities, mainly due to exposure to tobacco carcinogens.
  • Concomitantly, a series of morphological alterations of normal bronchial or bronchioloalveolar epithelium occur, resulting in preneoplastic and then neoplastic lesions.
  • The three pulmonary preneoplastic changes recognized to date in the lung include bronchial squamous dysplasia and in situ carcinoma, preceding invasive squamous cell carcinoma and basaloid carcinoma, atypical adenomatous hyperplasia, a preneoplastic condition of bronchioloalveolar carcinoma, and diffuse idiopathic pulmonary neuroendocrine cell hyperplasia, a proposed precursor for carcinoid tumours.
  • Although the gradual accumulation of molecular alterations has been widely investigated in bronchial carcinogenesis, with the aim of determining new biomarkers for early lung cancer detection in high-risk patients and targeted chemoprevention, lung adenocarcinoma pathogenesis has been only recently highlighted, with the recent discovery of epidermal growth factor receptor mutation pathway in non-smokers.
  • This review focuses on the current status of molecular pathology in lung cancer and pulmonary preneoplastic conditions.
  • [MeSH-major] Lung Neoplasms / genetics. Lung Neoplasms / pathology. Precancerous Conditions / genetics. Precancerous Conditions / pathology
  • [MeSH-minor] Adenocarcinoma / pathology. Humans. Lung / pathology. Small Cell Lung Carcinoma / pathology

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  • (PMID = 19187179.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 90
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95. 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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96. 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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97. Noguchi M: Stepwise progression of pulmonary adenocarcinoma--clinical and molecular implications. Cancer Metastasis Rev; 2010 Mar;29(1):15-21
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  • Pulmonary adenocarcinoma develops to invasive carcinoma through atypical adenomatous hyperplasia, adenocarcinoma in situ and minimally invasive adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Lung Neoplasms / genetics. Lung Neoplasms / pathology
  • [MeSH-minor] Carcinoma in Situ / pathology. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / pathology. Disease Progression. Humans. Neoplasm Invasiveness. Precancerous Conditions / pathology

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  • (PMID = 20108111.001).
  • [ISSN] 1573-7233
  • [Journal-full-title] Cancer metastasis reviews
  • [ISO-abbreviation] Cancer Metastasis Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 29
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98. Park CM, Goo JM, Lee HJ, Lee CH, Chun EJ, Im JG: Nodular ground-glass opacity at thin-section CT: histologic correlation and evaluation of change at follow-up. Radiographics; 2007 Mar-Apr;27(2):391-408
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  • The popularization of computed tomography (CT) in clinical practice and the introduction of mass screening for early lung cancer with the use of CT have increased the frequency of findings of subtle nodules or nodular ground-glass opacity.
  • Nodular ground-glass opacity may be observed in malignancies such as bronchioloalveolar carcinoma and adenocarcinoma, as well as in their putative precursors, such as atypical adenomatous hyperplasia.
  • [MeSH-minor] Humans. Lung Neoplasms / radiography. Practice Guidelines as Topic. Practice Patterns, Physicians'. Prognosis. Statistics as Topic

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  • [Copyright] (c) RSNA, 2007.
  • (PMID = 17374860.001).
  • [ISSN] 1527-1323
  • [Journal-full-title] Radiographics : a review publication of the Radiological Society of North America, Inc
  • [ISO-abbreviation] Radiographics
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 57
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99. 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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100. Kim TJ, Goo JM, Lee KW, Park CM, Lee HJ: Clinical, pathological and thin-section CT features of persistent multiple ground-glass opacity nodules: comparison with solitary ground-glass opacity nodule. Lung Cancer; 2009 May;64(2):171-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • RESULTS: Multiple GGO nodules (n=105) included atypical adenomatous hyperplasia (AAH) (n=31), bronchioloalveolar carcinoma (BAC) (n=33), adenocarcinoma (n=34) and focal interstitial fibrosis (n=7).
  • Female sex (P<.001), nonsmoker (P=.012) and multiple primary lung cancers (P<.001) were more frequent for multiple GGO nodules, which were smaller (12 mm+/-7.9) than solitary GGO nodules (17 mm+/-8.1) (P<.001).
  • [MeSH-major] Lung Neoplasms / pathology. Lung Neoplasms / radiography. Multiple Pulmonary Nodules / pathology. Multiple Pulmonary Nodules / radiography. Solitary Pulmonary Nodule / pathology. Solitary Pulmonary Nodule / radiography

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  • (PMID = 18799230.001).
  • [ISSN] 1872-8332
  • [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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