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1. 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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2. Job B, Bernheim A, Beau-Faller M, Camilleri-Broët S, Girard P, Hofman P, Mazières J, Toujani S, Lacroix L, Laffaire J, Dessen P, Fouret P, LG Investigators: Genomic aberrations in lung adenocarcinoma in never smokers. PLoS One; 2010;5(12):e15145
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  • [Title] Genomic aberrations in lung adenocarcinoma in never smokers.
  • BACKGROUND: Lung cancer in never smokers would rank as the seventh most common cause of cancer death worldwide.
  • METHODS AND FINDINGS: We performed high-resolution array comparative genomic hybridization analysis of lung adenocarcinoma in sixty never smokers and identified fourteen new minimal common regions (MCR) of gain or loss, of which five contained a single gene (MOCS2, NSUN3, KHDRBS2, SNTG1 and ST18).
  • NSD1 and FUS are oncogenes hitherto not known to be associated with lung cancer.
  • Multiple genetic pathways defined by gains of MYC, deletions of RB1 and WRN or gains on 7p and 7q are involved in lung adenocarcinoma in never smokers.
  • [MeSH-major] Adenocarcinoma / genetics. Chromosome Aberrations. Genomics. Lung Neoplasms / genetics
  • [MeSH-minor] Aged. DNA, Neoplasm / genetics. Female. Genes, Neoplasm. Genetic Predisposition to Disease. Humans. In Situ Hybridization, Fluorescence. Loss of Heterozygosity. Male. Middle Aged. Multigene Family. Receptor, Epidermal Growth Factor / genetics. Smoking

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  • (PMID = 21151896.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Other-IDs] NLM/ PMC2997777
  • [Investigator] Dartevelle P; Dulmet E; Leroy-Ladurie F; de Montpreville V; Monnet I; Bernard A; Piard F; Alifano M; Camilleri-Broët S; Régnard JF; Hofman P; Hofman V; Mouroux J; Trédaniel J; Beau-Faller M; Massard G; Neuville A; Antoine M; Cadranel J; Brouchet L; Mazières J; Rouquette I; Saint-Blancard P; Vaylet F; Berhneim A; Dessen P; Dufour F; Dorvault N; Fouret P; Job B; Lacroix L; Lazar V; Richon C; Roux V; Saulnier P; Taranchon E; Toujani S; Valent A; Girard P; Gossot D; Validire P; Laffaire J
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3. 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.
  • The high transcription of TACSTD2 and S100A2 in PL16T was confirmed by in situ hybridization.
  • 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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4. Song X, Song Z, Lv Y, Zhong M, Li X: [The Study on Gene Amplification of EGFR in Bronchioloalveolar Carcinoma and Conventional Adenocarcinoma of the Lung.]. Zhongguo Fei Ai Za Zhi; 2009 Aug 20;12(8):879-83
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  • [Title] [The Study on Gene Amplification of EGFR in Bronchioloalveolar Carcinoma and Conventional Adenocarcinoma of the Lung.].
  • BACKGROUND: Patients with adenocarcinoma of the lung have disproportionately response to the epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI).
  • The aim of this study is to analyze the difference of EGFR gene amplification in bronchioloalveolar carcinoma (BAC), adenocarcinma mixed subtype and conventional adenocarcinoma of the lung and provide some information to clinical therapies.
  • METHODS: Lung cancer cases were collected and reviewed from the archives of the Department of Pathology, Chinese PLA General Hospital during the time period from 2004 to 2006.
  • The definite diagnosis of BAC based on 2004 WHO classification of lung tumors was made by two pathologists.
  • Fluorescence in situ hybridization (FISH) was performed to detect EGFR gene amplification in pure BAC, adenocarcinma mixed subtype and conventional adenocarcinoma.
  • RESULTS: Conventional adenocarcinoma had higher EGFR amplification compared with pure BAC and adenocarcinma mixed subtype (Chi-square=11.632, P<0.05).
  • EGFR gene amplification was found in 45.45% of conventional adenocarcinoma, 14.81% in pure BACs, and 22.58% in adenocarcinma mixed subtype.
  • EGFR gene amplification might be associated with the development of adenocarcinoma of the lung.

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  • (PMID = 20719175.001).
  • [ISSN] 1999-6187
  • [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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5. Shen H, Zhu Y, Wu YJ, Qiu HR, Shu YQ: Genomic alterations in lung adenocarcinomas detected by multicolor fluorescence in situ hybridization and comparative genomic hybridization. Cancer Genet Cytogenet; 2008 Mar;181(2):100-7
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  • [Title] Genomic alterations in lung adenocarcinomas detected by multicolor fluorescence in situ hybridization and comparative genomic hybridization.
  • We used two molecular cytogenetic techniques, multicolor fluorescence in situ hybridization (M-FISH) and comparative genomic hybridization (CGH), to analyze three established lung adenocarcinoma cell lines (A549, H1650, and SPC-A-1) and primary lung adenocarcinoma samples, to identify common chromosomal aberrations.
  • The most common gains were found in 16p13 (in 50% of samples), and 16p13 amplification was associated with relatively poor differentiation and late stage.
  • M-FISH and CGH can be a powerful tool in identification of genomic alterations in lung cancer, as well as in diagnosis.
  • The overrepresented regions may harbor potential candidate genes involved in lung adenocarcinoma pathogenesis.
  • [MeSH-major] Adenocarcinoma / genetics. Chromosome Aberrations. In Situ Hybridization, Fluorescence / methods. Lung Neoplasms / genetics. Nucleic Acid Hybridization
  • [MeSH-minor] Carcinoma, Non-Small-Cell Lung / diagnosis. Carcinoma, Non-Small-Cell Lung / genetics. Cell Line, Tumor. Color. Genome, Human. Humans. Karyotyping

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  • (PMID = 18295661.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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6. Chiosea S, Shuai Y, Cieply K, Nikiforova MN, Dacic S: EGFR fluorescence in situ hybridization-positive lung adenocarcinoma: incidence of coexisting KRAS and BRAF mutations. Hum Pathol; 2010 Aug;41(8):1053-60
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  • [Title] EGFR fluorescence in situ hybridization-positive lung adenocarcinoma: incidence of coexisting KRAS and BRAF mutations.
  • Despite growing evidence that epidermal growth factor receptor (EGFR) and v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) mutation analysis is the most reliable predictor of the lung carcinoma response to EGFR-targeted therapies, there is still discussion about the role of EGFR fluorescence in situ hybridization (FISH).
  • The incidence of KRAS and V-raf murine sarcoma viral oncogene homolog B1 (BRAF) mutations in EGFR-amplified or EGFR FISH-positive lung adenocarcinomas remains unknown.
  • The aim of this study was to prospectively characterize the incidence of KRAS and BRAF mutations in EGFR FISH-positive surgically treated lung adenocarcinomas.
  • Of 386 primary lung adenocarcinomas, 77 (20%) were EGFR FISH positive by University of Colorado criteria.
  • The incidence of KRAS mutations in EGFR FISH-positive lung adenocarcinomas was 23% and was not significantly different from the incidence of KRAS mutations in EGFR FISH-negative subsets of adenocarcinoma (32%).
  • Our results showed significant number of EGFR FISH positive/amplified lung adenocarcinomas harboring KRAS mutation.
  • [MeSH-major] Adenocarcinoma / genetics. Biomarkers, Tumor / genetics. Carcinoma, Non-Small-Cell Lung / genetics. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins B-raf / genetics. Receptor, Epidermal Growth Factor / genetics. ras Proteins / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chromosomes, Human, Pair 7 / genetics. Chromosomes, Human, Pair 7 / ultrastructure. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Mutation. Polyribosomes / genetics. Prospective Studies

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20381121.001).
  • [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 / Biomarkers, Tumor; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 3.6.5.2 / ras Proteins
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7. Kalogeraki A, Tzardi M, Zoras O, Giannikaki E, Papadakis M, Tamiolakis D, Petraki PE, Diamantis A, Siafakas N, Stathopoulos E: Apoptosis and cell proliferation correlated with tumor grade in patients with lung adenocarcinoma. In Vivo; 2010 Sep-Oct;24(5):667-70
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  • [Title] Apoptosis and cell proliferation correlated with tumor grade in patients with lung adenocarcinoma.
  • BACKGROUND: Apoptosis and cell proliferation in patients with adenocarcinoma of the lung have not been well described with relation to fine-needle aspiration biopsies (FNABs).
  • To investigate the contribution of apoptosis to the growth of adenocarcinoma of the lung, both apoptosis and cell proliferation were analysed for correlation with the grade of the tumor.
  • PATIENTS AND METHODS: Fifty tumors from 50 patients with adenocarcinoma of the lung were studied.
  • The detection of DNA fragments in situ using the terminal deoxyribonucleotidyl transferase-mediated dUTP-digoxigenin nick-end labeling (TUNEL) assay was applied to investigate active cell death (apoptosis) and the MIB-1 antigen was used to investigate cell proliferation.
  • RESULTS: The TUNEL indices were 0.55±0.09, 0.90±0.33 and 3.1±0.99 in well-, moderately and poorly differentiated adenocarcinoma of the lung respectively.
  • The differences in both TUNEL and MIB-1 labeling indices were significant between well-, moderately and poorly differentiated adenocarcinoma of the lung and a positive correlation was found between the TUNEL indices and the MIB-1 indices.
  • CONCLUSION: Apoptosis (cell death) and cell proliferation increases as the grade of differentiation decreases in adenocarcinoma of the lung, suggesting a rapid turn over of the tumor cells in tumors with a lower grade of differentiation.
  • [MeSH-major] Adenocarcinoma / pathology. Apoptosis / physiology. Lung Neoplasms / pathology. Severity of Illness Index
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Biopsy, Fine-Needle. Cell Differentiation / physiology. Cell Division / physiology. Humans. In Situ Nick-End Labeling. Ki-67 Antigen / metabolism. Prognosis. Tumor Cells, Cultured

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  • (PMID = 20952731.001).
  • [ISSN] 1791-7549
  • [Journal-full-title] In vivo (Athens, Greece)
  • [ISO-abbreviation] In Vivo
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen
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8. Hatzibougias D, Bobos M, Karayannopoulou G, Karkavelas G, Karapanagiotidis GT, Foroulis CN, Kostopoulos I: A rare tumoral combination, synchronous lung adenocarcinoma and mantle cell lymphoma of the pleura. World J Surg Oncol; 2008;6:137
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  • [Title] A rare tumoral combination, synchronous lung adenocarcinoma and mantle cell lymphoma of the pleura.
  • BACKGROUND: Coexistence of adenocarcinoma and mantle cell lymphoma in the same or different anatomical sites is extremely rare.
  • We present a case of incidental discovery of primary lung adenocarcinoma and mantle cell lymphoma involving the pleura, during an axillary thoracotomy performed for a benign condition.
  • A bulla of the lung apex was resected en bloc with a scar-like lesion of the lung, which was located in proximity with the bulla origin, by a wide wedge resection.
  • Histologic examination of the stripped-off parietal pleura and of the bullectomy specimen revealed the synchronous occurrence of two distinct neoplasms, a lymphoma infiltrating the pleura and a primary, early lung adenocarcinoma.
  • Immunohistochemical and fluorescence in situ hybridization assays were performed.
  • The morphologic, immunophenotypic and genetic findings supported the diagnosis of primary lung adenocarcinoma (papillary subtype) coexisting with a non-Hodgkin, B-cell lineage, mantle cell lymphoma involving both, visceral and parietal pleura and without mediastinal lymph node involvement.
  • The patient received 6 cycles of chemotherapy, while pulmonary function tests precluded further pulmonary parenchyma resection (lobectomy) for his adenocarcinoma.
  • CONCLUSION: This is the first reported case of a rare tumoral combination involving simultaneously lung and pleura, emphasizing at the incidental discovery of the two coexisting neoplasms during a procedure performed for a benign condition.
  • [MeSH-major] Adenocarcinoma / pathology. Lung Neoplasms / pathology. Lymphoma, Mantle-Cell / pathology. Neoplasms, Multiple Primary / pathology. Pleural Neoplasms / pathology
  • [MeSH-minor] Aged. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male

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  • [Cites] Hum Pathol. 2001 Jan;32(1):129-32 [11172307.001]
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  • (PMID = 19114021.001).
  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2629472
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9. Shen H, Gao W, Wu YJ, Qiu HR, Shu YQ: Multicolor fluorescence in situ hybridization and comparative genomic hybridization reveal molecular events in lung adenocarcinomas and squamous cell lung carcinomas. Biomed Pharmacother; 2009 Jul;63(6):396-403
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  • [Title] Multicolor fluorescence in situ hybridization and comparative genomic hybridization reveal molecular events in lung adenocarcinomas and squamous cell lung carcinomas.
  • We have used the molecular cytogenetic techniques of multicolor fluorescence in situ hybridization (M-FISH) and comparative genomic hybridization (CGH) to analyze two established lung cancer cell lines (A549, H520), 80 primary lung adenocarcinoma samples and 80 squamous cell lung carcinoma samples in order to identify common chromosomal aberrations.
  • In lung adenocarcinomas the most common gains were found in 16p13 (50%); while in squamous cell lung carcinomas the common gains were found in 17q21 (45%) and these alterations were observed to be associated with their specific pathological subtype.
  • In conclusion, the present study contributes to the molecular biological characterization in lung adenocarcinomas and squamous cell lung carcinomas and through evaluation of molecular events to the recently emergent focus on novel markers for lung cancer treatment.
  • [MeSH-major] Adenocarcinoma / genetics. Comparative Genomic Hybridization / methods. In Situ Hybridization, Fluorescence / methods. Lung Neoplasms / genetics
  • [MeSH-minor] Adult. Aged. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / pathology. Cell Line, Tumor. Chromosome Aberrations. Female. Humans. Male. Middle Aged. Translocation, Genetic / genetics

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  • (PMID = 18848758.001).
  • [ISSN] 1950-6007
  • [Journal-full-title] Biomedicine & pharmacotherapy = Biomédecine & pharmacothérapie
  • [ISO-abbreviation] Biomed. Pharmacother.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] France
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10. Sakuma Y, Matsukuma S, Yoshihara M, Nakamura Y, Noda K, Nakayama H, Kameda Y, Tsuchiya E, Miyagi Y: Distinctive evaluation of nonmucinous and mucinous subtypes of bronchioloalveolar carcinomas in EGFR and K-ras gene-mutation analyses for Japanese lung adenocarcinomas: confirmation of the correlations with histologic subtypes and gene mutations. Am J Clin Pathol; 2007 Jul;128(1):100-8
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  • [Title] Distinctive evaluation of nonmucinous and mucinous subtypes of bronchioloalveolar carcinomas in EGFR and K-ras gene-mutation analyses for Japanese lung adenocarcinomas: confirmation of the correlations with histologic subtypes and gene mutations.
  • Although adenocarcinomas of the lung are associated with epidermal growth factor receptor (EGFR) gene mutations and sensitivity to EGFR tyrosine kinase inhibitors, it remains unclear whether bronchioloalveolar carcinoma (BAC) components and/or subtypes affect these associations.
  • We examined 141 non-small cell lung cancers (NSCLCs), including 118 adenocarcinomas, for mutations in exons 19 and 21 of the EGFR gene together with mutations in codon 12 of the K-ras gene using loop-hybrid mobility shift assays, a highly sensitive polymerase chain reaction-based method.
  • In NSCLCs, EGFR mutations were detected in 75 cases (53.2%) and were significantly associated with adenocarcinoma, female sex, and never smoking.
  • Because EGFR mutations were detected even in most pure nonmucinous BACs, ie, lung adenocarcinoma in situ, EGFR mutation is considered a critical event in the pathogenesis of nonmucinous BAC tumors.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma, Bronchiolo-Alveolar / genetics. Genes, ras. Lung Neoplasms / genetics. Mutation. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Adult. Aged. Carcinoma, Non-Small-Cell Lung / genetics. Female. Humans. Male. Middle Aged

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  • (PMID = 17580276.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [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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11. Tsuta K, Ishii G, Kim E, Shiono S, Nishiwaki Y, Endoh Y, Kodama T, Nagai K, Nagai K: Primary lung adenocarcinoma with massive lymphocyte infiltration. Am J Clin Pathol; 2005 Apr;123(4):547-52
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  • [Title] Primary lung adenocarcinoma with massive lymphocyte infiltration.
  • We report 6 cases of adenocarcinoma with massive lymphocyte infiltration.
  • This adenocarcinoma is found in 0.7% of surgically resected primary lung adenocarcinomas.
  • The mean follow-up period was 49.8 months; all patients were alive without recurrence despite advanced pathologic stage.
  • The lung parenchyma was destroyed by the severe inflammatory cell infiltration without dense fibrosis.
  • This type of adenocarcinoma occurs in old age, and good outcome and distinctive histologic features were observed.
  • We refer to it as primary lung adenocarcinoma with massive lymphocyte infiltration.
  • [MeSH-major] Adenocarcinoma / pathology. Lung Neoplasms / pathology. Lymphocyte Subsets / pathology. Lymphocytes, Tumor-Infiltrating / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Female. Humans. Immunohistochemistry. In Situ Hybridization. Lymphatic Metastasis / pathology. Male. Middle Aged

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  • (PMID = 15743751.001).
  • [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] 0 / Biomarkers, Tumor
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12. Wen J, Duan Y, Zou Y, Nie Z, Feng H, Lugnani F, Baust JG: Cryoablation induces necrosis and apoptosis in lung adenocarcinoma in mice. Technol Cancer Res Treat; 2007 Dec;6(6):635-40
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  • [Title] Cryoablation induces necrosis and apoptosis in lung adenocarcinoma in mice.
  • This study evaluated cryoablation on subcutaneously transplanted tumors of lung adenocarcinoma LA795 in T739 mice in vivo, in an effort to assess the feasibility of cryoablation in treatment of NSCLC.
  • Subcutaneously transplanted lung adenocarcinoma LA795 was implanted into T739 mice yielding tumors of approximately 2.5 cm in diameter.
  • Following cryoablation, the various modes of cell death were studied: necrosis in the central frozen zone by light microscopy and apoptosis in periphery of the frozen zone by in situ end labeling (TUNEL).
  • [MeSH-major] Adenocarcinoma / surgery. Apoptosis. Cryosurgery. Lung Neoplasms / surgery. Necrosis
  • [MeSH-minor] Animals. Blotting, Western. Caspase 3 / metabolism. Female. Immunohistochemistry. In Situ Nick-End Labeling. Male. Mice. Poly (ADP-Ribose) Polymerase-1. Poly(ADP-ribose) Polymerases / metabolism. bcl-2-Associated X Protein / metabolism

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  • (PMID = 17994794.001).
  • [ISSN] 1533-0346
  • [Journal-full-title] Technology in cancer research & treatment
  • [ISO-abbreviation] Technol. Cancer Res. Treat.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / bcl-2-Associated X Protein; EC 2.4.2.30 / Parp1 protein, mouse; EC 2.4.2.30 / Poly (ADP-Ribose) Polymerase-1; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / Caspase 3
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13. Choi CM, Seo KW, Jang SJ, Oh YM, Shim TS, Kim WS, Lee DS, Lee SD: Chromosomal instability is a risk factor for poor prognosis of adenocarcinoma of the lung: Fluorescence in situ hybridization analysis of paraffin-embedded tissue from Korean patients. Lung Cancer; 2009 Apr;64(1):66-70
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  • [Title] Chromosomal instability is a risk factor for poor prognosis of adenocarcinoma of the lung: Fluorescence in situ hybridization analysis of paraffin-embedded tissue from Korean patients.
  • BACKGROUND: In this study, we sought to evaluate the prognostic importance of chromosomal instability (CIN) in adenocarcinoma (AC) of the lung.
  • The relationship between CIN detected by fluorescence in situ hybridization (FISH) and survival in AC patients was examined.
  • METHODS: Sixty-three surgical specimens of lung AC were analyzed.
  • CONCLUSIONS: CIN can be effectively detected in primary AC of lung using FISH analysis.
  • [MeSH-major] Adenocarcinoma / genetics. Chromosomal Instability. Chromosomes, Human, Pair 6 / genetics. Lung Neoplasms / genetics. Neoplasm Proteins / genetics. Proto-Oncogene Proteins c-myc / genetics. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Adult. Aged. Female. Humans. In Situ Hybridization, Fluorescence. Korea. Male. Middle Aged. Paraffin Embedding. Prognosis. Risk Factors. Survival Rate

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  • (PMID = 18814932.001).
  • [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 / MYC protein, human; 0 / Neoplasm Proteins; 0 / P16 protein, human; 0 / Proto-Oncogene Proteins c-myc; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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14. Fukuoka M, Wu Y, Thongprasert S, Yang C, Chu D, Saijo N, Watkins C, Duffield E, Armour A, Mok T: Biomarker analyses from a phase III, randomized, open-label, first-line study of gefitinib (G) versus carboplatin/paclitaxel (C/P) in clinically selected patients (pts) with advanced non-small cell lung cancer (NSCLC) in Asia (IPASS). J Clin Oncol; 2009 May 20;27(15_suppl):8006

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  • [Title] Biomarker analyses from a phase III, randomized, open-label, first-line study of gefitinib (G) versus carboplatin/paclitaxel (C/P) in clinically selected patients (pts) with advanced non-small cell lung cancer (NSCLC) in Asia (IPASS).
  • : 8006^ Background: IPASS demonstrated overall superiority of first-line G vs C/P for progression-free survival (PFS) in never/light ex-smokers with stage IIIB/IV adenocarcinoma NSCLC in Asia.
  • EGFR gene-copy number was evaluable in 406 pts by fluorescence in situ hybridization (FISH; 61% FISH +).

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  • (PMID = 27962786.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. Ponz-Sarvisé M, Calvo A, Redrado M, Nguewa PA, Abella L, Catena R, García-Foncillas J, Panizo A, Gil-Bazo I: Inhibitor of differentiation-1 (Id1) characterization in poor-prognosis (PP) human bladder cancer (BCa) primary tumors and matched metastases (MTS) using a new monoclonal antibody (MoAb). J Clin Oncol; 2009 May 20;27(15_suppl):e16119

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  • : e16119 Background: Id1, involved in cell differentiation, proliferation, tumor angiogenesis and metastasis, has recently showed to mediate lung MTS from breast cancer (PNAS 2007).
  • 2009) and other non-adenocarcinoma tumors.
  • Most pts had PP advanced (22,7 % stage III; 68,2% stage IV) BCa.
  • We also observed Id1 exp. in tumor in situ areas near the invasive carcinoma in 16 out of 20 pts expressing Id1 in the primary tumor.
  • Id1 exp. in tumor in situ areas suggests Id1 as an initial factor in the BCa carcinogenic process and in the case of being confirmed Id1 could represent a target in BCa prophylaxis.

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  • (PMID = 27963310.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Okudera K, Kamata Y, Takanashi S, Hasegawa Y, Tsushima T, Ogura Y, Nakanishi K, Sato H, Okumura K: Small adenocarcinoma of the lung: prognostic significance of central fibrosis chiefly because of its association with angiogenesis and lymphangiogenesis. Pathol Int; 2006 Sep;56(9):494-502
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  • [Title] Small adenocarcinoma of the lung: prognostic significance of central fibrosis chiefly because of its association with angiogenesis and lymphangiogenesis.
  • To clarify the reason why central fibrosis (CF) is an important histological prognostic factor in small adenocarcinoma (SA) of the lung, tumor tissues from 50 patients with SA < or = 2 cm in diameter were investigated using immunohistochemical and in situ hybridization analysis for factors relating to extracellular matrix and vessels.
  • In adenocarcinoma areas, positive activity was observed with both primary antibodies and probes for matrix metalloproteinase-2 (MMP-2) in 11/50 patients (22%), membrane-type 1 matrix metalloproteinase (MT1-MMP) in 39/50 patients (78%) and tissue inhibitor of metalloproteinase-2 (TIMP-2) in 49/50 patients (98%).
  • [MeSH-major] Carcinoma, Small Cell / complications. Lung Neoplasms / complications. Lymphangiogenesis. Neovascularization, Pathologic. Pulmonary Fibrosis / complications
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease-Free Survival. Female. Humans. Immunohistochemistry. In Situ Hybridization. Male. Matrix Metalloproteinase 2 / metabolism. Matrix Metalloproteinases / metabolism. Matrix Metalloproteinases, Membrane-Associated. Middle Aged. Prognosis. Tissue Inhibitor of Metalloproteinases / metabolism

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  • (PMID = 16930329.001).
  • [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 / Tissue Inhibitor of Metalloproteinases; EC 3.4.24.- / Matrix Metalloproteinases; EC 3.4.24.- / Matrix Metalloproteinases, Membrane-Associated; EC 3.4.24.24 / Matrix Metalloproteinase 2
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17. Kim HG, Hwang YP, Jeong HG: Kahweol blocks STAT3 phosphorylation and induces apoptosis in human lung adenocarcinoma A549 cells. Toxicol Lett; 2009 May 22;187(1):28-34
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  • [Title] Kahweol blocks STAT3 phosphorylation and induces apoptosis in human lung adenocarcinoma A549 cells.
  • In this study, the apoptotic effect of kahweol in human lung adenocarcinoma A549 cells was investigated.
  • [MeSH-major] Adenocarcinoma / pathology. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Diterpenes / pharmacology. Lung Neoplasms / pathology. STAT3 Transcription Factor / metabolism
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Drug Screening Assays, Antitumor. Humans. In Situ Nick-End Labeling. Mitochondria / drug effects. Phosphorylation / drug effects. Proto-Oncogene Proteins c-bcl-2 / metabolism. Signal Transduction / drug effects. Time Factors. Tumor Cells, Cultured. bcl-2-Associated X Protein / metabolism

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  • (PMID = 19429240.001).
  • [ISSN] 0378-4274
  • [Journal-full-title] Toxicology letters
  • [ISO-abbreviation] Toxicol. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BAX protein, human; 0 / Diterpenes; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / bcl-2-Associated X Protein; 6894-43-5 / kahweol
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18. De Oliveira Duarte Achcar R, Nikiforova MN, Yousem SA: Micropapillary lung adenocarcinoma: EGFR, K-ras, and BRAF mutational profile. Am J Clin Pathol; 2009 May;131(5):694-700
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  • [Title] Micropapillary lung adenocarcinoma: EGFR, K-ras, and BRAF mutational profile.
  • Micropapillary lung adenocarcinoma (MPA) has been reported as an aggressive variant of adenocarcinoma, frequently manifesting at high stage with a poor prognosis.
  • We analyzed the clinical and molecular profile of 15 primary MPAs for K-ras, EGFR, and BRAF mutations and performed fluorescence in situ hybridization for EGFR amplification.
  • We conclude that K-ras, EGFR, and BRAF mutations are disproportionately seen in adenocarcinomas of lung with a dominant micropapillary growth pattern compared with conventional adenocarcinoma in our institutional experience.
  • [MeSH-major] Adenocarcinoma, Papillary / genetics. Genes, erbB-1 / genetics. Genes, ras / genetics. Lung Neoplasms / genetics. Proto-Oncogene Proteins B-raf / genetics
  • [MeSH-minor] Aged. Aged, 80 and over. DNA Mutational Analysis. DNA, Neoplasm / analysis. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Mucins / metabolism. Prognosis

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  • [CommentIn] Am J Clin Pathol. 2009 May;131(5):615-7 [19369618.001]
  • (PMID = 19369630.001).
  • [ISSN] 1943-7722
  • [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] 0 / DNA, Neoplasm; 0 / Mucins; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
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19. Li R, Wang H, Bekele BN, Yin Z, Caraway NP, Katz RL, Stass SA, Jiang F: Identification of putative oncogenes in lung adenocarcinoma by a comprehensive functional genomic approach. Oncogene; 2006 Apr 27;25(18):2628-35
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  • [Title] Identification of putative oncogenes in lung adenocarcinoma by a comprehensive functional genomic approach.
  • We used a functional genomic approach that integrated simultaneous genomic and transcript microarray, proteomics, and tissue microarray analyses to directly identify putative oncogenes in lung adenocarcinoma.
  • We first identified 183 genes with increases in both genomic copy number and transcript in six lung adenocarcinoma cell lines.
  • Parallel fluorescence in situ hybridization and immunohistochemical analyses of EEF1A2 and KCIP-1 in tissue microarrays from patients with lung adenocarcinoma showed that gene amplification was associated with high protein expression for both genes and that protein overexpression was related to tumor grade, disease stage, Ki-67 expression, and a shorter survival of patients.
  • The amplification of EEF1A2 and KCIP-1 and the presence of overexpressed protein in tumor samples strongly suggest that these genes could be oncogenes and hence potential targets for diagnosis and therapy in lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Gene Expression Regulation, Neoplastic. Lung Neoplasms / genetics. Neoplasm Proteins / genetics. Oncogenes / genetics
  • [MeSH-minor] Electrophoresis, Gel, Two-Dimensional. Gene Amplification. Gene Dosage. Gene Expression Profiling. Genomics. Humans. In Situ Hybridization, Fluorescence. Oligonucleotide Array Sequence Analysis. Peptide Elongation Factor 1 / antagonists & inhibitors. Peptide Elongation Factor 1 / genetics. Peptide Elongation Factor 1 / metabolism. RNA, Small Interfering / genetics. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization. Tissue Array Analysis. Tumor Cells, Cultured

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  • (PMID = 16369491.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA113707-01; United States / NCI NIH HHS / CA / P50 CA70907
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / EEF1A2 protein, human; 0 / Neoplasm Proteins; 0 / Peptide Elongation Factor 1; 0 / RNA, Small Interfering
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20. Lu HD, Huang T, Shen WZ, Zhen Y, Kong QZ: [Effect of tankyrase antisense oligonucleotide combined human telomerase reverse transcriptase antisense oligonucleotide on telomere dynamics in human lung adenocarcinoma A549 cells]. Ai Zheng; 2007 Nov;26(11):1164-9
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  • [Title] [Effect of tankyrase antisense oligonucleotide combined human telomerase reverse transcriptase antisense oligonucleotide on telomere dynamics in human lung adenocarcinoma A549 cells].
  • This study was to determine the effect of tankyrase antisense oligonucleotide (asTANKS) combined human telomerase reverse transcriptase antisense oligonucleotide (ashTERT) on telomere dynamics in human lung adenocarcinoma A549 cells.
  • Telomere length was analyzed by quantitative fluorescence in situ hybridization (Q-FISH).
  • [MeSH-major] Lung Neoplasms / pathology. Oligonucleotides, Antisense / pharmacology. Tankyrases / metabolism. Telomerase / metabolism. Telomere / pathology
  • [MeSH-minor] Adenocarcinoma / enzymology. Adenocarcinoma / pathology. Cell Aging / drug effects. Cell Line, Tumor. Humans. RNA, Messenger / metabolism. Transfection

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  • (PMID = 17991312.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Oligonucleotides, Antisense; 0 / RNA, Messenger; EC 2.4.2.30 / Tankyrases; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
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21. Lim WT, Chuah KL, Leong SS, Tan EH, Toh CK: Assessment of human papillomavirus and Epstein-Barr virus in lung adenocarcinoma. Oncol Rep; 2009 Apr;21(4):971-5
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  • [Title] Assessment of human papillomavirus and Epstein-Barr virus in lung adenocarcinoma.
  • The association of human papillomavirus (HPV) and Epstein-Barr virus (EBV) infection with non-small cell lung cancer is controversial.
  • HPV and EBV prevalence in a uniform population of lung adenocarcinoma was investigated, hypothesizing that there would be differences seen between smokers and non-smokers and between sexes.
  • Patients involved in this study were selected from a single institution database of lung cancer.
  • In total 497 patients with adenocarcinoma were identified and 110 patients had sufficient tissue for analysis with an in situ hybridization method that probed for high-risk and low-risk HPV and EBV.
  • There were 65 males and 45 females, 78 patients with stage I-IIIA disease and 32 patients with stage IIIB-IV disease.
  • It is unlikely that HPV or EBV is an important etiological agent in adenocarcinoma of the lung, even among the never-smokers.
  • [MeSH-major] Adenocarcinoma / virology. Herpesvirus 4, Human / isolation & purification. Lung Neoplasms / virology. Papillomaviridae / isolation & purification

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  • (PMID = 19287995.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, T-Lymphocyte; 0 / CD69 antigen; 0 / DNA, Viral; 0 / Lectins, C-Type; 0 / RNA, Viral
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22. Bonanno L, Schiavon M, Nardo G, Bertorelle R, Bonaldi L, Galligioni A, Indraccolo S, Pasello G, Rea F, Favaretto A: Prognostic and predictive implications of EGFR mutations, EGFR copy number and KRAS mutations in advanced stage lung adenocarcinoma. Anticancer Res; 2010 Dec;30(12):5121-8
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  • [Title] Prognostic and predictive implications of EGFR mutations, EGFR copy number and KRAS mutations in advanced stage lung adenocarcinoma.
  • BACKGROUND/AIM: Gefitinib and erlotinib were shown to be particularly effective in a clinically selected subpopulation of non-small cell lung cancer patients (NSCLC): adenocarcinoma histology, non-smoking status, Asian origin and female gender have been associated with improved clinical benefit compared to the unselected NSCLC population.
  • The aim of the present study was to investigate the prognostic and predictive role of EGFR and KRAS analysis in advanced lung adenocarcinomas, selected according to clinical features associated to better response to EGFR tyrosine kinase inhibitors (TKIs), namely female gender and non-smoker or former light smoker status.
  • CONCLUSION: In a group of clinically selected patients, EGFR and KRAS analysis was able to define distinct molecular subsets of lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Genes, erbB-1. Genes, ras. Lung Neoplasms / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Gene Dosage. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Mutation. Retrospective Studies

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  • (PMID = 21187500.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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23. Li F, Wang X, Xu H, Roggli VL: Small neuroendocrine lesions in intrathoracic lymph nodes of patients with primary lung adenocarcinoma: real metastasis? Am J Surg Pathol; 2010 Nov;34(11):1701-7
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  • [Title] Small neuroendocrine lesions in intrathoracic lymph nodes of patients with primary lung adenocarcinoma: real metastasis?
  • The presence of individual neuroendocrine cells in rare peripancreatic lymph nodes (LNs) suggests that neuroendocrine tumor or nested neuroendocrine cell proliferation can arise in situ from neuroendocrine cells native to any LN.
  • We encountered 4 cases of neuroendocrine proliferation in intrathoracic LNs (ILNs) of patients with primary lung adenocarcinoma.
  • All patients had a single lung mass without mediastinal lymphadenopathy based on computed tomography and positron emission tomography imaging.
  • Mediastinal staging was done by either mediastinoscopy or thoracotomy and none of them had metastasis from adenocarcinoma in any LN.
  • One patient had three ILNs positive for neuroendocrine proliferation measuring 1.7, 1.8, and 4.0 mm, respectively and a minute tumorlet less than 1.0 mm in the lung.
  • Three other patients had small areas of neuroendocrine proliferation no more than 1 mm in single ILN without any lung neuroendocrine lesion.
  • Neuroendocrine cells in ILNs often formed nests of varying size with similar morphology to carcinoid tumorlet in the lung.
  • [MeSH-major] Adenocarcinoma / pathology. Cell Proliferation. Lung Neoplasms / pathology. Lymph Nodes / pathology. Neuroendocrine Cells / pathology

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  • (PMID = 20871390.001).
  • [ISSN] 1532-0979
  • [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 / Biomarkers
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24. Jokoji R, Yamasaki T, Minami S, Komuta K, Sakamaki Y, Takeuchi K, Tsujimoto M: Combination of morphological feature analysis and immunohistochemistry is useful for screening of EML4-ALK-positive lung adenocarcinoma. J Clin Pathol; 2010 Dec;63(12):1066-70
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  • [Title] Combination of morphological feature analysis and immunohistochemistry is useful for screening of EML4-ALK-positive lung adenocarcinoma.
  • BACKGROUND: A subset of lung cancers harbours the fusion gene echinoderm microtubule-associated protein-like-4-anaplastic lymphoma kinase (EML4-ALK).
  • Recently, immunohistochemistry for ALK has shown sensitivity for the detection of EML4-ALK-positive lung adenocarcinoma almost equal to that of the fluorescence in situ hybridisation (FISH) assay.
  • AIMS: To study the clinicopathological features of EML4-ALK-positive lung adenocarcinoma in a large number of surgically resected samples using immunohistochemistry, in order to establish a useful screening method for EML4-ALK-positive lung adenocarcinoma.
  • METHODS: Immunohistochemistry for ALK was used to screen for EML4-ALK-positive lung adenocarcinomas in 254 cases of surgically resected samples.
  • RESULTS: EML4-ALK-positive cases were detected in 3.1% of lung adenocarcinomas (8/254).
  • EML4-ALK-positive lung adenocarcinomas showed significant associations with intra- and/or extra-cytoplasmic mucin (p=0.0001), and cribriform pattern with excessive extracytoplasmic mucin (p<0.0001).
  • CONCLUSION: EML4-ALK-positive lung adenocarcinoma has a tendency to express a characteristic morphological pattern.
  • The combined use of morphological feature analysis and immunohistochemistry may be a useful and cost effective screening method for EML4-ALK lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Biomarkers, Tumor / metabolism. Early Detection of Cancer / methods. Lung Neoplasms / pathology. Oncogene Proteins, Fusion / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Differentiation. Cytoplasm / enzymology. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Neoplasm Proteins / metabolism

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  • (PMID = 20935334.001).
  • [ISSN] 1472-4146
  • [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 / Biomarkers, Tumor; 0 / EML4-ALK fusion protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion
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25. Noguchi M, Minami Y, Iijima T, Matsuno Y: Reproducibility of the diagnosis of small adenocarcinoma of the lung and usefulness of an educational program for the diagnostic criteria. Pathol Int; 2005 Jan;55(1):8-13
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  • [Title] Reproducibility of the diagnosis of small adenocarcinoma of the lung and usefulness of an educational program for the diagnostic criteria.
  • Using 32 small adenocarcinomas of the lung including bronchioloalveolar carcinoma (BAC), the reproducibility of diagnosis by the modified diagnostic criteria for small adenocarcinoma (Cancer 75; 2844, 1995) and the effectiveness of an educational program for 27 volunteer general pathologists were examined.
  • The average coincidence rate of the diagnosis before and after the program was 42.4% and 56.6%, respectively.
  • In contrast, the average coincidence rate of six lung cancer specialists was 71.4%, and this was significantly higher than that for general pathologists after the program (P < 0.05).
  • When the cases were divided into two groups (in situ adenocarcinoma (BAC and BAC with alveolar collapse) and early invasive adenocarcinoma), the average coincidence rate for the general pathologists after the program increased to 85.3%, which was significantly higher than that before the program (80.3%; P < 0.05).
  • This trial was thought to provide a theoretical background for the histological diagnosis of peripheral type adenocarcinoma of the lung and to justify the existing diagnostic criteria.
  • [MeSH-major] Adenocarcinoma / diagnosis. Carcinoma in Situ / diagnosis. Lung Neoplasms / diagnosis. Pathology, Surgical / education
  • [MeSH-minor] Diagnosis, Differential. Humans. Reproducibility of Results

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  • (PMID = 15660697.001).
  • [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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26. Noguchi M: Stepwise progression of pulmonary adenocarcinoma--clinical and molecular implications. Cancer Metastasis Rev; 2010 Mar;29(1):15-21
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  • [Title] Stepwise progression of pulmonary adenocarcinoma--clinical and molecular implications.
  • Stepwise progression of pulmonary adenocarcinoma is described from the viewpoint of both pathology and molecular biology.
  • Pulmonary adenocarcinoma develops to invasive carcinoma through atypical adenomatous hyperplasia, adenocarcinoma in situ and minimally invasive adenocarcinoma.
  • On the other hand, in terms of molecular biology, p16 gene inactivation, EGFR mutation and KRAS mutation are early events, and tumors progress to invasive adenocarcinoma as a result of p53 mutation, loss of various chromosomes and other genetic abnormalities.
  • [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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27. Chang JW, Liu HP, Hsieh MH, Fang YF, Hsieh MS, Hsieh JJ, Chiu YT, Tsai HY, Chen YH, Chen YT, Hsu HY, Chen YT, Tsai SF, Chen YR, Hsi BL, Huang SF: Increased epidermal growth factor receptor (EGFR) gene copy number is strongly associated with EGFR mutations and adenocarcinoma in non-small cell lung cancers: a chromogenic in situ hybridization study of 182 patients. Lung Cancer; 2008 Sep;61(3):328-39
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  • [Title] Increased epidermal growth factor receptor (EGFR) gene copy number is strongly associated with EGFR mutations and adenocarcinoma in non-small cell lung cancers: a chromogenic in situ hybridization study of 182 patients.
  • SUMMARY: To evaluate the association of epidermal growth factor receptor (EGFR) gene copy number with EGFR and k-ras mutation status and tyrosine kinase inhibitor (TKI) sensitivity in non-small cell lung cancer (NSCLC), EGFR gene copy number of 182 NSCLC tumor specimens were analyzed by chromogenic in situ hybridization (CISH).
  • CISH-positive tumors were strongly associated with adenocarcinoma (56.8%) compared with squamous cell carcinoma (15.9%) (p<0.0001).
  • Our results suggest Increased EGFR copy number was highly correlated with EGFR mutation in adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Carcinoma, Non-Small-Cell Lung / genetics. Genes, erbB-1 / drug effects. Genes, ras / genetics. Lung Neoplasms / genetics. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Chi-Square Distribution. Erlotinib Hydrochloride. Female. Gene Dosage / drug effects. Humans. In Situ Hybridization. Male. Middle Aged. Mutation. Protein Kinase Inhibitors / therapeutic use. Quinazolines / therapeutic use. Survival Analysis

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  • (PMID = 18304690.001).
  • [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 / Protein Kinase Inhibitors; 0 / Quinazolines; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
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28. Li CM, Han GL, Zhang SJ: [Detection of Epstein-Barr virus in lung carcinoma tissue by in situ hybridization]. Zhonghua Shi Yan He Lin Chuang Bing Du Xue Za Zhi; 2007 Sep;21(3):288-90
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  • [Title] [Detection of Epstein-Barr virus in lung carcinoma tissue by in situ hybridization].
  • OBJECTIVES: To examine the Epstein-Barr virus (EBV) in primary lung carcinoma tissue, and to investigate the relationship between EBV infection and tumorigenesis of lung cancer.
  • METHODS: Formalin-fixed and paraffin-embedded lung tissue specimens from surgically resected lung carcinoma tissues of 108 cases treated in Tanshan area from 2001 to 2006, which were confirmed further by histopathological examination after hematoxylin-eosin (HE) staining, were used to observe the EBV encoded RNA-1 (EBER1) using in situ hybridization (ISH).
  • RESULTS: EBER1 was detected in 36 of the 108 primary lung carcinoma cases, and in 1 of the 22 normal lung tissues.
  • The positive rates of EBV infection in squamous cell carcinoma, adenocarcinoma, small cell carcinoma and large cell carcinoma were 35.9%, 31.6% 31.0%, 1/2, respectively.
  • Gender, age and clinicohistopathological type were not found to have any correlation with EBER1 expression, but EBER1 expression in groups of cases with poorly and moderately differentiated carcinomas was significantly higher than those in the group of cases with well differentiated carcinoma, and the EBER1 expression in the right lung was higher than in the left lung.
  • CONCLUSIONS: The frequency of EBV infection in this series of patients from Tangshan area was 33.3%, the results suggest that there is a relationship between EBV infection and the occurrence of the primary lung carcinoma, EBV infection might be one of the potential causes to induce lung cancer.
  • [MeSH-major] Epstein-Barr Virus Infections / virology. Herpesvirus 4, Human / genetics. In Situ Hybridization / methods. Lung Neoplasms / virology

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  • (PMID = 17971949.001).
  • [ISSN] 1003-9279
  • [Journal-full-title] Zhonghua shi yan he lin chuang bing du xue za zhi = Zhonghua shiyan he linchuang bingduxue zazhi = Chinese journal of experimental and clinical virology
  • [ISO-abbreviation] Zhonghua Shi Yan He Lin Chuang Bing Du Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Epstein-Barr virus encoded RNA 1; 0 / RNA, Viral
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29. El-Zammar OA, Zhang S, Katzenstein AL: Comparison of FISH, PCR, and immunohistochemistry in assessing EGFR status in lung adenocarcinoma and correlation with clinicopathologic features. Diagn Mol Pathol; 2009 Sep;18(3):133-7
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  • [Title] Comparison of FISH, PCR, and immunohistochemistry in assessing EGFR status in lung adenocarcinoma and correlation with clinicopathologic features.
  • The purpose of this study is to investigate the relationship between mutation status, copy number, and protein expression of epidermal growth factor receptor (EGFR) in lung adenocarcinoma, and to correlate the genetic status and clinicopathologic features.
  • Forty-nine adenocarcinomas were tested by polymerase chain reaction (PCR) for EGFR gene mutations, by fluorescence in situ hybridization (FISH) for increased EGFR gene copy number, and by immunohistochemistry (IHC) for EGFR protein expression.
  • No statistically significant differences in mitotic count, age, sex, smoking status, degree of differentiation, or stage were seen.
  • [MeSH-major] Adenocarcinoma / pathology. Immunohistochemistry / methods. In Situ Hybridization, Fluorescence / methods. Lung Neoplasms / pathology. Polymerase Chain Reaction / methods. Receptor, Epidermal Growth Factor / biosynthesis. Receptor, Epidermal Growth Factor / genetics

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  • (PMID = 19704257.001).
  • [ISSN] 1533-4066
  • [Journal-full-title] Diagnostic molecular pathology : the American journal of surgical pathology, part B
  • [ISO-abbreviation] Diagn. Mol. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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30. 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.
  • 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
  • [MeSH-minor] Adult. Aged. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Precancerous Conditions / genetics. Sex Factors. Smoking

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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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31. Motoi N, Szoke J, Riely GJ, Seshan VE, Kris MG, Rusch VW, Gerald WL, Travis WD: Lung adenocarcinoma: modification of the 2004 WHO mixed subtype to include the major histologic subtype suggests correlations between papillary and micropapillary adenocarcinoma subtypes, EGFR mutations and gene expression analysis. Am J Surg Pathol; 2008 Jun;32(6):810-27
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  • [Title] Lung adenocarcinoma: modification of the 2004 WHO mixed subtype to include the major histologic subtype suggests correlations between papillary and micropapillary adenocarcinoma subtypes, EGFR mutations and gene expression analysis.
  • The histologic heterogeneity of lung adenocarcinoma creates a variety of complex challenges to pathologists in analyzing the various subtypes.
  • The tumors were analyzed for KRAS mutation and epidermal growth factor receptor (EGFR) by mutation, chromogenic in situ hybridization, and immunohistochemistry for EGFR and phosphorylated EGFR.
  • Papillary adenocarcinoma strongly correlated with EGFR mutation (P<0.001) and gene profile Cluster 1 (P=0.006) with weaker correlations with low grade (P=0.038) and favorable behavior in Stage 1 patients (P=0.047).
  • Solid adenocarcinoma strongly correlated with gene profile Cluster 3 (P=0.001) and worse survival (P=0.001).
  • No correlation was found with BAC and EGFR by mutation, chromogenic in situ hybridization or immunohistochemistry.
  • Higher stage (P<0.001), grade (P<0.001), and solid subtype (P=0.001) correlated with shorter survival.
  • Our data suggest that EGFR mutations are associated with papillary adenocarcinoma and gene profile Cluster 1.
  • As we do not know the major genetic pathways of 30% to 70% of lung adenocarcinomas, the comprehensive histologic subtyping we propose gives advantage for recognition of unanticipated histologic-genetic correlations that might not be detected using classification systems that focus primarily on specific aspects of adenocarcinomas such as BAC or EGFR mutations.

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  • (PMID = 18391747.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA084999; United States / NCI NIH HHS / CA / UO1CA84999
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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32. Sholl LM, John Iafrate A, Chou YP, Wu MT, Goan YG, Su L, Huang YT, Christiani DC, Chirieac LR: Validation of chromogenic in situ hybridization for detection of EGFR copy number amplification in nonsmall cell lung carcinoma. Mod Pathol; 2007 Oct;20(10):1028-35
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  • [Title] Validation of chromogenic in situ hybridization for detection of EGFR copy number amplification in nonsmall cell lung carcinoma.
  • Epidermal growth factor receptor (EGFR) gene copy number correlates with response to tyrosine kinase inhibitors in patients with nonsmall cell lung carcinoma.
  • Fluorescence in situ hybridization (FISH), a standard methodology to detect EGFR copy number abnormalities in nonsmall cell lung carcinoma, is limited by instrumentation and cost.
  • Chromogenic in situ hybridization (CISH) is an emerging alternative detection technique using light microscopy, but its utility in assessing EGFR copy number in lung cancer is not established.
  • To address the utility of CISH, we studied paraffin-embedded nonsmall cell lung carcinoma specimens from 77 Taiwanese nonsmoking women treated by surgery alone.
  • Tumors were classified as adenocarcinoma (n=28), mixed adenocarcinoma with bronchioloalveolar features (n=25), bronchioloalveolar carcinoma (n=2), squamous cell carcinoma (n=15), and adenosquamous carcinoma (n=7).
  • CISH is an alternative assay to FISH in determining EGFR copy number status that may contribute to stratification of patients with nonsmall cell lung carcinoma for clinical trials and identify a subset of patients that should be treated with tyrosine kinase inhibitors.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Gene Dosage. Genes, erbB-1. In Situ Hybridization / methods. Lung Neoplasms / genetics. Receptor, Epidermal Growth Factor / metabolism
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Cell Nucleus / metabolism. Cell Nucleus / pathology. Chromogenic Compounds / chemistry. Discriminant Analysis. Female. Gene Amplification. Humans. In Situ Hybridization, Fluorescence / methods. Sensitivity and Specificity

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  • (PMID = 17673923.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / CA074386; United States / NCI NIH HHS / CA / CA092824; United States / NCI NIH HHS / CA / CA90578
  • [Publication-type] Comparative Study; 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 / Biomarkers, Tumor; 0 / Chromogenic Compounds; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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33. Morio A, Miyamoto H, Izumi H: Risk of recurrence after surgical resection of small-sized invasive lung adenocarcinoma: analysis based on apoptotic index. Jpn J Thorac Cardiovasc Surg; 2005 Jul;53(7):345-53
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  • [Title] Risk of recurrence after surgical resection of small-sized invasive lung adenocarcinoma: analysis based on apoptotic index.
  • OBJECTIVE: It has been reported that small-sized invasive lung adenocarcinomas, i.e., those classified as type C through type F according to Noguchi's classification, may also recur even after complete resection.
  • We evaluated the prognostic value of molecular biologic markers (apoptosis, Ki-67, p53, epidermal growth factor) and clinicopathological factors in patients with small-sized invasive lung adenocarcinomas.
  • METHODS: The clinical records of all patients who had had a peripheral adenocarcinoma surgically resected between 1996 and 2002, and histologically diagnosed as type C through type F according to Noguchi's classification were retrospectively reviewed.
  • CONCLUSION: Peripheral small-sized invasive lung adenocarcinomas with a low AI carry an increased risk of distant metastases, indicating that adjuvant chemotherapy after complete resection might be needed.
  • [MeSH-major] Adenocarcinoma / surgery. Apoptosis. Lung Neoplasms / surgery. Neoplasm Recurrence, Local
  • [MeSH-minor] Aged. Biomarkers / analysis. Female. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Ki-67 Antigen / analysis. Male. Middle Aged. Neoplasm Invasiveness. Receptor, Epidermal Growth Factor / analysis. Retrospective Studies. Tumor Suppressor Protein p53 / analysis

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  • (PMID = 16095233.001).
  • [ISSN] 1344-4964
  • [Journal-full-title] The Japanese journal of thoracic and cardiovascular surgery : official publication of the Japanese Association for Thoracic Surgery = Nihon Kyōbu Geka Gakkai zasshi
  • [ISO-abbreviation] Jpn. J. Thorac. Cardiovasc. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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34. Shibata T, Uryu S, Kokubu A, Hosoda F, Ohki M, Sakiyama T, Matsuno Y, Tsuchiya R, Kanai Y, Kondo T, Imoto I, Inazawa J, Hirohashi S: Genetic classification of lung adenocarcinoma based on array-based comparative genomic hybridization analysis: its association with clinicopathologic features. Clin Cancer Res; 2005 Sep 1;11(17):6177-85
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  • [Title] Genetic classification of lung adenocarcinoma based on array-based comparative genomic hybridization analysis: its association with clinicopathologic features.
  • To analyze the genetic alterations of primary lung adenocarcinoma in a high-throughput way, we used laser-capture microdissection of cancer cells and array comparative genomic hybridization focusing on 800 chromosomal loci containing cancer-related genes.
  • Unsupervised hierarchical clustering analysis of multiple alterations revealed three subgroups of lung adenocarcinoma that were characterized by the accumulation of distinct genetic alterations and associated with smoking history and gender.
  • Our results suggest that there exist multiple molecular carcinogenesis pathways in lung adenocarcinoma that may associate with smoking habits and gender, and that genetic cancer profiling will reveal previously uncharacterized genetic heterogeneity of cancer and be beneficial in estimating patient prognosis and discovering novel cancer-related genes including therapeutic targets.
  • [MeSH-major] Adenocarcinoma / classification. Adenocarcinoma / genetics. Lung Neoplasms / classification. Lung Neoplasms / genetics. Nucleic Acid Hybridization. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Adult. Aged. Chromosomes, Artificial, Bacterial. Chromosomes, Human / genetics. DNA, Neoplasm / genetics. Female. Gene Amplification. Gene Deletion. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Genes, erbB-1 / physiology. Humans. In Situ Hybridization, Fluorescence. Male. Microarray Analysis. Middle Aged. Mutation / genetics

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  • (PMID = 16144918.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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35. Striebel JM, Dacic S, Yousem SA: Gross cystic disease fluid protein-(GCDFP-15): expression in primary lung adenocarcinoma. Am J Surg Pathol; 2008 Mar;32(3):426-32
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  • [Title] Gross cystic disease fluid protein-(GCDFP-15): expression in primary lung adenocarcinoma.
  • A total of 211 cases of primary lung adenocarcinoma were tested for expression of gross cystic disease fluid protein-15 (GCDFP-15) and only 11 cases (5.2%) were positive.
  • This report details the first 11 cases of pulmonary adenocarcinoma to express GCDFP-15 and their distinctive morphology with frequent mucin production and coexpression of thyroid transcription factor-1 and synaptophysin.
  • [MeSH-major] Adenocarcinoma / chemistry. Adenocarcinoma / pathology. Carrier Proteins / analysis. Glycoproteins / analysis. Lung Neoplasms / chemistry. Lung Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma, Papillary / chemistry. Adenocarcinoma, Papillary / pathology. Aged. Female. Histocytochemistry. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Mucins / analysis. Nuclear Proteins / analysis. Synaptophysin / analysis. Transcription Factors / analysis

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  • (PMID = 18300807.001).
  • [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 / Carrier Proteins; 0 / Glycoproteins; 0 / Mucins; 0 / Nuclear Proteins; 0 / PIP protein, human; 0 / Synaptophysin; 0 / Transcription Factors; 0 / thyroid nuclear factor 1
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36. Ilie MI, Hofman V, Bonnetaud C, Havet K, Lespinet-Fabre V, Coëlle C, Gavric-Tanga V, Vénissac N, Mouroux J, Hofman P: Usefulness of tissue microarrays for assessment of protein expression, gene copy number and mutational status of EGFR in lung adenocarcinoma. Virchows Arch; 2010 Oct;457(4):483-95
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  • [Title] Usefulness of tissue microarrays for assessment of protein expression, gene copy number and mutational status of EGFR in lung adenocarcinoma.
  • Specific inhibitors targeting the epidermal growth factor receptor (EGFR) can increase survival rates in certain lung adenocarcinoma patients with mutations in the EGFR gene.
  • Although such EGFR-targeted therapies have been approved for use, there is no general consensus among surgical pathologists on how the EGFR status should be tested in lung adenocarcinoma tissues and whether the results of immunohistochemistry (IHC), fluorescence in situ hybridization (FISH), and mutational analysis by molecular methods correlate.
  • We evaluated the EGFR status in 61 lung adenocarcinomas by IHC (using total and mutant-specific antibodies against EGFR), by FISH analysis on tissue microarrays (TMAs), and by direct sequencing.
  • Taken together, these results demonstrate the high potential of TMAs to test for the major mechanisms of EGFR activation in patients with lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / chemistry. Gene Dosage. Lung Neoplasms / chemistry. Mutation. Receptor, Epidermal Growth Factor / analysis. Tissue Array Analysis / methods
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Middle Aged

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  • (PMID = 20803030.001).
  • [ISSN] 1432-2307
  • [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] EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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37. Anagnostou VK, Bepler G, Syrigos KN, Tanoue L, Gettinger S, Homer RJ, Boffa D, Detterbeck F, Rimm DL: High expression of mammalian target of rapamycin is associated with better outcome for patients with early stage lung adenocarcinoma. Clin Cancer Res; 2009 Jun 15;15(12):4157-64
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  • [Title] High expression of mammalian target of rapamycin is associated with better outcome for patients with early stage lung adenocarcinoma.
  • Despite the well known role of mTOR in carcinogenesis, its prognostic potential in lung cancer has not been investigated.
  • EXPERIMENTAL DESIGN: Automated quantitative analysis (AQUA), a fluorescent-based method for analysis of in situ protein expression, was used to assess mTOR expression in a training cohort of 167 lung cancer patients.
  • An independent cohort of 235 lung cancer patients (from a second institution) was used for validation.
  • Patients with high mTOR expression had a longer median overall survival compared with the low expressers (52.7 versus 38.5 months; log rank P = 0.06), which was more prominent in the adenocarcinoma group (55.7 versus 38.88 months; log rank P = 0.018).
  • Multivariate analysis revealed an independent lower risk of death for adenocarcinoma and adenocarcinoma stage IA patients with mTOR-expressing tumors (hazard ratio, 0.48; 95% confidence interval, 0.24-0.98; P = 0.04, and hazard ratio, 0.12; 95% confidence interval, 0.03-0.72; P = 0.019, respectively).
  • CONCLUSIONS: mTOR expression defines a subgroup of patients with a favorable outcome and may be useful for prognostic stratification of lung adenocarcinoma patients as well as incorporation of mTOR into clinical decisions.
  • [MeSH-major] Adenocarcinoma / pathology. Biomarkers, Tumor / biosynthesis. Lung Neoplasms / pathology. Protein Kinases / biosynthesis

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  • (PMID = 19509151.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases
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38. Barletta JA, Perner S, Iafrate AJ, Yeap BY, Weir BA, Johnson LA, Johnson BE, Meyerson M, Rubin MA, Travis WD, Loda M, Chirieac LR: Clinical significance of TTF-1 protein expression and TTF-1 gene amplification in lung adenocarcinoma. J Cell Mol Med; 2009 Aug;13(8B):1977-86
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  • [Title] Clinical significance of TTF-1 protein expression and TTF-1 gene amplification in lung adenocarcinoma.
  • The majority of lung adenocarcinomas express the lineage-specific thyroid transcription factor-1 (TTF-1).
  • We recently reported that in a subset of lung adenocarcinomas the TTF-1 gene is amplified.
  • We studied 89 consecutive patients with lung adenocarcinomas treated by surgery at Brigham and Women's Hospital between 1997 and 1999 and performed immunohistochemical analysis for TTF-1 expression and fluorescence in situ hybridization for TTF-1 amplification.
  • In patients with lung adenocarcinoma, TTF-1 expression is a predictor of good outcome.

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  • (PMID = 19040416.001).
  • [ISSN] 1582-4934
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P20 CA090578; United States / NCI NIH HHS / CA / R01 CA092824; United States / NCI NIH HHS / CA / CA092824; United States / NCI NIH HHS / CA / R01 CA074386; United States / NCI NIH HHS / CA / CA074386; United States / NCI NIH HHS / CA / CA90578; United States / NCI NIH HHS / CA / CA090578-01A10003; United States / NCI NIH HHS / CA / P50 CA090578; United States / NCI NIH HHS / CA / P20 CA090578-01A10003
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / thyroid nuclear factor 1
  • [Other-IDs] NLM/ NIHMS120847; NLM/ PMC2830395
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39. 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).
  • [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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40. Bubendorf L, Savic S: [Predictive EGFR gene analyses in cytology]. Pathologe; 2009 Dec;30 Suppl 2:136-9
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  • [Transliterated title] Prädiktive EGFR-Genanalysen in der Zytologie.
  • EGFR mutations and EGFR gene copy number are considered as predictive markers for response to EGFR tyrosine kinase inhibitors in non-small cell lung cancer (NSCLC).NSCLC are often diagnosed by cytology alone.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Genetic Markers / genetics. Lung Neoplasms / genetics. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / genetics. Adenocarcinoma / pathology. Antineoplastic Agents / therapeutic use. Biopsy, Fine-Needle. DNA Mutational Analysis. DNA, Neoplasm / analysis. DNA, Neoplasm / genetics. False Positive Reactions. Humans. In Situ Hybridization, Fluorescence. Lung / pathology. Microdissection / instrumentation. Polymerase Chain Reaction. Predictive Value of Tests. Prognosis. Protein-Tyrosine Kinases / antagonists & inhibitors. Sequence Analysis, DNA

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  • (PMID = 19859710.001).
  • [ISSN] 1432-1963
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA, Neoplasm; 0 / Genetic Markers; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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41. Rodig SJ, Mino-Kenudson M, Dacic S, Yeap BY, Shaw A, Barletta JA, Stubbs H, Law K, Lindeman N, Mark E, Janne PA, Lynch T, Johnson BE, Iafrate AJ, Chirieac LR: Unique clinicopathologic features characterize ALK-rearranged lung adenocarcinoma in the western population. Clin Cancer Res; 2009 Aug 15;15(16):5216-23
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  • [Title] Unique clinicopathologic features characterize ALK-rearranged lung adenocarcinoma in the western population.
  • PURPOSE: The anaplastic large cell kinase gene (ALK) is rearranged in approximately 5% of lung adenocarcinomas within the Asian population.
  • We evaluated the incidence and the characteristics of ALK-rearranged lung adenocarcinomas within the western population and the optimal diagnostic modality to detect ALK rearrangements in routine clinical practice.
  • EXPERIMENTAL DESIGN: We tested 358 lung adenocarcinomas from three institutions for ALK rearrangements by fluorescent in situ hybridization (FISH) and immunohistochemistry with and without tyramide amplification.
  • RESULTS: We identified 20 (5.6%) lung adenocarcinomas with ALK rearrangements within our cohort of western patients.
  • ALK rearrangement was associated with younger age (P = 0.0002), never smoking (P < 0.0001), advanced clinical stage (P = 0.0001), and a solid histology with signet-ring cells (P < 0.0001).
  • CONCLUSIONS: Lung adenocarcinomas with ALK rearrangements are uncommon in the western population and represent a distinct entity of carcinomas with unique characteristics.
  • For suspected cases, dual diagnostic testing, with FISH and immunohistochemistry, should be considered to accurately identify lung adenocarcinomas with ALK rearrangement.

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  • (PMID = 19671850.001).
  • [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 / CA136851-02; United States / PHS HHS / / R01-135257; United States / PHS HHS / / R01-136851; United States / NCI NIH HHS / CA / P50 CA090578; United States / NCI NIH HHS / CA / R01 CA136851-02; United States / NCI NIH HHS / CA / R01 CA136851; United States / NCI NIH HHS / CA / 2P50 CA090578-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Other-IDs] NLM/ NIHMS198972; NLM/ PMC2865649
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42. 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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43. Kim YT, Kim TY, Lee DS, Park SJ, Park JY, Seo SJ, Choi HS, Kang HJ, Hahn S, Kang CH, Sung SW, Kim JH: Molecular changes of epidermal growth factor receptor (EGFR) and KRAS and their impact on the clinical outcomes in surgically resected adenocarcinoma of the lung. Lung Cancer; 2008 Jan;59(1):111-8
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  • [Title] Molecular changes of epidermal growth factor receptor (EGFR) and KRAS and their impact on the clinical outcomes in surgically resected adenocarcinoma of the lung.
  • Recent studies have reported that clinical response to epidermal growth factor receptor (EGFR) inhibitors is associated with somatic changes of EGFR in the advanced stage of lung cancer.
  • However, there is no clear data demonstrating whether such molecular changes of EGFR per se can affect the clinical outcome of early stage cancer after surgical resection.
  • DNA mutations of EGFR and KRAS were investigated in 71 adenocarcinoma patients who received surgical resection.
  • Fluorescence in situ hybridization (FISH) of EGFR gene amplification was performed in 48 samples.
  • However, the EGFR mutation was not associated with age, gender, or clinical stage.
  • The amplification of EGFR copy was frequently observed in the female gender (12/29 (41.4%):3/19 (15.8%); p=0.061) and in the advanced stage (> or =Stage IIIA, 9/19 (47.4%):6/29 (20.7%); p=0.051).
  • KRAS mutations (p=0.000), male gender (p=0.001), absence of BAC feature (p=0.003), advanced stage (p=0.039), and smoking history (p=0.030) were poor prognostic factors for overall survival, whereas EGFR mutation (p=0.184) and amplification (p=0.756) were not.
  • The presence of EGFR mutation was not a prognostic factor of the clinical outcome of early lung cancer after surgical resection.
  • This result provides an important message for the protocol design of future trials of EGFR inhibitors in early lung cancer.
  • DNA mutations of EGFR and KRAS were investigated in 71 adenocarcinoma patients who received surgical resection.
  • Whereas KRAS mutation was a poor prognostic factor, EGFR mutation was not, and its presence per se did not affect the clinical outcome of early lung cancer after surgical resection.
  • [MeSH-major] Adenocarcinoma / genetics. Genes, ras. Lung Neoplasms / genetics. Mutation. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged

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  • (PMID = 17904685.001).
  • [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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44. Kume M, Taguchi T, Okada H, Anayama T, Tominaga A, Shuin T, Sasaguri S: Establishment and molecular cytogenetic characterization of non-small cell lung cancer cell line KU-T1 by multicolor fluorescence in situ hybridization, comparative genomic hybridization, and chromosome microdissection. Cancer Genet Cytogenet; 2007 Dec;179(2):93-101
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  • [Title] Establishment and molecular cytogenetic characterization of non-small cell lung cancer cell line KU-T1 by multicolor fluorescence in situ hybridization, comparative genomic hybridization, and chromosome microdissection.
  • A human lung adenocarcinoma cell line, designated KU-T1, was established from a Japanese man in Kochi Medical School.
  • Conventional banding and multicolor fluorescence in situ hybridization (M-FISH) analyses of KU-T1 cells revealed a hyperdiploid chromosomal constitution and complex karyotypes.
  • [MeSH-major] Adenocarcinoma / genetics. Carcinoma, Non-Small-Cell Lung / genetics. Cell Line, Tumor. Cytogenetic Analysis / methods. Lung Neoplasms / genetics
  • [MeSH-minor] Aged. Chromosome Aberrations. Chromosome Banding. Humans. Hybridization, Genetic. In Situ Hybridization, Fluorescence. Karyotyping. Male. Microdissection

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  • (PMID = 18036395.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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45. Liu K, Jiang L, Zhou X: Association of p73 G4C14-to-A4T14 polymorphism at exon 2 with the response of human lung adenocarcinoma cell lines to chemotherapy. Cell Biol Int; 2010 Feb;34(2):185-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association of p73 G4C14-to-A4T14 polymorphism at exon 2 with the response of human lung adenocarcinoma cell lines to chemotherapy.
  • In order to assess the effect of p73 gene polymorphism G4C14-A4T14 on cisplatin-based chemosensitivity of human lung adenocarcinoma cell lines, we examined the differences in biological character and drug sensitivity affected by cisplatin between human lung adenocarcinoma cell lines A549 and P15.
  • P73 G4C14-A4T14 polymorphisms at exon 2 existed in human NSCLC (non-small-cell lung cancer) cell lines.
  • Our data in vitro suggest that p73 G4C14-A4T14 polymorphism has no significant relationship to the cisplatin-based chemosensitivity in human lung adenocarcinoma.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / drug therapy. DNA-Binding Proteins / genetics. Lung Neoplasms / drug therapy. Nuclear Proteins / genetics. Polymorphism, Genetic. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Alleles. Antineoplastic Agents / pharmacology. Apoptosis. Cell Line, Tumor. Cisplatin / pharmacology. Exons. Genotype. Homozygote. Humans. In Situ Nick-End Labeling

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  • (PMID = 19947923.001).
  • [ISSN] 1095-8355
  • [Journal-full-title] Cell biology international
  • [ISO-abbreviation] Cell Biol. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Tumor Suppressor Proteins; 0 / tumor suppressor protein p73; Q20Q21Q62J / Cisplatin
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46. Ikeda S, Takabe K, Inagaki M, Funakoshi N, Suzuki K: [Detection of ALK positive pulmonary adenocarcinoma using immunostaining]. Rinsho Byori; 2010 Jun;58(6):565-70
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  • [Title] [Detection of ALK positive pulmonary adenocarcinoma using immunostaining].
  • Although ALK-positive lung cancer cases have been recently reported, it is impossible to detect using only morphology technique.
  • We investigated whether ALK-positive lung cancer could be detected using a conventional immunostaining method.
  • Resected lung adenocarcinoma samples from 88 nonsmoker cases were selected and screening was performed using ALK immunostaining in 24 cases that did not have the EGFR or k-ras mutation.
  • Detection by immunostaining was found useful for ALK mutated lung cancer cases, though the pretreatment and detection methods utilized are important.
  • [MeSH-major] Adenocarcinoma / diagnosis. Biomarkers, Tumor / analysis. Biomarkers, Tumor / genetics. Lung Neoplasms / diagnosis. Mutation. Oncogene Proteins, Fusion / analysis. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Aged. Aged, 80 and over. Chimerin Proteins / genetics. Female. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 20662267.001).
  • [ISSN] 0047-1860
  • [Journal-full-title] Rinsho byori. The Japanese journal of clinical pathology
  • [ISO-abbreviation] Rinsho Byori
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Chimerin Proteins; 0 / EML4-ALK fusion protein, human; 0 / Oncogene Proteins, Fusion
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47. Sholl LM, Yeap BY, Iafrate AJ, Holmes-Tisch AJ, Chou YP, Wu MT, Goan YG, Su L, Benedettini E, Yu J, Loda M, Jänne PA, Christiani DC, Chirieac LR: Lung adenocarcinoma with EGFR amplification has distinct clinicopathologic and molecular features in never-smokers. Cancer Res; 2009 Nov 1;69(21):8341-8
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  • [Title] Lung adenocarcinoma with EGFR amplification has distinct clinicopathologic and molecular features in never-smokers.
  • In a subset of lung adenocarcinomas, the epidermal growth factor receptor (EGFR) is activated by kinase domain mutations and/or gene amplification, but the interaction between the two types of abnormalities is complex and unclear.
  • For this study, we selected 99 consecutive never-smoking women of East Asian origin with lung adenocarcinomas that were characterized by histologic subtype.
  • We analyzed EGFR mutations by PCR-capillary sequencing, EGFR copy number abnormalities by fluorescence and chromogenic in situ hybridization and quantitative PCR, and EGFR expression by immunohistochemistry with both specific antibodies against exon 19 deletion-mutated EGFR and total EGFR.
  • Lung adenocarcinomas with EGFR amplification had significantly more EGFR exon 19 deletion mutations than adenocarcinomas with disomy, and low and high polysomy (100% versus 54%, P = 0.009).
  • EGFR amplification occurred invariably on the mutated and not the wild-type allele (median mutated/wild-type ratios 14.0 versus 0.33, P = 0.003), was associated with solid histology (P = 0.008), and advanced clinical stage (P = 0.009).
  • EGFR amplification was focally distributed in lung cancer specimens, mostly in regions with solid histology.
  • Patients with EGFR amplification had a significantly worse outcome in univariate analysis (median disease-free survival, 16 versus 31 months, P = 0.01) and when adjusted for stage (P = 0.027).
  • Lung adenocarcinomas with EGFR amplification have a unique association with exon 19 deletion mutations and show distinct clinicopathologic features associated with a significantly worsened prognosis.

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  • (PMID = 19826035.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P20 CA090578; United States / NCI NIH HHS / CA / CA092824; United States / NCI NIH HHS / CA / CA074386; United States / NCI NIH HHS / CA / CA090578-01A10003; United States / NCI NIH HHS / CA / P50 CA090578; United States / NCI NIH HHS / CA / R0I CA114465; United States / NCI NIH HHS / CA / R01 CA114465; United States / NCI NIH HHS / CA / P20 CA090578-01A10003
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 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
  • [Other-IDs] NLM/ NIHMS143923; NLM/ PMC2783286
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48. Ikeda S, Takabe K, Inagaki M, Funakoshi N, Suzuki K: Detection of gene point mutation in paraffin sections using in situ loop-mediated isothermal amplification. Pathol Int; 2007 Sep;57(9):594-9
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  • [Title] Detection of gene point mutation in paraffin sections using in situ loop-mediated isothermal amplification.
  • An in situ LAMP method was used, along with an amplification refractory mutation system (ARMS) to directly detect a specific point mutation, L858R, which is a mutation of epidermal growth factor receptor (EGFR), useful for the prediction of the effects of the anti-lung cancer drug gefitinib.
  • The investigation was done using two types of cultured cells as well as paraffin-sectioned specimens collected from 26 cases of surgically resected lung cancer.
  • Twelve of the specimens had an L858R mutation and in situ LAMP showed reactions in the nuclei of all cancer cells present in those.
  • Such reactions were also shown on in situ LAMP in three of the remaining 14 cases that were without the L858R mutation.
  • In addition, a few cases showed responses in the nuclei of bronchial epithelium cells located in non-cancerous areas in the vicinity of a positive tumor, which suggested that the mutation had already occurred in the tumorigenic early stage.
  • [MeSH-major] Adenocarcinoma / genetics. DNA Mutational Analysis / methods. DNA, Neoplasm / analysis. Lung Neoplasms / genetics. Nucleic Acid Amplification Techniques / methods. Paraffin Embedding. Point Mutation

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  • (PMID = 17685931.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Validation Studies
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / DNA, Neoplasm; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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49. Tanaka R, Ishiyama T, Uchihara T, Inadome Y, Iijima T, Morishita Y, Kano J, Goya T, Noguchi M: Expression of the Bax inhibitor-1 gene in pulmonary adenocarcinoma. Cancer; 2006 Feb 1;106(3):648-53
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  • [Title] Expression of the Bax inhibitor-1 gene in pulmonary adenocarcinoma.
  • METHODS: Surgically resected lung specimens were obtained from 32 patients with peripheral adenocarcinomas, and BI-1 gene expression was examined and compared with expression of the p53, bcl-2 and Bax genes.
  • RESULTS: Fourteen of 32 tumors (43.8%) were positive for BI-1 gene expression by in situ hybridization.
  • Patients who had BI-1-positive adenocarcinoma showed a relatively favorable prognosis compared with patients who had BI-1-negative adenocarcinoma.
  • CONCLUSIONS: BI-1 gene expression was restricted to tumor cells with lepidic growth and was a prognostic factor for peripheral-type adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Apoptosis / genetics. Lung Neoplasms / genetics. Proteins / analysis

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  • [Copyright] Copyright (c) 2005 American Cancer Society.
  • (PMID = 16353209.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Membrane Proteins; 0 / Proteins; 0 / TMBIM6 protein, human
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50. Park EA, Lee HJ, Kim YT, Kang CH, Kang KW, Jeon YK, Goo JM, Lee CH, Park CM: EGFR gene copy number in adenocarcinoma of the lung by FISH analysis: investigation of significantly related factors on CT, FDG-PET, and histopathology. Lung Cancer; 2009 May;64(2):179-86
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  • [Title] EGFR gene copy number in adenocarcinoma of the lung by FISH analysis: investigation of significantly related factors on CT, FDG-PET, and histopathology.
  • However, imaging features related to EGFR gene copy number status in adenocarcinoma are still unknown.
  • We therefore retrospectively analyzed CT, FDG-PET, and histopathologic slides of surgical resected lung adenocarcinoma in 132 patients.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / radiography. Adenocarcinoma / radionuclide imaging. Lung Neoplasms / genetics. Lung Neoplasms / radiography. Lung Neoplasms / radionuclide imaging. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Adult. Aged. Female. Fluorodeoxyglucose F18. Gene Dosage. Humans. Image Interpretation, Computer-Assisted. In Situ Hybridization, Fluorescence. Male. Middle Aged. Positron-Emission Tomography. Radiopharmaceuticals. Retrospective Studies. Tomography, X-Ray Computed

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  • (PMID = 18819724.001).
  • [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
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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51. Li X, Zhang Q, Cai L, Wang Y, Wang Q, Huang X, Fu S, Bai J, Liu J, Zhang G, Qi J: Inhibitor of growth 4 induces apoptosis in human lung adenocarcinoma cell line A549 via Bcl-2 family proteins and mitochondria apoptosis pathway. J Cancer Res Clin Oncol; 2009 Jun;135(6):829-35
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  • [Title] Inhibitor of growth 4 induces apoptosis in human lung adenocarcinoma cell line A549 via Bcl-2 family proteins and mitochondria apoptosis pathway.
  • In present study, the effects of ING4 on apoptosis and its mechanisms were investigated through the transduction of ING4 cDNA into lung adenocarcinoma cell line A549.
  • [MeSH-major] Adenocarcinoma / physiopathology. Apoptosis / physiology. Cell Cycle Proteins / physiology. Homeodomain Proteins / physiology. Lung Neoplasms / physiopathology. Mitochondria / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Tumor Suppressor Proteins / physiology
  • [MeSH-minor] Animals. Blotting, Western. Caspase 3 / metabolism. Cell Line, Tumor. Cytochromes c / metabolism. Flow Cytometry. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Lung / metabolism. Lung / pathology. Lung / ultrastructure. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Microscopy, Electron. Neoplasm Transplantation. Signal Transduction / physiology. Transfection. Transplantation, Heterologous

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  • (PMID = 19034511.001).
  • [ISSN] 1432-1335
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Homeodomain Proteins; 0 / ING4 protein, human; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Proteins; 9007-43-6 / Cytochromes c; EC 3.4.22.- / Caspase 3
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52. Aviel-Ronen S, Coe BP, Lau SK, da Cunha Santos G, Zhu CQ, Strumpf D, Jurisica I, Lam WL, Tsao MS: Genomic markers for malignant progression in pulmonary adenocarcinoma with bronchioloalveolar features. Proc Natl Acad Sci U S A; 2008 Jul 22;105(29):10155-60
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  • [Title] Genomic markers for malignant progression in pulmonary adenocarcinoma with bronchioloalveolar features.
  • Bronchioloalveolar carcinoma (BAC), a subtype of lung adenocarcinoma (ADC) without stromal, vascular, or pleural invasion, is considered an in situ tumor with a 100% survival rate.
  • BAC-like areas may accompany otherwise invasive adenocarcinoma, referred to as mixed type adenocarcinoma with BAC features (AWBF).
  • Correlative gene expression analyses demonstrated a high percentage of them to be poor prognosis markers in early stage ADC.
  • Quantitative PCR also validated the amplification and overexpression of PDCD6 and TERT on chromosome 5p and the prognostic significance of PDCD6 in early stage ADC patients.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma, Bronchiolo-Alveolar / genetics. Biomarkers, Tumor / genetics. Lung Neoplasms / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Apoptosis Regulatory Proteins / genetics. Calcium-Binding Proteins / genetics. Chromosomal Instability. Chromosome Aberrations. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Neoplasm Invasiveness / genetics. Oligonucleotide Array Sequence Analysis. Polymerase Chain Reaction. Prognosis. Telomerase / genetics

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  • (PMID = 18632575.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE11945
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Biomarkers, Tumor; 0 / Calcium-Binding Proteins; 0 / PDCD6 protein, human; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
  • [Other-IDs] NLM/ PMC2465804
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53. Sun W, Iijima T, Kano J, Kobayashi H, Li D, Morishita Y, Okubo C, Anami Y, Noguchi M: Frequent aberrant methylation of the promoter region of sterile alpha motif domain 14 in pulmonary adenocarcinoma. Cancer Sci; 2008 Nov;99(11):2177-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Frequent aberrant methylation of the promoter region of sterile alpha motif domain 14 in pulmonary adenocarcinoma.
  • In order to identify novel hypermethylated genes in early stage lung adenocarcinoma, we carried out methylated CpG island amplification, modified suppression subtractive hybridization, and methylation-specific polymerase chain reaction to identify aberrant methylation of CpG islands in the A/J mouse lung adenoma model, which histologically mimics the early stage of human pulmonary adenocarcinoma.
  • Two of them showed downregulation of their expression in human lung adenocarcinoma.
  • Most of the lung adenocarcinoma cell lines showed suppressed expression of SAMD14 together with hypermethylation at the promoter region, although an immortalized bronchial epithelium cell line (PL16B) did not show hypermethylation and did express SAMD14.
  • Hypermethylation at the CpG site of the SAMD14 promoter region was detected frequently in early invasive adenocarcinoma (8/24, 33.3%) but not in in situ adenocarcinoma (0/7, 0%) or normal lung tissue (0/31, 0%).
  • [MeSH-major] Adenocarcinoma / genetics. DNA Methylation. Lung Neoplasms / genetics. Promoter Regions, Genetic / genetics. Tumor Suppressor Proteins / genetics

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  • (PMID = 18823374.001).
  • [ISSN] 1349-7006
  • [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 / DNA, Neoplasm; 0 / KIF21A protein, human; 0 / Kif21a protein, mouse; 0 / Tumor Suppressor Proteins; EC 3.6.1.- / Kinesin
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54. Sung JS, Park KH, Kim YH: Genomic alterations of chromosome region 11p as predictive marker by array comparative genomic hybridization in lung adenocarcinoma patients. Cancer Genet Cytogenet; 2010 Apr 1;198(1):27-34
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  • [Title] Genomic alterations of chromosome region 11p as predictive marker by array comparative genomic hybridization in lung adenocarcinoma patients.
  • In this study, we used aCGH to compare genomic alterations in fresh-frozen lung cancer tissues of 21 adenocarcinomas (AdCCs) (11 early relapse and 10 nonrelapse) and identified genomic alterations that showed significant by different frequency between early relapse and nonrelapse AdCCs.
  • To further validate the gain of chromosome 11p region that was identified by array CGH, fluorescence in situ hybridization (FISH) was performed.
  • [MeSH-major] Adenocarcinoma / genetics. Chromosomes, Human, Pair 11. Comparative Genomic Hybridization / methods. DNA Copy Number Variations. Lung Neoplasms / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chromosome Aberrations. Female. Genetic Markers. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Recurrence

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20303011.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers
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55. 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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56. Zhang W, Liu JN, Tan XY: Vaccination with xenogeneic tumor endothelial proteins isolated in situ inhibits tumor angiogenesis and spontaneous metastasis. Int J Cancer; 2009 Jul 1;125(1):124-32
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  • [Title] Vaccination with xenogeneic tumor endothelial proteins isolated in situ inhibits tumor angiogenesis and spontaneous metastasis.
  • In our study, the rat tumor endothelial proteins (EP) were isolated in situ via biotinylation of tumor vascular endothelial luminal surface followed by streptavidin affinity chromatography.
  • [MeSH-major] Adenocarcinoma / blood supply. Carcinoma, Lewis Lung / blood supply. Endothelium, Vascular / chemistry. Lung Neoplasms / blood supply. Mammary Neoplasms, Experimental / blood supply. Neoplasm Proteins / therapeutic use. Neovascularization, Pathologic / prevention & control

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  • (PMID = 19350628.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Immunoglobulin G; 0 / Neoplasm Proteins
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57. Collins BT, Janney CG, Ong M, Cortese C: Fine needle aspiration biopsy of monophasic spindle synovial sarcoma of lung with fluorescence in situ hybridization identification of t(x;18) translocation: a case report. Acta Cytol; 2009 Jan-Feb;53(1):105-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fine needle aspiration biopsy of monophasic spindle synovial sarcoma of lung with fluorescence in situ hybridization identification of t(x;18) translocation: a case report.
  • The diagnosis can be challenging because of the ability to mimic other spindle cell neoplasms.
  • Within the lung, these neoplasms are rare and cytologic descriptions are limited.
  • CASE: A 58-year-old woman was diagnosed with colonic adenocarcinoma; chest computed tomography (CT) revealed a 5-cm solitary pulmonary mass, and CT-guided fine needle aspiration was performed.
  • A diagnosis of spindle cell neoplasm was rendered; it was believed to be a second neoplasm unrelated to the colonic adenocarcinoma.
  • On resection, the neoplasm demonstrated t(x:1 8) chromosomal translocation by fluorescence in situ hybridization.
  • CONCLUSION: In a spindled cell neoplasm arising as a single peripheral pulmonary nodule, monophacir spindle synorvial sarcoma should be considered in the differential diagnosis; detection of the t(x;18) chromosomal translocation can confirm the diagnosis.
  • [MeSH-major] Lung Neoplasms / diagnosis. Neoplasms, Second Primary / diagnosis. Sarcoma, Synovial / diagnosis
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / pathology. Biopsy, Fine-Needle. Chromosomes, Human, Pair 18 / genetics. Colonic Neoplasms / diagnosis. Colonic Neoplasms / pathology. Diagnosis, Differential. Female. Humans. In Situ Hybridization, Fluorescence. Middle Aged. Proto-Oncogene Proteins c-bcl-2 / analysis. Translocation, Genetic. Vimentin / analysis

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  • (PMID = 19248564.001).
  • [ISSN] 0001-5547
  • [Journal-full-title] Acta cytologica
  • [ISO-abbreviation] Acta Cytol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Vimentin
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58. Ishiyama T, Kano J, Anami Y, Onuki T, Iijima T, Morisita Y, Yokota J, Noguchi M: OCIA domain containing 2 is highly expressed in adenocarcinoma mixed subtype with bronchioloalveolar carcinoma component and is associated with better prognosis. Cancer Sci; 2007 Jan;98(1):50-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] OCIA domain containing 2 is highly expressed in adenocarcinoma mixed subtype with bronchioloalveolar carcinoma component and is associated with better prognosis.
  • Although lung adenocarcinoma is a major cause of cancer death worldwide, details of its molecular carcinogenesis and stepwise progression are still unclear.
  • To characterize the sequential progression from bronchioloalveolar adenocarcinoma of the lung (BAC, in situ carcinoma) to adenocarcinoma mixed subtype with BAC component polymerase chain reaction-based cDNA suppression subtractive hybridization (SSH) was carried out using two representative cases of BAC (non-invasive tumors) and adenocarcinoma mixed subtype with BAC (invasive tumors).
  • Through differential screening, virtual reverse northern hybridization and quantitative real-time reverse-transcription-polymerase chain reaction (qRT-PCR) we selected five genes (TncRNA, OCIAD2, ANXA2, TMED4 and LGALS4) that were expressed at significantly higher levels in invasive adenocarcinoma mixed subtype with BAC than in BAC.
  • After in situ hybridization and qRT-PCR analyses, we confirmed that only the OCIAD2 gene showed significantly higher expression in the tumor cells of invasive adenocarcinoma mixed subtype with BAC than in BAC (P = 0.026).
  • We then carried out in situ hybridization of OCIAD2 in 56 adenocarcinoma mixed subtype with BAC component and assessed the correlation between OCIAD2 expression and clinicopathological features.
  • These results suggest that OCIAD2 begins to express at the progression from in situ to invasive carcinoma, and is associated with the favorable prognosis of adenocarcinoma mixed subtype with BAC component.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Lung Neoplasms / genetics. Lung Neoplasms / pathology. Neoplasm Proteins / genetics
  • [MeSH-minor] Aged. Blotting, Northern. Disease Progression. Female. Gene Expression. Gene Expression Profiling. Humans. In Situ Hybridization. Male. Middle Aged. Prognosis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17054434.001).
  • [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 / Neoplasm Proteins; 0 / OCIAD2 protein, human
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59. Zheng Z, Li X, Schell MJ, Chen T, Boulware D, Robinson L, Sommers E, Bepler G: Thymidylate synthase in situ protein expression and survival in stage I nonsmall-cell lung cancer. Cancer; 2008 Jun 15;112(12):2765-73
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  • [Title] Thymidylate synthase in situ protein expression and survival in stage I nonsmall-cell lung cancer.
  • High levels of expression of 2 other genes important in DNA synthesis and repair, RRM1 and ERCC1, are prognostic of survival in early stage nonsmall-cell lung cancer (NSCLC) patients.
  • We hypothesized that intratumoral TS expression would be prognostic of outcome in stage I NSCLC.
  • METHODS: Cytoplasmic tumoral TS was determined by automated in situ protein quantification (AQUA) in 160 patients with completely resected NSCLC that had not received chemotherapy or radiation.
  • In a multivariate analysis adjusting for tumor stage, TS remained significantly prognostic of survival (P=.0013, adjusted P=.032).
  • CONCLUSIONS: In situ cytoplasmic TS protein expression in tumors of patients with resected stage I NSCLC is a clinically important determinant of survival.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / metabolism. Lung Neoplasms / metabolism. Thymidylate Synthase / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Biomarkers, Tumor / analysis. Carcinoma, Large Cell / metabolism. DNA-Binding Proteins / metabolism. Endonucleases / metabolism. Female. Humans. Male. Neoplasms, Squamous Cell / metabolism. Prognosis. RNA, Messenger / metabolism. Smoking. Survival Analysis. Tumor Suppressor Proteins / metabolism

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  • [Copyright] Copyright (c) 2008 American Cancer Society.
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  • (PMID = 18442042.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA102726; United States / NCI NIH HHS / CA / R01 CA102726
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / RNA, Messenger; 0 / RRM1 protein, human; 0 / Tumor Suppressor Proteins; EC 2.1.1.45 / Thymidylate Synthase; EC 3.1.- / ERCC1 protein, human; EC 3.1.- / Endonucleases
  • [Other-IDs] NLM/ NIHMS530227; NLM/ PMC3857609
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60. Lindholm PM, Soini Y, Myllärniemi M, Knuutila S, Heikinheimo M, Kinnula VL, Salmenkivi K: Expression of GATA-6 transcription factor in pleural malignant mesothelioma and metastatic pulmonary adenocarcinoma. J Clin Pathol; 2009 Apr;62(4):339-44
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  • [Title] Expression of GATA-6 transcription factor in pleural malignant mesothelioma and metastatic pulmonary adenocarcinoma.
  • New markers for the prediction of prognosis in MM and in pulmonary adenocarcinoma of the pleura are valuable.
  • AIM: To clarify the distribution and possible function of GATA-6 transcription factor in MM and in pleural metastasis of lung adenocarcinomas.
  • RESULTS: Nuclear immunoreactivity for GATA-6 was stronger and more frequent in MM than in metastatic pleural adenocarcinoma.
  • GATA-6 was not associated with spontaneous proliferation or apoptosis of the tumour cells in situ.
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adenocarcinoma / secondary. Adenocarcinoma / surgery. Apoptosis. Cell Proliferation. Humans. Immunoenzyme Techniques. In Situ Nick-End Labeling / methods. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Lung Neoplasms / secondary. Lung Neoplasms / surgery. Neoplasm Proteins / metabolism. Prognosis. Survival Analysis. Tumor Cells, Cultured

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  • (PMID = 19060016.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / GATA6 Transcription Factor; 0 / Neoplasm Proteins
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61. Zakowski MF, Hussain S, Pao W, Ladanyi M, Ginsberg MS, Heelan R, Miller VA, Rusch VW, Kris MG: Morphologic features of adenocarcinoma of the lung predictive of response to the epidermal growth factor receptor kinase inhibitors erlotinib and gefitinib. Arch Pathol Lab Med; 2009 Mar;133(3):470-7
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  • [Title] Morphologic features of adenocarcinoma of the lung predictive of response to the epidermal growth factor receptor kinase inhibitors erlotinib and gefitinib.
  • CONTEXT: A subset of lung adenocarcinomas appears preferentially sensitive to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs).
  • Adenocarcinoma subtypes and morphologic features were defined in histologic and cytologic material.
  • EGFR mutations were detected by sequencing, copy number by chromogenic in situ hybridization, and expression by immunohistochemistry.
  • Immunohistochemistry and chromogenic in situ hybridization results were not significantly correlated with EGFR mutations or response to TKIs in this study.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Lung Neoplasms / drug therapy. Lung Neoplasms / pathology. Quinazolines / therapeutic use. Receptor, Epidermal Growth Factor / antagonists & inhibitors

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  • (PMID = 19260752.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA121210
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Quinazolines; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
  • [Other-IDs] NLM/ NIHMS578987; NLM/ PMC4016915
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62. Guerra C, Schuhmacher AJ, Cañamero M, Grippo PJ, Verdaguer L, Pérez-Gallego L, Dubus P, Sandgren EP, Barbacid M: Chronic pancreatitis is essential for induction of pancreatic ductal adenocarcinoma by K-Ras oncogenes in adult mice. Cancer Cell; 2007 Mar;11(3):291-302
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  • [Title] Chronic pancreatitis is essential for induction of pancreatic ductal adenocarcinoma by K-Ras oncogenes in adult mice.
  • Pancreatic ductal adenocarcinoma (PDA), one of the deadliest human cancers, often involves somatic activation of K-Ras oncogenes.
  • [MeSH-major] Carcinoma in Situ / pathology. Carcinoma, Pancreatic Ductal / pathology. Genes, ras. Pancreatic Neoplasms / pathology. Pancreatitis, Chronic / pathology
  • [MeSH-minor] Animals. Cell Lineage. Cell Transformation, Neoplastic. Ceruletide. Doxycycline / pharmacology. Liver Neoplasms / secondary. Lung Neoplasms / secondary. Mice. Mice, Mutant Strains. Mutation. Neoplasm Invasiveness. Pancreas / pathology. Signal Transduction


63. Gupta R, Dastane AM, Forozan F, Riley-Portuguez A, Chung F, Lopategui J, Marchevsky AM: Evaluation of EGFR abnormalities in patients with pulmonary adenocarcinoma: the need to test neoplasms with more than one method. Mod Pathol; 2009 Jan;22(1):128-33
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  • [Title] Evaluation of EGFR abnormalities in patients with pulmonary adenocarcinoma: the need to test neoplasms with more than one method.
  • Patients with advanced pulmonary adenocarcinoma exhibiting overexpression or mutation of epidermal growth factor receptor tend to respond better to targeted therapy with tyrosine kinase inhibitors such as gefitinib and erlotinib.
  • There is no consensus regarding how these neoplasms should be routinely tested for epidermal growth factor receptor (EGFR) and whether the results of immunohistochemistry (IHC), mutation analysis and fluorescent in situ hybridization correlate with each other or are independent predictive variables.
  • We tested 100 pulmonary adenocarcinomas from patients with stage III or IV disease for EGFR abnormalities using IHC, PCR and fluorescent in situ hybridization (FISH) and compared the results using kappa and other statistical methods.
  • The need to standardize the approach to EGFR testing in patients with advanced pulmonary adenocarcinoma is discussed.
  • [MeSH-major] Adenocarcinoma / metabolism. Immunohistochemistry / standards. In Situ Hybridization, Fluorescence / standards. Lung Neoplasms / metabolism. Polymerase Chain Reaction / standards. Receptor, Epidermal Growth Factor / biosynthesis

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  • (PMID = 18997733.001).
  • [ISSN] 1530-0285
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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64. Kalinina T, Güngör C, Thieltges S, Möller-Krull M, Penas EM, Wicklein D, Streichert T, Schumacher U, Kalinin V, Simon R, Otto B, Dierlamm J, Schwarzenbach H, Effenberger KE, Bockhorn M, Izbicki JR, Yekebas EF: Establishment and characterization of a new human pancreatic adenocarcinoma cell line with high metastatic potential to the lung. BMC Cancer; 2010;10:295
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Establishment and characterization of a new human pancreatic adenocarcinoma cell line with high metastatic potential to the lung.
  • Numerous genes were overexpressed, some of which have previously been implicated in pancreatic adenocarcinoma (GATA6, IGFBP3, IGFBP6), while others were detected for the first time (MEMO1, RIOK3).
  • Subcutaneous transplantation of PaCa 5061 into pfp-/-/rag2-/- mice resulted in formation of primary tumors and spontaneous lung metastasis.
  • [MeSH-major] Adenocarcinoma / secondary. Lung Neoplasms / secondary. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Cell Culture Techniques. Cell Line, Tumor. Cell Proliferation. Cell Separation. Cell Shape. DNA-Binding Proteins / deficiency. DNA-Binding Proteins / genetics. Dose-Response Relationship, Drug. Female. Gene Expression Profiling / methods. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Karyotyping. Male. Mice. Mice, Inbred C57BL. Mice, Knockout. Middle Aged. Mutation. Oligonucleotide Array Sequence Analysis. Pore Forming Cytotoxic Proteins / deficiency. Pore Forming Cytotoxic Proteins / genetics. Time Factors. Tumor Burden. Xenograft Model Antitumor Assays


65. Hirsch FR, Dziadziuszko R, Varella-Garcia M, Franklin WA, Gandara DR, Bunn PA Jr: First-generation epidermal growth factor receptor inhibitors in non-small cell lung cancer: clinical impact of the epidermal growth factor receptor fluorescence in situ hybridization assay. J Thorac Oncol; 2008 Jun;3(6 Suppl 2):S138-42
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  • [Title] First-generation epidermal growth factor receptor inhibitors in non-small cell lung cancer: clinical impact of the epidermal growth factor receptor fluorescence in situ hybridization assay.
  • Epidermal growth factor receptor (EGFR) inhibitors have been proven to improve survival in advanced non-small cell lung cancer patients, even after failure of previous chemotherapy.
  • Clinical and demographic factors, i.e., females, never-smokers, patients with Asian ethnicity, or histology of adenocarcinoma, seem all to be favorable factors for clinical outcome, but not sufficient for patient selection.
  • Increased EGFR gene copy number detected by fluorescence in situ hybridization has consistently been shown in several retrospective studies to be a good predictive "marker," especially for EGFR tyrosine kinase inhibitors.
  • The current review summarizes the clinical data based on the first generation EGFR inhibitors and discusses future strategies for exploring the role of EGFR fluorescence in situ hybridization as a selection marker for EGFR inhibitor therapy in non-small cell lung cancer.
  • [MeSH-major] Angiogenesis Inhibitors / administration & dosage. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Receptor, Epidermal Growth Factor / antagonists & inhibitors
  • [MeSH-minor] Biomarkers, Tumor / genetics. Female. Follow-Up Studies. Genetic Predisposition to Disease / epidemiology. Humans. In Situ Hybridization, Fluorescence. Male. Neoplasm Staging. Neovascularization, Pathologic / prevention & control. Risk Assessment. Survival Analysis. Treatment Outcome

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  • (PMID = 18520298.001).
  • [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; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Biomarkers, Tumor; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Number-of-references] 41
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66. Chen YM, Liu JM, Chou TY, Perng RP, Tsai CM, Whang-Peng J: Phase II randomized study of daily gefitinib treatment alone or with vinorelbine every 2 weeks in patients with adenocarcinoma of the lung who failed at least 2 regimens of chemotherapy. Cancer; 2007 May 1;109(9):1821-8
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  • [Title] Phase II randomized study of daily gefitinib treatment alone or with vinorelbine every 2 weeks in patients with adenocarcinoma of the lung who failed at least 2 regimens of chemotherapy.
  • BACKGROUND: The objective of this study was to assess the efficacy of adding chronic, intermittent, low-dose vinorelbine to gefitinib treatment for patients who had adenocarcinoma of the lung who failed>or=2 regimens of chemotherapy.
  • Epidermal growth factor receptor (EGFR) exon 18 through 21 nucleotide sequence analysis and fluorescence in situ hybridization were performed in patients who had tumor tissue specimens available for analysis.
  • CONCLUSIONS: Gefitinib was highly effective in ethnic Chinese patients with adenocarcinoma of the lung who failed previous platinum and taxane treatment.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. DNA Mutational Analysis. Disease-Free Survival. Drug Resistance, Neoplasm. Female. Humans. In Situ Hybridization, Fluorescence. Kaplan-Meier Estimate. Male. Middle Aged. Polymerase Chain Reaction. Quinazolines / administration & dosage. Quinazolines / adverse effects. Receptor, Epidermal Growth Factor / genetics. Vinblastine / administration & dosage. Vinblastine / adverse effects. Vinblastine / analogs & derivatives

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  • [Copyright] Copyright (c) 2007 American Cancer Society
  • (PMID = 17351950.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Quinazolines; 5V9KLZ54CY / Vinblastine; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; Q6C979R91Y / vinorelbine; S65743JHBS / gefitinib
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67. Savai R, Schermuly RT, Voswinckel R, Renigunta A, Reichmann B, Eul B, Grimminger F, Seeger W, Rose F, Hänze J: HIF-1alpha attenuates tumor growth in spite of augmented vascularization in an A549 adenocarcinoma mouse model. Int J Oncol; 2005 Aug;27(2):393-400
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  • [Title] HIF-1alpha attenuates tumor growth in spite of augmented vascularization in an A549 adenocarcinoma mouse model.
  • The aim of this study was to analyze the overall effect of HIF-1 on tumor growth in a mouse model, employing human lung adenocarcinoma A549 cells.
  • We conclude that in lung A549 cells, overexpression of HIF-1alpha negatively affects tumor growth due to decreased proliferation and increased apoptosis, despite augmented angiogenesis.
  • [MeSH-major] Adenocarcinoma / pathology. Cell Proliferation. Lung Neoplasms / pathology. Xenograft Model Antitumor Assays / methods
  • [MeSH-minor] Animals. Apoptosis. Cell Line, Tumor. Cell Survival. Humans. In Situ Nick-End Labeling. Mice. Mice, Nude. Transfection. Vascular Endothelial Growth Factor A / analysis

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  • (PMID = 16010420.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Vascular Endothelial Growth Factor A
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68. Willmore-Payne C, Holden JA, Layfield LJ: Detection of epidermal growth factor receptor and human epidermal growth factor receptor 2 activating mutations in lung adenocarcinoma by high-resolution melting amplicon analysis: correlation with gene copy number, protein expression, and hormone receptor expression. Hum Pathol; 2006 Jun;37(6):755-63
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  • [Title] Detection of epidermal growth factor receptor and human epidermal growth factor receptor 2 activating mutations in lung adenocarcinoma by high-resolution melting amplicon analysis: correlation with gene copy number, protein expression, and hormone receptor expression.
  • Activating mutations in the epidermal growth factor receptor (EGFR) (7p12.3-p12.1) and in the human epidermal growth factor receptor 2 (HER2) (17q21.1) characterize a subset of lung carcinomas.
  • In this study, we used high-resolution melting amplicon analysis to screen for EGFR and human HER2 activating mutations in 39 patients with primary lung adenocarcinoma.
  • The HER2 mutation-positive case was in an adenocarcinoma with bronchioloalveolar features.
  • [MeSH-major] Adenocarcinoma / genetics. Gene Dosage. Lung Neoplasms / genetics. Mutation. Nucleic Acid Amplification Techniques. Receptor, Epidermal Growth Factor / genetics. Receptor, ErbB-2 / genetics
  • [MeSH-minor] Chromosomes, Human, Pair 7. DNA Mutational Analysis. DNA, Neoplasm / analysis. Exons. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Sequence Analysis, DNA


69. Neumann J, Feuerhake F, Kayser G, Wiech T, Aumann K, Passlick B, Fisch P, Werner M, Zur Hausen A: Gene expression profiles of lung adenocarcinoma linked to histopathological grading and survival but not to EGF-R status: a microarray study. BMC Cancer; 2010;10:77
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene expression profiles of lung adenocarcinoma linked to histopathological grading and survival but not to EGF-R status: a microarray study.
  • BACKGROUND: Several different gene expression signatures have been proposed to predict response to therapy and clinical outcome in lung adenocarcinoma.
  • METHODS: Affymetrix Human Genome U133A platform was used to obtain gene expression profiles of 28 pathologically and clinically annotated adenocarcinomas of the lung.
  • EGFR status was determined by fluorescent in situ hybridization and immunohistochemistry.
  • [MeSH-major] Adenocarcinoma / metabolism. Gene Expression Profiling. Lung Neoplasms / metabolism. Receptor, Epidermal Growth Factor / biosynthesis
  • [MeSH-minor] Aged. Aged, 80 and over. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry / methods. In Situ Hybridization, Fluorescence. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Prognosis

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  • (PMID = 20196851.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Other-IDs] NLM/ PMC2843676
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70. Yendamuri S, Vaporciyan AA, Zaidi T, Feng L, Fernandez R, Bekele NB, Hofstetter WL, Jiang F, Mehran RJ, Rice DC, Spitz MR, Swisher SG, Walsh GL, Roth JA, Katz RL: 3p22.1 and 10q22.3 deletions detected by fluorescence in situ hybridization (FISH): a potential new tool for early detection of non-small cell lung Cancer (NSCLC). J Thorac Oncol; 2008 Sep;3(9):979-84
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  • [Title] 3p22.1 and 10q22.3 deletions detected by fluorescence in situ hybridization (FISH): a potential new tool for early detection of non-small cell lung Cancer (NSCLC).
  • BACKGROUND: Our objective was to study the feasibility of detecting chromosomal deletions at 3p22.1 and 10q22.3 by fluorescent in situ hybridization (FISH) and to examine their distribution in different areas of the airway in patients with non-small cell lung cancer.
  • Touch preparations from the tumor (TTP), normal lung parenchyma, and bronchi adjacent to the tumor were also obtained.
  • A significantly higher deletion rate was seen at TTP compared with normal lung parenchyma at both the 3p22.1 and 10 q22.3 (p < 0.0001).
  • This suggests that, FISH analysis of bronchoscopic brushes may be useful for identifying patients at high risk for developing non-small cell lung cancer.

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  • (PMID = 18758299.001).
  • [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 CA070907; United States / NCI NIH HHS / CA / R01 CA055769; United States / NCI NIH HHS / CA / CA 55769; United States / NCI NIH HHS / CA / P50CA70907
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS381558; NLM/ PMC3370669
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71. Nicolas MM, Nayar R, Yeldandi A, De Frias DV: Pulmonary metastasis of a postradiation breast epithelioid angiosarcoma mimicking adenocarcinoma. A case report. Acta Cytol; 2006 Nov-Dec;50(6):672-6
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  • [Title] Pulmonary metastasis of a postradiation breast epithelioid angiosarcoma mimicking adenocarcinoma. A case report.
  • We report a case of metastatic postradiation EAS to the lungs that was mistaken for adenocarcinoma.
  • CASE: A 45-year-old woman who received radiotherapy for ductal carcinoma in situ (DCIS) 5 years previously had a local recurrence a year earlier and recent development of bilateral small pulmonary nodules.
  • Fine needle aspiration biopsy of the lung lesions showed round to oval tumor cells with amphophilic cytoplasm.
  • An interpretation of adenocarcinoma was rendered during assessment for specimen adequacy.
  • Review of the recurrent breast tumor (initially reported as DCIS) and a prior wedge resection of the lung nodules (reported as EAS) showed an epithelial-appearing tumor exhibiting an endothelial immunophenotype CONCLUSION: The cytologic features of EAS may resemble those of other neoplasms.
  • [MeSH-major] Adenocarcinoma / pathology. Breast Neoplasms / pathology. Carcinoma, Intraductal, Noninfiltrating / radiotherapy. Hemangiosarcoma / secondary. Lung Neoplasms / secondary. Neoplasms, Radiation-Induced / pathology. Radiotherapy / adverse effects
  • [MeSH-minor] Biopsy, Fine-Needle / methods. Diagnosis, Differential. Epithelioid Cells / pathology. Female. Humans. Middle Aged

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  • (PMID = 17152281.001).
  • [ISSN] 0001-5547
  • [Journal-full-title] Acta cytologica
  • [ISO-abbreviation] Acta Cytol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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72. Zheng H, Abdel Aziz HO, Nakanishi Y, Masuda S, Saito H, Tsuneyama K, Takano Y: Oncogenic role of JC virus in lung cancer. J Pathol; 2007 Jul;212(3):306-15
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  • [Title] Oncogenic role of JC virus in lung cancer.
  • Here, JCV was examined by targeting its T-antigen in lung carcinomas (n=103) and normal lung tissues (n=18) by nested-PCR followed by Southern blot, real-time PCR, immunohistochemistry, in situ hybridization and in situ PCR.
  • Additionally, expression of Ki-67, caspase-3, beta-catenin, p53, and Rb was analysed by immunohistochemistry on tissue microarrays of lung carcinomas.
  • Normal lung tissue was positive significantly less frequently, and contained a lower copy number of JCV than lung carcinomas (p<0.05), and copies were lower in lung adenocarcinomas than in squamous, small or large cell carcinomas (p<0.05).
  • In situ PCR and immunolabelling revealed JCV positivity in the nuclei of lung carcinoma cells.
  • Age and UICC staging were independent prognostic factors for lung carcinoma patients.
  • These data suggest that JCV may be involved in lung carcinogenesis, especially in tumour types other than adenocarcinoma.
  • Lung carcinomas with higher JCV copy numbers display high proliferation and down-regulation of cell adhesion mediated by membrane beta-catenin.
  • [MeSH-major] Carcinoma / virology. JC Virus / pathogenicity. Lung Neoplasms / virology. Oncogenic Viruses
  • [MeSH-minor] Aged. Aged, 80 and over. Antigens, Viral, Tumor / genetics. Blotting, Southern / methods. Carcinoma, Large Cell / pathology. Carcinoma, Large Cell / virology. Carcinoma, Small Cell / pathology. Carcinoma, Small Cell / virology. Carcinoma, Squamous Cell / pathology. Carcinoma, Squamous Cell / virology. DNA, Viral / analysis. Female. Gene Expression Profiling. Humans. In Situ Hybridization. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Sequence Analysis, DNA

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  • [Copyright] Copyright (c) 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • (PMID = 17534844.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Viral, Tumor; 0 / DNA, Viral; 0 / RNA, Messenger
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73. Anagnostou VK, Syrigos KN, Bepler G, Homer RJ, Rimm DL: Thyroid transcription factor 1 is an independent prognostic factor for patients with stage I lung adenocarcinoma. J Clin Oncol; 2009 Jan 10;27(2):271-8
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  • [Title] Thyroid transcription factor 1 is an independent prognostic factor for patients with stage I lung adenocarcinoma.
  • PURPOSE: Thyroid transcription factor 1 (TTF1) is a transcription factor that regulates the expression of multiple genes involved in lung development.
  • It is preferentially expressed in adenocarcinomas of the lung and has been investigated as a potential prognostic parameter in patients with lung cancer, with conflicting results.
  • PATIENTS AND METHODS: Automated quantitative analysis, a fluorescent-based method for analysis of in situ protein expression, was used to assess a series of cell lines to find the threshold of detection of TTF1 expression.
  • TTF1 was consistently expressed in adenocarcinomas (n = 61 and 73; Spearman rho = 0.313 and 0.4 for the first and second set, respectively; P < .0001) independent of their differentiation and stage.
  • Survival analysis showed that patients with stage I adenocarcinoma with TTF1 expression had a longer median overall survival than those without expression (n = 43, 44.3 v 26.2 months, P = .05 for the first cohort; n = 87; 49.7 v 38.5 months, P = .03 for the second cohort) Multivariate analysis revealed an independent lower risk of death for patients with stage I adenocarcinoma with TTF1-expressing tumors (hazard ratio = 0.479, 95% CI, 0.235 to 0.977; P = .043).
  • CONCLUSION: TTF1 expression defines a subgroup of patients with a favorable outcome and may be useful for prognostic stratification of patients with stage I lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor / biosynthesis. Lung Neoplasms / metabolism. Nuclear Proteins / biosynthesis. Transcription Factors / biosynthesis

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  • (PMID = 19064983.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / thyroid nuclear factor 1
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74. Abdullah M, Schultz H, Kähler D, Branscheid D, Dalhoff K, Zabel P, Vollmer E, Goldmann T: Expression of the acute phase protein haptoglobin in human lung cancer and tumor-free lung tissues. Pathol Res Pract; 2009;205(9):639-47
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  • [Title] Expression of the acute phase protein haptoglobin in human lung cancer and tumor-free lung tissues.
  • As part of an investigation that aimed at illuminating the role of acute phase proteins in the local defense of the lungs, this study is the first to describe the expression and synthesis of haptoglobin in human lung tissues and lung tumors.
  • Prompted by the results obtained from a transcription array study, we analyzed 115 lung (cancer) specimens using immunohistochemistry.
  • Thirty-seven specimens were subjected to mRNA-in situ hybridization.
  • One small cell lung cancer displayed haptoglobin expression.
  • In situ hybridization verified the results of immunohistochemistry.
  • The results were further verified by RT-PCR and Western blot compared to liver tissues, which both showed comparable amounts of haptoglobin mRNA and protein in NSCLC and in liver, while tumor-free lung tissues showed lower expression.
  • Due to the known immunomodulatory effects of haptoglobin, its broad expression and synthesis within human lung tissues strongly suggests a function as a fundamental pulmonary local defense element.
  • [MeSH-major] Haptoglobins / biosynthesis. Lung / metabolism. Lung Neoplasms / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Blotting, Western. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / pathology. Humans. Immunohistochemistry. In Situ Hybridization. Reverse Transcriptase Polymerase Chain Reaction. Small Cell Lung Carcinoma / metabolism. Small Cell Lung Carcinoma / pathology. Tissue Array Analysis

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  • (PMID = 19501987.001).
  • [ISSN] 1618-0631
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Haptoglobins
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75. Wrage M, Ruosaari S, Eijk PP, Kaifi JT, Hollmén J, Yekebas EF, Izbicki JR, Brakenhoff RH, Streichert T, Riethdorf S, Glatzel M, Ylstra B, Pantel K, Wikman H: Genomic profiles associated with early micrometastasis in lung cancer: relevance of 4q deletion. Clin Cancer Res; 2009 Mar 1;15(5):1566-74
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  • [Title] Genomic profiles associated with early micrometastasis in lung cancer: relevance of 4q deletion.
  • PURPOSE: Bone marrow is a common homing organ for early disseminated tumor cells (DTC) and their presence can predict the subsequent occurrence of overt metastasis and survival in lung cancer.
  • EXPERIMENTAL DESIGN: DTCs were identified in bone marrow from lung cancer patients by an immunocytochemical cytokeratin assay.
  • Genomic aberrations and expression profiles of the respective primary tumors were assessed by microarrays and fluorescence in situ hybridization analyses.
  • The most significant results were validated on an independent set of primary lung tumors and brain metastases.
  • Fluorescence in situ hybridization analyses on further primary lung tumor samples confirmed the association between loss of 4q and bone marrow-positive status.
  • The same loss was also found to be common in brain metastases from both small and non-small cell lung cancer patients (39%).
  • [MeSH-major] Brain Neoplasms / genetics. Chromosome Deletion. Chromosomes, Human, Pair 4 / genetics. Gene Expression Profiling. Lung Neoplasms / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / secondary. Adult. Aged. Aged, 80 and over. Carcinoma, Large Cell / genetics. Carcinoma, Large Cell / secondary. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / secondary. Comparative Genomic Hybridization. Female. Gene Dosage. Genome, Human. Humans. In Situ Hybridization, Fluorescence. Lymphatic Metastasis. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Small Cell Lung Carcinoma / genetics. Small Cell Lung Carcinoma / secondary


76. Tanaka H, Yanagisawa K, Shinjo K, Taguchi A, Maeno K, Tomida S, Shimada Y, Osada H, Kosaka T, Matsubara H, Mitsudomi T, Sekido Y, Tanimoto M, Yatabe Y, Takahashi T: Lineage-specific dependency of lung adenocarcinomas on the lung development regulator TTF-1. Cancer Res; 2007 Jul 1;67(13):6007-11
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  • [Title] Lineage-specific dependency of lung adenocarcinomas on the lung development regulator TTF-1.
  • TTF-1 has a decisive role as a master regulatory transcription factor in lung development and in the maintenance of the functions of terminal respiratory unit (TRU) cells.
  • We show that a subset of lung adenocarcinoma cell lines expressing TTF-1, which presumably represent those derived from the TRU lineage, exhibit marked dependence on the persistent expression of TTF-1.
  • The inhibition of TTF-1 by RNA interference (RNAi) significantly and specifically induced growth inhibition and apoptosis in these adenocarcinoma cell lines.
  • Furthermore, a fraction of TTF-1-expressing tumors and cell lines displayed an increase in the gene dosage of TTF-1 in the analysis of 214 patients with non-small-cell lung cancer, including 174 adenocarcinomas, showing a tendency of higher frequency of increased gene copies at metastatic sites than at primary sites (P=0.07, by two-sided Fisher's exact test).
  • These findings strongly suggest that in addition to the development and maintenance of TRU lineages in normal lung, sustained TTF-1 expression may be crucial for the survival of a subset of adenocarcinomas that express TTF-1, providing credence for the lineage-specific dependency model.
  • [MeSH-major] Adenocarcinoma / pathology. DNA-Binding Proteins / physiology. Gene Expression Regulation, Neoplastic. Lung / pathology. Lung Neoplasms / pathology. Nuclear Proteins / metabolism. Transcription Factors / metabolism
  • [MeSH-minor] Apoptosis. Carcinoma, Non-Small-Cell Lung / pathology. Cell Line, Tumor. Cell Lineage. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. RNA Interference. Stem Cells

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  • (PMID = 17616654.001).
  • [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 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / thyroid nuclear factor 1
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77. Dacic S: EGFR assays in lung cancer. Adv Anat Pathol; 2008 Jul;15(4):241-7
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  • [Title] EGFR assays in lung cancer.
  • The development of small-molecule inhibitors of the epidermal growth factor receptor (EGFR) resulted in new therapeutic options for patients with advanced lung cancer.
  • This observation revolutionized understanding of EGFR in lung carcinogenesis and resulted in numerous retrospective studies that correlated patient's response and molecular profile of the lung adenocarcinoma.
  • Multiple methodologic approaches were used including mutational analysis, fluorescence in situ hybridization, and immunohistochemistry.
  • [MeSH-major] Lung Neoplasms / genetics. Mutation / genetics. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / drug therapy. Adenocarcinoma / genetics. Carcinoma, Non-Small-Cell Lung / diagnosis. Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / genetics. Humans. In Situ Hybridization, Fluorescence. Polymerase Chain Reaction. Prognosis

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  • (PMID = 18580100.001).
  • [ISSN] 1533-4031
  • [Journal-full-title] Advances in anatomic pathology
  • [ISO-abbreviation] Adv Anat Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Number-of-references] 61
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78. Saad RS, Liu YL, Silverman JF: Distribution of basal/myoepithelial markers in benign and malignant bronchioloalveolar proliferations of the lung. Appl Immunohistochem Mol Morphol; 2010 May;18(3):219-25
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  • [Title] Distribution of basal/myoepithelial markers in benign and malignant bronchioloalveolar proliferations of the lung.
  • We investigated the staining pattern of commonly used basal cell/myoepithelial markers, such as p63 (a p53-homologous nuclear protein), basal cell-specific cytokeratin antibody (34betaE12, K903), and smooth muscle myosin heavy chain (SMMHC) in benign and malignant bronchioloalveolar proliferations of the lung.
  • We studied 85 lung lesions consisting of 35 bronchioloalveolar carcinoma, 30 well-differentiated adenocarcinoma, and 20 cases of benign lung lesions.
  • In normal lung, p63, K903, and SMMHC decorated the basal cells of large and small airways and occasional cells of terminal bronchioles.
  • For adenocarcinoma, a majority of the cases (28/30, 93%) were negative for p63 and K903; however, SMMHC showed artifactual staining in the desmoplastic stroma in 6/30 (20%) cases.
  • The staining pattern of basal cells in bronchioloalveolar carcinoma supports that these neoplasms may actually be carcinoma in-situ.

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  • (PMID = 20065853.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CKAP4 protein, human; 0 / Membrane Proteins; 68238-35-7 / Keratins; EC 3.6.1.- / Smooth Muscle Myosins
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79. Sartori G, Bettelli S, Schirosi L, Bigiani N, Maiorana A, Cavazza A, Rossi G: Microsatellite and EGFR, HER2 and K-RAS analyses in sclerosing hemangioma of the lung. Am J Surg Pathol; 2007 Oct;31(10):1512-20
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  • [Title] Microsatellite and EGFR, HER2 and K-RAS analyses in sclerosing hemangioma of the lung.
  • We investigated 11 cases of SH by immunohistochemistry, fluorescence in situ hybridization, and polymerase chain reaction-based microsatellite and mutational analyses with particular emphasis on possible alterations of microsatellite loci located at tumor suppressor genes (FHIT, p16, Rb, and p53) involved in lung adenocarcinoma genesis and EGFR, HER2, and K-RAS genes.
  • Fluorescence in situ hybridization and mutational analysis of EGFR and HER2 and also K-RAS sequencing did not reveal molecular alterations, whereas allelic losses at p16 and Rb loci (4 and 2 out of 9 tested cases, respectively) with an identical microsatellite allelic loss pattern in both cuboidal and polygonal cells were observed.
  • The finding of microsatellite alterations in chromosomal regions related to genes deeply involved in early stage lung adenocarcinoma could suggest a possible link between SH and bronchioloalveolar carcinoma, but tumor pathway promoted by EGFR, HER2, and K-RAS does not represent a common molecular mechanism of tumorigenesis.
  • [MeSH-major] Adenocarcinoma / genetics. Microsatellite Repeats. Proto-Oncogene Proteins p21(ras) / genetics. Pulmonary Sclerosing Hemangioma / genetics. Receptor, Epidermal Growth Factor / genetics. Receptor, ErbB-2 / genetics
  • [MeSH-minor] Adult. Biomarkers, Tumor / metabolism. Clone Cells. DNA, Neoplasm / analysis. Disease-Free Survival. Female. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Loss of Heterozygosity. Male. Middle Aged. Polymerase Chain Reaction

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  • (PMID = 17895751.001).
  • [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 / Biomarkers, Tumor; 0 / DNA, Neoplasm; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
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80. Cupp JS, Wrede JE, Cherry AM, Arber DA, George TI: Chromosomal aberrations in a case of synchronous extranodal marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue type and bronchogenic adenocarcinoma. Appl Immunohistochem Mol Morphol; 2008 May;16(3):296-300
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  • [Title] Chromosomal aberrations in a case of synchronous extranodal marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue type and bronchogenic adenocarcinoma.
  • We present the chromosomal aberrations in a case of synchronous extranodal marginal zone B-cell lymphoma and bronchogenic adenocarcinoma with bronchioloalveolar features.
  • Using fluorescence in situ hybridization, we identified deletion of the immunoglobulin heavy chain gene in the lymphomatous component, but not the carcinomatous component.

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  • (PMID = 18301237.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 0 / Neoplasm Proteins; EC 3.4.22.- / Caspases; EC 3.4.22.- / MALT1 protein, human
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81. Dennis JL, Hvidsten TR, Wit EC, Komorowski J, Bell AK, Downie I, Mooney J, Verbeke C, Bellamy C, Keith WN, Oien KA: Markers of adenocarcinoma characteristic of the site of origin: development of a diagnostic algorithm. Clin Cancer Res; 2005 May 15;11(10):3766-72
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  • [Title] Markers of adenocarcinoma characteristic of the site of origin: development of a diagnostic algorithm.
  • PURPOSE: Patients with metastatic adenocarcinoma of unknown origin are a common clinical problem.
  • In the first (training) round, we studied 352 primary adenocarcinomas, from seven main sites (breast, colon, lung, ovary, pancreas, prostate and stomach) and their differential diagnoses.
  • CONCLUSIONS: This classification scheme should enable better prediction on biopsy material of the primary site in patients with metastatic adenocarcinoma of unknown origin, leading to improved management and therapy.
  • [MeSH-major] Adenocarcinoma / diagnosis. Biomarkers, Tumor / analysis. Neoplasms, Unknown Primary / diagnosis
  • [MeSH-minor] Biopsy. Diagnosis, Differential. Humans. Immunohistochemistry. In Situ Hybridization. Predictive Value of Tests. Sensitivity and Specificity

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  • (PMID = 15897574.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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82. Gómez-Román JJ, Martínez MN, Fernández SL, Val-Bernal JF: Epstein-Barr virus-associated adenocarcinomas and squamous-cell lung carcinomas. Mod Pathol; 2009 Apr;22(4):530-7
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  • [Title] Epstein-Barr virus-associated adenocarcinomas and squamous-cell lung carcinomas.
  • Five carcinomas presented typical features of Lymphoepithelioma-like lung carcinomas; but six cases could be classified as squamous-cell carcinomas and eight as adenocarcinomas.
  • A semiquantitative polymerase chain reaction method, Early RNA genes 1 and 2 in situ hybridization as well as Latent membrane protein immunostaining for Epstein-Barr virus DNA, RNA and protein detection methods were used in every case.
  • Otherwise four squamous-cell carcinomas and eight adenocarcinomas (12 cases) demonstrated viral sequences in polymerase chain reaction and/or in situ hybridization analysis in neoplastic cells.
  • [MeSH-major] Adenocarcinoma / virology. Carcinoma, Squamous Cell / virology. Epstein-Barr Virus Infections / epidemiology. Lung Neoplasms / virology
  • [MeSH-minor] Aged. DNA, Viral / analysis. DNA, Viral / isolation & purification. Enzyme-Linked Immunosorbent Assay. Female. Herpesvirus 4, Human / isolation & purification. Humans. Immunohistochemistry. In Situ Hybridization. Male. Middle Aged. Polymerase Chain Reaction. RNA, Viral / analysis. RNA, Viral / isolation & purification

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  • (PMID = 19252476.001).
  • [ISSN] 1530-0285
  • [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 / DNA, Viral; 0 / RNA, Viral
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83. Yoo KJ, Lee HJ, Lee H, Lee KY, Lee SH, Chung HM, Baek KH: Expression and functional analyses of mHAUSP regulating apoptosis of cervical adenocarcinoma cells. Int J Oncol; 2005 Jul;27(1):97-104
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  • [Title] Expression and functional analyses of mHAUSP regulating apoptosis of cervical adenocarcinoma cells.
  • In situ hybridization study showed the global expression of mHAUSP in various organs of embryos, including mesencephalon, spinal cord, lung and genital eminence.
  • [MeSH-minor] Amino Acid Sequence. Animals. Blotting, Northern. Catalytic Domain. Conserved Sequence. Female. Genitalia / embryology. HeLa Cells. Humans. In Situ Hybridization. Lung / embryology. Mesencephalon / metabolism. Mice. Models, Genetic. Molecular Sequence Data. Mutagenesis, Site-Directed. Plasmids / metabolism. Point Mutation. Protein Structure, Tertiary. Spinal Cord / embryology. Time Factors. Tissue Distribution. Tumor Suppressor Protein p53 / metabolism. Ubiquitin / metabolism. Ubiquitin Thiolesterase

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  • (PMID = 15942648.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53; 0 / Ubiquitin; EC 3.1.2.15 / USP7 protein, human; EC 3.1.2.15 / Ubiquitin Thiolesterase; EC 3.4.- / Endopeptidases
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84. Gupta R, Dastane AM, McKenna R Jr, Marchevsky AM: The predictive value of epidermal growth factor receptor tests in patients with pulmonary adenocarcinoma: review of current "best evidence" with meta-analysis. Hum Pathol; 2009 Mar;40(3):356-65
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  • [Title] The predictive value of epidermal growth factor receptor tests in patients with pulmonary adenocarcinoma: review of current "best evidence" with meta-analysis.
  • Epidermal growth factor receptor signaling pathway plays an important role in pulmonary adenocarcinoma biology.
  • Several RCT and other studies have evaluated the value of various tests such as immunohistochemistry, polymerase chain reaction, and fluorescent in situ hybridization for epidermal growth factor receptor detection.
  • Estimated positive predictive values of immunohistochemistry, polymerase chain reaction, and fluorescent in situ hybridization range from 6.5% to 82%%, 7% to 100%, and 11% to 89%, respectively.
  • Meta-analysis of nearly 5000 cases in the literature estimates that all 3 tests significantly predict response to gefitinib in patients with lung cancer.
  • Further studies are needed to clarify the predictive value of epidermal growth factor receptor tests in patients with pulmonary adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / metabolism. Lung Neoplasms / metabolism. Receptor, Epidermal Growth Factor / metabolism

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  • (PMID = 18976796.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Quinazolines; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
  • [Number-of-references] 50
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85. Dacic S, Shuai Y, Yousem S, Ohori P, Nikiforova M: Clinicopathological predictors of EGFR/KRAS mutational status in primary lung adenocarcinomas. Mod Pathol; 2010 Feb;23(2):159-68
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  • [Title] Clinicopathological predictors of EGFR/KRAS mutational status in primary lung adenocarcinomas.
  • Screening for EGFR and KRAS mutations in patients with lung adenocarcinomas can be used to predict the patient's response to EGFR tyrosine kinase inhibitors, but there is a lack of guidelines for testing in clinical practice.
  • We analyzed the morphological and clinicopathological characteristics, including tumor stage, size, presence of scar, inflammatory response, angiolymphatic and pleural invasion, of 345 surgically treated primary lung adenocarcinomas with respect to their EGFR and KRAS mutational profile and EGFR FISH.
  • EGFR and KRAS mutations were found in 33 (10%) and 78 (23%) of lung adenocarcinomas, respectively, whereas 226 (67%) cases were negative for both mutations.
  • The cost-effectiveness of lung carcinoma mutational testing would be improved by initial determination of KRAS mutational status as negative predictor of the patient's response to EGFR tyrosine kinase inhibitors, followed by EGFR mutational analysis, if necessary.
  • [MeSH-major] Adenocarcinoma / genetics. DNA Mutational Analysis. Lung Neoplasms / genetics. Proto-Oncogene Proteins / genetics. Receptor, Epidermal Growth Factor / genetics. ras Proteins / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Base Sequence. Cost-Benefit Analysis. Drug Resistance, Neoplasm / genetics. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Mutation. Neoplasm Staging

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  • (PMID = 19855375.001).
  • [ISSN] 1530-0285
  • [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 / 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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86. Keith RL: Chemoprevention of lung cancer. Proc Am Thorac Soc; 2009 Apr 15;6(2):187-93
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  • [Title] Chemoprevention of lung cancer.
  • Lung cancer is the leading cause of cancer death in the United States, and the majority of diagnoses are made in former smokers.
  • While avoidance of tobacco abuse and smoking cessation clearly will have the greatest impact on lung cancer development, effective chemoprevention could prove to be more effective than treatment of established disease.
  • Chemoprevention is the use of dietary or pharmaceutical agents to reverse or inhibit the carcinogenic process and has been successfully applied to common malignancies other than lung.
  • Despite previous studies in lung cancer chemoprevention failing to identify effective agents, our ability to determine higher risk populations and the understanding of lung tumor and pre-malignant biology continues to advance.
  • The World Health Organization/International Association for the Study of Lung Cancer classification for lung cancer now recognizes distinct histologic lesions that can be reproducibly graded as precursors of non-small cell lung cancer.
  • For example, carcinogenesis in the bronchial epithelium starts with normal epithelium and progresses through hyperplasia, metaplasia, dysplasia, and carcinoma in situ to invasive squamous cell cancer.
  • Similar precursor lesions exist for adenocarcinoma, and these pre-malignant lesions are targeted by chemopreventive agents in current and future trials.
  • [MeSH-major] Chemoprevention / methods. Lung Neoplasms / prevention & control. Precancerous Conditions / drug therapy

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  • (PMID = 19349487.001).
  • [ISSN] 1546-3222
  • [Journal-full-title] Proceedings of the American Thoracic Society
  • [ISO-abbreviation] Proc Am Thorac Soc
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers
  • [Number-of-references] 86
  • [Other-IDs] NLM/ PMC2674227
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87. 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.
  • 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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88. Chi S, Huang S, Li C, Zhang X, He N, Bhutani MS, Jones D, Castro CY, Logrono R, Haque A, Zwischenberger J, Tyring SK, Zhang H, Xie J: Activation of the hedgehog pathway in a subset of lung cancers. Cancer Lett; 2006 Nov 28;244(1):53-60
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  • [Title] Activation of the hedgehog pathway in a subset of lung cancers.
  • Activation of the hedgehog pathway is reported in lung cancer, but its frequency remains unknown.
  • We examine activation of this pathway in lung cancers by in situ hybridization and immunohistochemstry, and find that less than 10% of the tumors have elevated hedgehog target gene expression.
  • These data indicate that activation of the hedgehog pathway is activated through Shh over-expression or Su(Fu) inactivation in only a subset of lung cancers.
  • [MeSH-major] Hedgehog Proteins / metabolism. Lung Neoplasms / metabolism. Signal Transduction
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Blotting, Northern. Blotting, Western. Carcinoma, Large Cell / genetics. Carcinoma, Large Cell / metabolism. Carcinoma, Small Cell / genetics. Carcinoma, Small Cell / metabolism. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / metabolism. Cell Proliferation. Colony-Forming Units Assay. Female. Humans. Immunoblotting. Immunoenzyme Techniques. In Situ Hybridization. Male. Oncogene Proteins / genetics. Oncogene Proteins / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Receptors, Cell Surface / genetics. Receptors, Cell Surface / metabolism. Repressor Proteins / genetics. Repressor Proteins / metabolism. Trans-Activators / genetics. Trans-Activators / metabolism. Tumor Cells, Cultured

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  • (PMID = 16446029.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / ES06676; United States / NCI NIH HHS / CA / R01-CA94160
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Gli protein; 0 / Hedgehog Proteins; 0 / Oncogene Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, Cell Surface; 0 / Repressor Proteins; 0 / SUFU protein, human; 0 / Trans-Activators; 0 / patched receptors
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89. 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.
  • High expression of both SP-A and lysozyme in tumor cells was confirmed by in situ hybridization (ISH).
  • 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-minor] Animals. Apoproteins / metabolism. DNA, Complementary / metabolism. DNA-Directed RNA Polymerases / metabolism. Female. In Situ Hybridization. Lasers. Lung / cytology. Lung / pathology. Mice. Microscopy, Electron, Transmission. Muramidase / chemistry. Muramidase / metabolism. Phenotype. Promoter Regions, Genetic. Pulmonary Surfactant-Associated Protein A / metabolism. RNA / metabolism. RNA, Messenger / metabolism. Surface-Active Agents / metabolism. Time Factors. Viral Proteins

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  • [Copyright] Copyright 2004 Wiley-Liss, Inc.
  • (PMID = 15584020.001).
  • [ISSN] 0899-1987
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoproteins; 0 / Carcinogens; 0 / DNA, Complementary; 0 / Nitrosamines; 0 / Pulmonary Surfactant-Associated Protein A; 0 / RNA, Messenger; 0 / Surface-Active Agents; 0 / Viral Proteins; 63231-63-0 / RNA; 64091-91-4 / 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone; EC 2.7.7.- / bacteriophage T7 RNA polymerase; EC 2.7.7.6 / DNA-Directed RNA Polymerases; EC 3.2.1.17 / Muramidase
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90. Dziadziuszko R, Merrick DT, Witta SE, Mendoza AD, Szostakiewicz B, Szymanowska A, Rzyman W, Dziadziuszko K, Jassem J, Bunn PA Jr, Varella-Garcia M, Hirsch FR: Insulin-like growth factor receptor 1 (IGF1R) gene copy number is associated with survival in operable non-small-cell lung cancer: a comparison between IGF1R fluorescent in situ hybridization, protein expression, and mRNA expression. J Clin Oncol; 2010 May 1;28(13):2174-80
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  • [Title] Insulin-like growth factor receptor 1 (IGF1R) gene copy number is associated with survival in operable non-small-cell lung cancer: a comparison between IGF1R fluorescent in situ hybridization, protein expression, and mRNA expression.
  • PURPOSE: The purpose of this study was to characterize insulin-like growth factor-1 receptor (IGF1R) protein expression, mRNA expression, and gene copy number in surgically resected non-small-cell lung cancers (NSCLC) in relation to epidermal growth factor receptor (EGFR) protein expression, patient characteristics, and prognosis.
  • IGF1R gene copy number was assessed by fluorescent in situ hybridization using customized probes (n = 181).
  • RESULTS: IGF1R IHC score was higher in squamous cell carcinomas versus other histologies (P < .001) and associated with stage (P = .03) but not survival (P = .46).
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Squamous Cell / genetics. Gene Dosage. Gene Expression Regulation, Neoplastic. In Situ Hybridization, Fluorescence. Lung Neoplasms / genetics. Pulmonary Surgical Procedures. RNA, Messenger / analysis. Receptor, IGF Type 1 / genetics
  • [MeSH-minor] Adenocarcinoma / chemistry. Adenocarcinoma / genetics. Adenocarcinoma / surgery. Adult. Aged. Aged, 80 and over. Aneuploidy. Carcinoma, Large Cell / chemistry. Carcinoma, Large Cell / genetics. Carcinoma, Large Cell / surgery. Disease-Free Survival. Female. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Middle Aged. Neoplasm Staging. Proportional Hazards Models. Receptor, Epidermal Growth Factor / genetics. Reverse Transcriptase Polymerase Chain Reaction. Risk Assessment. Risk Factors. Time Factors. Tissue Array Analysis. Treatment Outcome

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  • (PMID = 20351332.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA058187; United States / NCI NIH HHS / CA / P50 CA058187
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, IGF Type 1
  • [Other-IDs] NLM/ PMC2860435
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91. Brouchet L, Valmary S, Dahan M, Didier A, Galateau-Salle F, Brousset P, Degano B: Detection of oncogenic virus genomes and gene products in lung carcinoma. Br J Cancer; 2005 Feb 28;92(4):743-6
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  • [Title] Detection of oncogenic virus genomes and gene products in lung carcinoma.
  • We investigated a series of 122 cases of small cell lung carcinomas and non-small cell lung carcinomas for the presence of several viruses that are known to be oncogenic in humans.
  • Thus, viral genomes (DNA) and/or RNA transcripts and/or proteins of human papillomaviruses (HPV) 16, 18, 31, 33, 51, Epstein-Barr virus (EBV), human herpesvirus 8 (HHV-8), human cytomegalovirus (HCMV) and simian virus 40 (SV40) were investigated on tissue sections (prepared in tissue microarrays) with different techniques of immunohistochemistry and in situ hybridisation.
  • Taken together, our data strongly suggest that the conventional human oncogenic viruses (HPV, EBV, HCMV, HHV-8 and SV40) are unlikely to play some role in the development of lung carcinomas..
  • [MeSH-major] Genome, Viral. Lung Neoplasms / virology. Oncogenic Viruses / genetics. Viral Proteins / isolation & purification
  • [MeSH-minor] Adenocarcinoma / virology. Antibodies, Viral / analysis. Carcinoid Tumor / virology. Carcinoma, Large Cell / virology. Carcinoma, Neuroendocrine / virology. Carcinoma, Non-Small-Cell Lung / virology. Carcinoma, Small Cell / virology. Carcinoma, Squamous Cell / virology. Cytomegalovirus / genetics. DNA, Viral / isolation & purification. Herpesvirus 4, Human / genetics. Herpesvirus 8, Human / genetics. Humans. Immunohistochemistry. In Situ Hybridization. Papillomaviridae / genetics. Polymerase Chain Reaction. RNA, Viral / isolation & purification. Simian virus 40 / genetics

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  • (PMID = 15700034.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Viral; 0 / DNA, Viral; 0 / RNA, Viral; 0 / Viral Proteins
  • [Other-IDs] NLM/ PMC2361883
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92. O'Donoghue K, Sultan HA, Al-Allaf FA, Anderson JR, Wyatt-Ashmead J, Fisk NM: Microchimeric fetal cells cluster at sites of tissue injury in lung decades after pregnancy. Reprod Biomed Online; 2008 Mar;16(3):382-90
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  • [Title] Microchimeric fetal cells cluster at sites of tissue injury in lung decades after pregnancy.
  • Specimens were obtained from women undergoing surgery for suspected lung cancer.
  • Y-fluorescence in-situ hybridization was performed on paraffin-embedded sections, with the investigator blinded to medical histories.
  • Male cells were identified in lung/thymus tissue from all women with known male pregnancies, but not in those without sons.
  • The frequency of male microchimeric cells was seven-fold greater in lung/thymus tissues than marrow and was two-fold greater than normal bone from the same women.
  • Male cells in lung were clustered in tumour rather than surrounding healthy tissues.
  • [MeSH-major] Adenocarcinoma / pathology. Chimerism. Fetal Stem Cells / pathology. Lung / pathology. Lung Neoplasms / pathology. Wound Healing / physiology

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  • (PMID = 18339261.001).
  • [ISSN] 1472-6483
  • [Journal-full-title] Reproductive biomedicine online
  • [ISO-abbreviation] Reprod. Biomed. Online
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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93. Maekawa S, Hishima T, Yamada Y, Ichikawa H, Natsui S, Shinohara M: [A case of primary urethral adenocarcinoma accompanied by vaginal wall infiltration in which the CA19-9 level was very high]. Hinyokika Kiyo; 2009 Aug;55(8):513-6

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  • [Title] [A case of primary urethral adenocarcinoma accompanied by vaginal wall infiltration in which the CA19-9 level was very high].
  • Computed tomography confirmed a urethral tumor, and transurethral biopsy confirmed adenocarcinoma.
  • However, the majority of the tumor was located in the bladder and urethra, a duct with intestinal metaplasia was present around the urethra, and carcinoma in situ was seen in the urethral mucosa.
  • Based on the above findings, the patient was diagnosed as having primary urethral adenocarcinoma.
  • Six months after surgery, the patient developed bone metastasis, followed by peritoneal and pleural dissemination, as well as multiple lung metastases.
  • [MeSH-major] Adenocarcinoma / pathology. Biomarkers, Tumor / blood. CA-19-9 Antigen / blood. Urethral Neoplasms / pathology. Vagina / pathology

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  • (PMID = 19764540.001).
  • [ISSN] 0018-1994
  • [Journal-full-title] Hinyokika kiyo. Acta urologica Japonica
  • [ISO-abbreviation] Hinyokika Kiyo
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CA-19-9 Antigen
  • [Number-of-references] 11
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94. Bai XY, Shen H: [Quantitative analysis of thyroid transcription factor-1 mRNA expressions in primary lung cancer and its metastatic foci]. Nan Fang Yi Ke Da Xue Xue Bao; 2008 Jan;28(1):20-5
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  • [Title] [Quantitative analysis of thyroid transcription factor-1 mRNA expressions in primary lung cancer and its metastatic foci].
  • OBJECTIVE: To observe the expression of thyroid transcription factor-1 (TTF-1) mRNA in human normal adult type II alveolar epithelial cells, embryonic alveolar epithelial cells, and primary lung carcinoma and lymph nodes, thereby exploring the role of TTF-1 mRNA expression in the tumorigenesis, development and metastasis of lung carcinoma.
  • METHODS: TTF-1 mRNA was detected using tissue microarray and in situ hybridization in 1320 different paraffin-embedded tissue specimens.
  • RESULTS: TTF-1 mRNA expression was significantly less intense in embryonic lung than in normal adult lung tissues (P= 0.000), and the two tissues both had significantly greater expression than lung adenocarcinoma, squamous cell carcinoma, small cell carcinoma and large cell carcinoma (P=0.000).
  • Lung adenocarcinoma and small cell carcinoma, with similar expression intensity (P= 0.068), showed stronger expression than squamous cell carcinoma and large cell carcinoma (P=0.000), and squamous cell carcinoma showed stronger expression than large cell carcinoma (P=0.018).
  • In lung adenocarcinoma, squamous cell carcinoma and large cell carcinoma, the intensity of TTF-1 mRNA expression was stronger in lymph node metastases than in the primary foci (P=0.003, P=0.000, P=0.019, respectively).
  • The lymph node metastases had more intense expression than the primary foci of small cell lung carcinoma (P=0.078).
  • The intensity of TTF-1 mRNA expression was greater in primary lung carcinomas with lymph node metastases than in those without metastases (P=0.026).
  • Tumors of TNM stage II-IV had stronger expression than those of stage I (P=0.010).
  • CONCLUSION: The amount of TTF-1 mRNA expression lowers in the order of normal adult lung, embryonic lung and lung carcinoma tissues.
  • In lung carcinomas, TTF-1 mRNA expression differs between the histological types, high in lung adenocarcinoma and small cell carcinoma and rather low in squamous cell carcinoma and large cell carcinoma.
  • Strong expression of TTF-1 mRNA often indicates high likeliness of lung carcinoma metastasis, and highlights the high metastatic potentials of lung adenocarcinoma, squamous cell carcinoma and large cell carcinoma.
  • [MeSH-major] Carcinoma, Squamous Cell / genetics. Lung Neoplasms / genetics. Nuclear Proteins / genetics. Transcription Factors / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Female. Humans. In Situ Hybridization. Lymphatic Metastasis. Male. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Thyroid Gland / metabolism. Tissue Array Analysis / methods

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  • (PMID = 18227018.001).
  • [ISSN] 1673-4254
  • [Journal-full-title] Nan fang yi ke da xue xue bao = Journal of Southern Medical University
  • [ISO-abbreviation] Nan Fang Yi Ke Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Nuclear Proteins; 0 / RNA, Messenger; 0 / Transcription Factors; 0 / thyroid nuclear factor 1
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95. Liao WT, Lin P, Cheng TS, Yu HS, Chang LW: Arsenic promotes centrosome abnormalities and cell colony formation in p53 compromised human lung cells. Toxicol Appl Pharmacol; 2007 Dec 1;225(2):162-70
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  • [Title] Arsenic promotes centrosome abnormalities and cell colony formation in p53 compromised human lung cells.
  • Epidemiological evidence indicated that residents, especially cigarette smokers, in arseniasis areas had significantly higher lung cancer risk than those living in non-arseniasis areas.
  • Thus, an interaction between arsenic and cigarette smoking in lung carcinogenesis was suspected. p53 dysfunction or mutation in lung epithelial cells was frequently observed in cigarette smokers.
  • Our present study was to explore the differential effects by arsenic on H1355 cells (human lung adenocarcinoma cell line with mutation in p53), BEAS-2B (immortalized lung epithelial cell with functional p53) and pifithrin-alpha-treated BEAS-2B cells (p53-inhibited cells).
  • [MeSH-major] Arsenites / toxicity. Centrosome / drug effects. Enzyme Inhibitors / toxicity. Lung / drug effects. Sodium Compounds / toxicity. Tumor Suppressor Protein p53 / physiology
  • [MeSH-minor] Adenocarcinoma / metabolism. Apoptosis / drug effects. Cell Cycle Proteins / drug effects. Cell Cycle Proteins / genetics. Cell Line. Cell Line, Tumor. Cell Survival / drug effects. Chromosome Aberrations / drug effects. Chromosome Segregation / drug effects. Cyclin-Dependent Kinase Inhibitor p21 / drug effects. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Dose-Response Relationship, Drug. Epithelial Cells / drug effects. Epithelial Cells / metabolism. Gene Expression Regulation / drug effects. Humans. In Situ Nick-End Labeling. Mutation. Nuclear Proteins / drug effects. Nuclear Proteins / genetics

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  • (PMID = 17945324.001).
  • [ISSN] 0041-008X
  • [Journal-full-title] Toxicology and applied pharmacology
  • [ISO-abbreviation] Toxicol. Appl. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arsenites; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Enzyme Inhibitors; 0 / GADD45A protein, human; 0 / Nuclear Proteins; 0 / Sodium Compounds; 0 / Tumor Suppressor Protein p53; 48OVY2OC72 / sodium arsenite
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96. Zudaire I, Lozano MD, Vazquez MF, Pajares MJ, Agorreta J, Pio R, Zulueta JJ, Yankelevitz DF, Henschke CI, Montuenga LM: Molecular characterization of small peripheral lung tumors based on the analysis of fine needle aspirates. Histol Histopathol; 2008 01;23(1):33-40
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  • [Title] Molecular characterization of small peripheral lung tumors based on the analysis of fine needle aspirates.
  • The computed tomography (CT)-based early lung cancer diagnostic technologies allow the detection of very small stage I lung tumors.
  • Fine Needle Aspiration (FNA) cytology is a well-recognised method for a rapid and accurate diagnosis of small lung tumors.
  • Molecular analysis of the FNA specimens could complement cytology diagnosis by the characterization of the biological traits at the preoperative stage.
  • In this study, we aimed to characterize the biological profile of 33 paraffin-embedded transthoracic FNA samples obtained from three groups of lung cancer patients: two groups of small early-detected lung adenocarcinomas (radiologically subsolid and solid nodules) and a third group of small metastatic adenocarcinomas.
  • Genetic analysis was performed by fluorescence in situ hybridization using the four-color LAVysion probe. p53 and Ki-67 protein expression was also evaluated by immunocytochemistry.
  • [MeSH-major] Adenocarcinoma / pathology. Biopsy, Fine-Needle / methods. Lung Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Immunohistochemistry / methods. In Situ Hybridization, Fluorescence / methods. Ki-67 Antigen / metabolism. Male. Middle Aged. Neoplasm Staging. Paraffin Embedding / methods. Proto-Oncogene Proteins c-myc / metabolism. Receptor, Epidermal Growth Factor / metabolism. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 17952855.001).
  • [ISSN] 1699-5848
  • [Journal-full-title] Histology and histopathology
  • [ISO-abbreviation] Histol. Histopathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-myc; 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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97. Pajares MJ, Zudaire I, Lozano MD, Agorreta J, Bastarrika G, Torre W, Remírez A, Pio R, Zulueta JJ, Montuenga LM: Molecular profiling of computed tomography screen-detected lung nodules shows multiple malignant features. Cancer Epidemiol Biomarkers Prev; 2006 Feb;15(2):373-80
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  • [Title] Molecular profiling of computed tomography screen-detected lung nodules shows multiple malignant features.
  • RATIONALE AND PURPOSE: Low-dose spiral computerized axial tomography (spiral CT) is effective for the detection of small early lung cancers.
  • The objective of the current study was to analyze the phenotypic and genetic alterations in the small pulmonary malignancies resected after detection in the University of Navarra/International Early Lung Cancer Action Project spiral CT screening trial and to determine whether their malignant molecular features are similar to those of resected lung tumors diagnosed conventionally.
  • EXPERIMENTAL DESIGN: We analyzed 17 biomarkers of lung epithelial malignancy in a series of 11 tumors resected at our institution during the last 4 years (1,004 high-risk individuals screened), using immunohistochemistry and fluorescence in situ hybridization (FISH).
  • A parallel series of 11 gender-, stage-, and histology-matched lung cancers diagnosed by other means except screening was used as control.
  • RESULTS: The molecular alterations and the frequency of phenotypic or genetic aberrations were very similar when screen-detected and nonscreen-detected lung cancers were compared.
  • Furthermore, most of the alterations found in the screen-detected cancers from this study were concordant with what has been described previously for stage I-II lung cancer.
  • CONCLUSIONS: Small early-stage lung cancers resected after detection in a spiral CT-based screening trial reveal malignant molecular features similar to those found in conventionally diagnosed lung cancers, suggesting that the screen-detected cancers are not overdiagnosed.
  • [MeSH-major] Adenocarcinoma / genetics. Biomarkers, Tumor / analysis. Carcinoma, Squamous Cell / genetics. Lung Neoplasms / genetics. Tomography, Spiral Computed
  • [MeSH-minor] Early Diagnosis. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Mass Screening. Neoplasm Staging. Phenotype. Sensitivity and Specificity. Smoking

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  • (PMID = 16492931.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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98. Chitale D, Gong Y, Taylor BS, Broderick S, Brennan C, Somwar R, Golas B, Wang L, Motoi N, Szoke J, Reinersman JM, Major J, Sander C, Seshan VE, Zakowski MF, Rusch V, Pao W, Gerald W, Ladanyi M: An integrated genomic analysis of lung cancer reveals loss of DUSP4 in EGFR-mutant tumors. Oncogene; 2009 Aug 6;28(31):2773-83
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  • [Title] An integrated genomic analysis of lung cancer reveals loss of DUSP4 in EGFR-mutant tumors.
  • To address the biological heterogeneity of lung cancer, we studied 199 lung adenocarcinomas by integrating genome-wide data on copy number alterations and gene expression with full annotation for major known somatic mutations in this cancer.
  • DUSP4 is involved in negative feedback control of EGFR signaling, and we provide functional validation for its role as a growth suppressor in EGFR-mutant lung adenocarcinoma.
  • DUSP4 loss also associates with p16/CDKN2A deletion and defines a distinct clinical subset of lung cancer patients.

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  • (PMID = 19525976.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA129243-029001; United States / NCI NIH HHS / CA / U01 CA084999; United States / NCI NIH HHS / CA / P01 CA129243-029001; United States / NCI NIH HHS / CA / P01-CA129243; United States / NCI NIH HHS / CA / P01 CA129243; United States / NCI NIH HHS / CA / U01-CA84999
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.1.3.- / Mitogen-Activated Protein Kinase Phosphatases; EC 3.1.3.48 / DUSP4 protein, human; EC 3.1.3.48 / Dual-Specificity Phosphatases
  • [Other-IDs] NLM/ NIHMS108311; NLM/ PMC2722688
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99. Levy MJ, Clain JE, Clayton A, Halling KC, Kipp BR, Rajan E, Roberts LR, Root RM, Sebo TJ, Topazian MD, Wang KK, Wiersema MJ, Gores GJ: Preliminary experience comparing routine cytology results with the composite results of digital image analysis and fluorescence in situ hybridization in patients undergoing EUS-guided FNA. Gastrointest Endosc; 2007 Sep;66(3):483-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Preliminary experience comparing routine cytology results with the composite results of digital image analysis and fluorescence in situ hybridization in patients undergoing EUS-guided FNA.
  • BACKGROUND: Studies indicate enhanced diagnostic accuracy for digital image analysis (DIA) and fluorescence in situ hybridization (FISH) versus routine cytology examination (RC) when biliary strictures are evaluated.
  • The final diagnosis was based on strict cytopathologic and imaging criteria and 12-month follow-up.
  • RESULTS: Malignancy was diagnosed in 30 of 42 patients, including esophageal squamous cell carcinoma, esophageal adenocarcinoma, gastric adenocarcinoma, pancreatic adenocarcinoma, pancreatic mucinous cystic neoplasia, intraductal papillary mucinous neoplasia, metastatic forearm sarcoma, small cell and non-small cell lung cancer, thyroid carcinoma, malignant GI stromal tumor, melanoma, adenocarcinoma of unknown primary, and lymphoma.
  • [MeSH-major] Biopsy, Fine-Needle. Endosonography. Esophageal Neoplasms / pathology. Image Processing, Computer-Assisted. In Situ Hybridization, Fluorescence. Lymphatic Metastasis / pathology. Pancreatic Neoplasms / pathology. Stomach Neoplasms / pathology. Thyroid Neoplasms / pathology


100. Zhao R, Yang W, Wang Z, Li G, Qin W, Wang J: Treatment of transplanted tumor of lung adenocarcinoma A549 transfected by human somatostatin receptor subtype 2 (hsstr2) gene with 188Re-RC-160. Nucl Med Biol; 2010 Nov;37(8):977-87

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of transplanted tumor of lung adenocarcinoma A549 transfected by human somatostatin receptor subtype 2 (hsstr2) gene with 188Re-RC-160.
  • BACKGROUND AND AIM: Radionuclide-labeled somatostatin analogues selectively target somatostatin receptor (SSTR)-expressing tumors as a basis for diagnosis and treatment of these tumors.
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adenocarcinoma / radiotherapy. Animals. Blotting, Western. Cell Line, Tumor. Cell Transformation, Neoplastic. Cloning, Molecular. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Lung Neoplasms / genetics. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Lung Neoplasms / radiotherapy. Male. Mice. Mice, Inbred BALB C. Tomography, Emission-Computed, Single-Photon. Transfection

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 21055629.001).
  • [ISSN] 1872-9614
  • [Journal-full-title] Nuclear medicine and biology
  • [ISO-abbreviation] Nucl. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Radioisotopes; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 2PK59M9GFF / vapreotide; 51110-01-1 / Somatostatin; 7440-15-5 / Rhenium; Adenocarcinoma of lung
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