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1. Silva BA, Silva IS, Pereira DM, Aydos RD, Carvalho Pde T, Facco GG: Experimental model of pulmonary carcinogenesis in Wistar rats. Acta Cir Bras; 2007 Mar-Apr;22 Suppl 1:16-20
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  • RESULTS: The presence of diffuse inflammatory alterations was observed in all groups; however, at the analysis of the pulmonary tissue of the experimental groups had been observed hyperplasic alterations (BALT hyperplasia), and in one of the animals of the experimental group 20mg/kg (12 weeks) was noticed the presence of cellular epithelial tracheal pleomorphism, suggesting the adenocarcinoma formation in situ.
  • The association of an activator agent of the pulmonary metabolic reply is necessary to establish the ideal reply-dose to the development of the lung cancer.

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  • (PMID = 17505650.001).
  • [ISSN] 0102-8650
  • [Journal-full-title] Acta cirurgica brasileira
  • [ISO-abbreviation] Acta Cir Bras
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Carcinogens; 3417WMA06D / Benzo(a)pyrene
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2. 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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3. Monaco SE, Nikiforova MN, Cieply K, Teot LA, Khalbuss WE, Dacic S: A comparison of EGFR and KRAS status in primary lung carcinoma and matched metastases. Hum Pathol; 2010 Jan;41(1):94-102
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  • [Title] A comparison of EGFR and KRAS status in primary lung carcinoma and matched metastases.
  • Epidermal growth factor receptor (EGFR) and v-Ki-ras 2 (KRAS; viral Kirsten rat sacoma 2 oncogene homolog) oncogenes are predictors of response to EGFR-targeted therapy in lung carcinomas.
  • Morphologic heterogeneity of lung carcinomas is reflected at the molecular level and may confound interpretation of immunohistochemistry, fluorescence in situ hybridization, and mutational assays, which are all used for analysis of KRAS and EGFR genes.
  • The aim of this study was to determine if the KRAS and/or EGFR status of primary and metastatic lung carcinoma differs.
  • Three hundred thirty-six cases of primary lung carcinomas were tested for EGFR and KRAS, and 85 cases had a metastasis (25%).
  • Of the cases with EGFR fluorescence in situ hybridization results, there were 3 (8%) primary tumors and 8 (24%) metastases that were fluorescence in situ hybridization positive.
  • Overall, there were 9 cases (22.5%) with discordant KRAS status and 11 cases (32.5%) with discordant EGFR fluorescence in situ hybridization status.
  • Our results suggest that the EGFR and KRAS status of primary lung carcinomas may not predict the status in the corresponding metastases.
  • [MeSH-major] Adenocarcinoma / metabolism. Lung Neoplasms / metabolism. Proto-Oncogene Proteins / metabolism. Receptor, Epidermal Growth Factor / metabolism. ras Proteins / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. DNA Mutational Analysis. DNA, Neoplasm / analysis. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Mutation. Predictive Value of Tests. Prognosis

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  • (PMID = 19740513.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.6.5.2 / ras Proteins
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4. 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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5. 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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6. Zendehrokh N, Franzen L, Dejmek A: Weak telomerase activity in malignant cells in metastatic serous effusions: correlation to short survival time. Acta Cytol; 2007 May-Jun;51(3):412-6
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  • STUDY DESIGN: Telomere repeat amplification protocol (TRAP) in situ was applied to 46 effusions containing metastatic cancer cells.
  • [MeSH-major] Adenocarcinoma / mortality. Adenocarcinoma / secondary. Lung Neoplasms / mortality. Lung Neoplasms / pathology. Pleural Effusion, Malignant / mortality. Pleural Effusion, Malignant / pathology. Telomerase / metabolism

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  • (PMID = 17536544.001).
  • [ISSN] 0001-5547
  • [Journal-full-title] Acta cytologica
  • [ISO-abbreviation] Acta Cytol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.7.49 / Telomerase
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7. 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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8. Pelosi G, Del Curto B, Dell'Orto P, Pasini F, Veronesi G, Spaggiari L, Maisonneuve P, Iannucci A, Terzi A, Lonardoni A, Viale G: Lack of prognostic implications of HER-2/neu abnormalities in 345 stage I non-small cell carcinomas (NSCLC) and 207 stage I-III neuroendocrine tumours (NET) of the lung. Int J Cancer; 2005 Jan 1;113(1):101-8
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  • [Title] Lack of prognostic implications of HER-2/neu abnormalities in 345 stage I non-small cell carcinomas (NSCLC) and 207 stage I-III neuroendocrine tumours (NET) of the lung.
  • Irrespective of protein overexpression, HER-2/neu gene amplification is rare in lung cancer and studies on its prevalence and clinicopathological implications in early stage non-small cell lung cancer (NCSLC) and neuroendocrine tumours (NET) of the lung are lacking.
  • We evaluated HER-2/neu abnormalities in 345 Stage I NSCLC and 207 Stage I-III NET of the lung of all the diverse histological types, by using immunohistochemistry and fluorescent in situ hybridization in selected cases.
  • HER-2/neu gene amplification and protein overexpression are not closely correlated in lung carcinomas and do not bear any prognostic implication.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Chromosome Aberrations. Gene Amplification. Genes, erbB-2. Lung Neoplasms / genetics. Receptor, ErbB-2 / metabolism
  • [MeSH-minor] Adenocarcinoma / genetics. Adolescent. Adult. Aged. Aged, 80 and over. Carcinoma, Neuroendocrine / genetics. Carcinoma, Squamous Cell / genetics. Chromosomes, Human, Pair 17. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Middle Aged. Neoplasm Staging. Predictive Value of Tests. Prognosis. Retrospective Studies. Up-Regulation

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  • (PMID = 15386424.001).
  • [ISSN] 0020-7136
  • [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] EC 2.7.10.1 / Receptor, ErbB-2
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9. Zeng X, Hood BL, Sun M, Conrads TP, Day RS, Weissfeld JL, Siegfried JM, Bigbee WL: Lung cancer serum biomarker discovery using glycoprotein capture and liquid chromatography mass spectrometry. J Proteome Res; 2010 Dec 3;9(12):6440-9
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  • [Title] Lung cancer serum biomarker discovery using glycoprotein capture and liquid chromatography mass spectrometry.
  • Here we report its application to a set of pooled nonsmall cell lung cancer (NSCLC) case sera (9 adenocarcinoma and 6 squamous cell carcinoma pools from 54 patients) and matched controls pools, including 8 clinical control pools with computed tomography detected nodules but being nonmalignant as determined by biopsy from 54 patients, and 8 matched healthy control pools from 106 cancer-free subjects.
  • The goal of the study is to discover biomarkers that may enable improved early detection and diagnosis of lung cancer.
  • Hydrazide resin in situ trypsin digestion was used to release nonglycosylated peptides.

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  • (PMID = 20931982.001).
  • [ISSN] 1535-3907
  • [Journal-full-title] Journal of proteome research
  • [ISO-abbreviation] J. Proteome Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA090440; United States / NCI NIH HHS / CA / U01 CA084968-10; United States / NCI NIH HHS / CA / P50CA90440; United States / NCI NIH HHS / CA / U01 CA084968; United States / NCI NIH HHS / CA / P50 CA090440-10
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Glycopeptides; 0 / Glycoproteins
  • [Other-IDs] NLM/ NIHMS249067; NLM/ PMC3184639
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10. 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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11. 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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12. Barbetakis N, Asteriou C, Kleontas A, Tsilikas C: eComment: Therapeutic options for bronchial stump infiltration following lung cancer surgery. Interact Cardiovasc Thorac Surg; 2009 Aug;9(2):186
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  • [Title] eComment: Therapeutic options for bronchial stump infiltration following lung cancer surgery.
  • [MeSH-major] Adenocarcinoma / surgery. Bronchi / surgery. Carcinoma in Situ / surgery. Carcinoma, Non-Small-Cell Lung / surgery. Carcinoma, Squamous Cell / surgery. Lung Neoplasms / surgery. Thoracotomy

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  • [CommentOn] Interact Cardiovasc Thorac Surg. 2009 Aug;9(2):182-6 [19470498.001]
  • (PMID = 19628536.001).
  • [ISSN] 1569-9285
  • [Journal-full-title] Interactive cardiovascular and thoracic surgery
  • [ISO-abbreviation] Interact Cardiovasc Thorac Surg
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] England
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13. 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


14. Bean J, Brennan C, Shih JY, Riely G, Viale A, Wang L, Chitale D, Motoi N, Szoke J, Broderick S, Balak M, Chang WC, Yu CJ, Gazdar A, Pass H, Rusch V, Gerald W, Huang SF, Yang PC, Miller V, Ladanyi M, Yang CH, Pao W: MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib. Proc Natl Acad Sci U S A; 2007 Dec 26;104(52):20932-7
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  • [Title] MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib.
  • In human lung adenocarcinomas harboring EGFR mutations, a second-site point mutation that substitutes methionine for threonine at position 790 (T790M) is associated with approximately half of cases of acquired resistance to the EGFR kinase inhibitors, gefitinib and erlotinib.
  • We also found that an existing EGFR mutant lung adenocarcinoma cell line, NCI-H820, harbors MET amplification in addition to a drug-sensitive EGFR mutation and the T790M change.

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  • (PMID = 18093943.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / U01 CA084999; United States / NCI NIH HHS / CA / K08 CA097980; United States / NCI NIH HHS / CA / K08-CA097980; United States / NCI NIH HHS / CA / R01-CA121210; United States / NCI NIH HHS / CA / P50CA75907; United States / NCI NIH HHS / CA / R01 CA121210; United States / NCI NIH HHS / CA / R21-CA115051; United States / NCI NIH HHS / CA / R21 CA115051; 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] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Proto-Oncogene Proteins c-met; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
  • [Other-IDs] NLM/ PMC2409244
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15. 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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16. Maley SN, Schwartz SM, Johnson LG, Malkki M, Du Q, Daling JR, Li SS, Zhao LP, Petersdorf EW, Madeleine MM: Genetic variation in CXCL12 and risk of cervical carcinoma: a population-based case-control study. Int J Immunogenet; 2009 Dec;36(6):367-75
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  • Cases (n = 917) were residents of western Washington State diagnosed with invasive squamous cell cervical carcinoma (SCC), invasive adenocarcinoma or adenosquamous carcinoma, or adenocarcinoma in situ of the cervix.

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  • (PMID = 19788587.001).
  • [ISSN] 1744-313X
  • [Journal-full-title] International journal of immunogenetics
  • [ISO-abbreviation] Int. J. Immunogenet.
  • [Language] ENG
  • [Grant] United States / NHGRI NIH HHS / HG / T32HG00035; United States / NCI NIH HHS / CA / CA112512-02; United States / NCI NIH HHS / CA / R01CA112512; United States / NCI NIH HHS / CA / R01 CA112512-02; United States / NCI NIH HHS / CA / P01 CA042792-219003; United States / NCI NIH HHS / CA / P01CA04279; United States / NCI NIH HHS / CA / R25 CA094880; United States / NCI NIH HHS / CA / CA112512-01; United States / NIEHS NIH HHS / ES / P30ES07033; United States / NHGRI NIH HHS / HG / T32 HG000035; United States / NCI NIH HHS / CA / CA112512-04; United States / NCI NIH HHS / CA / R01 CA112512-01; United States / NCI NIH HHS / CA / R01 CA112512-03; United States / NIEHS NIH HHS / ES / P30 ES007033; United States / NCI NIH HHS / CA / R01 CA112512-04; United States / NCI NIH HHS / CA / R25CA094880; United States / NCI NIH HHS / PC / N01-PC-35412; United States / NCI NIH HHS / CA / CA042792-219003; United States / NCI NIH HHS / CA / P01 CA042792; United States / NCI NIH HHS / CA / CA112512-03; United States / NCI NIH HHS / CA / CA112512-05; United States / NCI NIH HHS / CA / R01 CA112512-05; United States / NCI NIH HHS / CA / R01 CA112512
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 3' Untranslated Regions; 0 / CXCL12 protein, human; 0 / Chemokine CXCL12
  • [Other-IDs] NLM/ NIHMS144226; NLM/ PMC2784202
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17. Bono F: Pleural mesothelioma in situ and its adenocarcinoma simulator. Int J Surg Pathol; 2010 Dec;18(6):519-20
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  • [Title] Pleural mesothelioma in situ and its adenocarcinoma simulator.
  • [MeSH-major] Adenocarcinoma / pathology. Carcinoma in Situ / pathology. Lung Neoplasms / pathology. Mesothelioma / pathology. Pleural Neoplasms / pathology
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Diagnosis, Differential. Humans. Immunohistochemistry. Male

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  • (PMID = 21081535.001).
  • [ISSN] 1940-2465
  • [Journal-full-title] International journal of surgical pathology
  • [ISO-abbreviation] Int. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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18. Soh J, Toyooka S, Ichihara S, Asano H, Kobayashi N, Suehisa H, Otani H, Yamamoto H, Ichimura K, Kiura K, Gazdar AF, Date H: Sequential molecular changes during multistage pathogenesis of small peripheral adenocarcinomas of the lung. J Thorac Oncol; 2008 Apr;3(4):340-7
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  • [Title] Sequential molecular changes during multistage pathogenesis of small peripheral adenocarcinomas of the lung.
  • INTRODUCTION: We investigated EGFR and KRAS alterations among atypical adenomatous hyperplasia and small lung adenocarcinomas with bronchioloalveolar features to understand their role during multistage pathogenesis.
  • EGFR copy number was evaluated using fluorescence in situ hybridization.
  • CONCLUSIONS: EGFR and KRAS mutations occur early during the multistage pathogenesis of peripheral lung adenocarcinomas.
  • By contrast, increased EGFR copy number is a late event during tumor development and plays a role in the progression of lung adenocarcinoma independent of the initiating molecular events.

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  • (PMID = 18379350.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA084971-09; United States / NCI NIH HHS / CA / CA084971-09; United States / NCI NIH HHS / CA / P50CA70907; United States / NCI NIH HHS / CA / U01 CA084971; United States / NCI NIH HHS / CA / P50 CA070907-05S30003; United States / NCI NIH HHS / CA / P50 CA070907; United States / NCI NIH HHS / CA / CA070907-05S30003
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ NIHMS137273; NLM/ PMC2758162
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19. Dacic S, Flanagan M, Cieply K, Ramalingam S, Luketich J, Belani C, Yousem SA: Significance of EGFR protein expression and gene amplification in non-small cell lung carcinoma. Am J Clin Pathol; 2006 Jun;125(6):860-5
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  • [Title] Significance of EGFR protein expression and gene amplification in non-small cell lung carcinoma.
  • We evaluated epidermal growth factor receptor (EGFR) protein expression by immunohistochemical analysis and EGFR gene amplification by fluorescence in situ hybridization in 199 consecutive newly diagnosed and surgically treated patients with primary non-small cell lung carcinoma (NSCLC) and correlated results with clinicopathologic findings.
  • EGFR protein expression was more common in squamous cell carcinoma (SCC; 17 [26.2%]) than in adenocarcinoma (14 [11.1%]; (P = .0076) and more frequently associated with EGFR amplification (8 [14.5%] vs 4 [3.6%] cases; P = .0208).
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / metabolism. Gene Amplification. Lung Neoplasms / metabolism. Receptor, Epidermal Growth Factor / genetics. Receptor, Epidermal Growth Factor / metabolism
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / secondary. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Carcinoma, Large Cell / genetics. Carcinoma, Large Cell / metabolism. Carcinoma, Large Cell / secondary. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / secondary. Chromosomes, Human, Pair 7. Disease-Free Survival. Gene Dosage. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Middle Aged. Neoplasm Staging. Prospective Studies


20. 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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21. Perner S, Wagner PL, Soltermann A, LaFargue C, Tischler V, Weir BA, Weder W, Meyerson M, Giordano TJ, Moch H, Rubin MA: TTF1 expression in non-small cell lung carcinoma: association with TTF1 gene amplification and improved survival. J Pathol; 2009 Jan;217(1):65-72
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  • [Title] TTF1 expression in non-small cell lung carcinoma: association with TTF1 gene amplification and improved survival.
  • Such genetic alterations occur in a significant proportion of non-small cell lung carcinomas (NSCLCs) and include amplification of 14q13.3, which contains the TTF1 gene.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Carcinoma, Non-Small-Cell Lung / metabolism. DNA-Binding Proteins / metabolism. Lung Neoplasms / metabolism
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Aged. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / pathology. Female. Gene Amplification. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Neoplasm Staging. Prognosis. Retrospective Studies. Survival Analysis. Thyroid Neoplasms / genetics. Thyroid Neoplasms / metabolism

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  • (PMID = 18932182.001).
  • [ISSN] 1096-9896
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / TTF1 protein, human
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22. Dar AA, Zaika A, Piazuelo MB, Correa P, Koyama T, Belkhiri A, Washington K, Castells A, Pera M, El-Rifai W: Frequent overexpression of Aurora Kinase A in upper gastrointestinal adenocarcinomas correlates with potent antiapoptotic functions. Cancer; 2008 Apr 15;112(8):1688-98
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  • [Title] Frequent overexpression of Aurora Kinase A in upper gastrointestinal adenocarcinomas correlates with potent antiapoptotic functions.
  • BACKGROUND: Upper gastrointestinal adenocarcinomas are a common cause of cancer-related deaths.
  • In this study, the authors investigated the prevalence and biological significance of Aurora Kinase A (AURKA) overexpression in upper gastrointestinal adenocarcinomas.
  • METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemical staining on tumor tissue microarrays (TMA) were used to study the expression of AURKA in upper gastrointestinal adenocarcinomas.
  • To investigate the biological and signaling impact of AURKA, the authors used multiple in vitro assays that included 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT), TUNEL (terminal deoxynucleotidyl transferase-mediated nick-end labeling), cytochrome C release, flow cytometry, luciferase reporter, and Western blot analysis.
  • RESULTS: Frequent overexpression of AURKA transcript in upper gastrointestinal adenocarcinomas was detected compared with normal samples (47%; P= .001).
  • The immunohistochemical analysis of 130 tumors demonstrated moderate-to-strong immunostaining of AURKA in >50% of upper gastrointestinal adenocarcinomas.
  • By using camptothecin as a drug-induced apoptosis in vitro model, the authors demonstrated that the expression of AURKA provided protection against apoptosis to gastrointestinal cancer cells (AGS and RKO) (P= .006) and RIE-1 primary intestinal epithelial cells (P= .001).
  • The AURKA overexpression mediated an increase in phosphorylation of AKT(Ser473) with an increase in HDM2 level.
  • The shRNA-knockdown of AKT in AURKA-overexpressing cells reversed this effect and showed a significant increase in the p53 protein level, indicating a possible nexus of AURKA/AKT/p53.
  • Indeed, overexpression of AURKA led to a remarkable reduction in the transcription activity of p53, with subsequent reductions in transcript and protein levels of its downstream proapoptotic transcription targets (p21, BAX, NOXA, and PUMA).
  • CONCLUSIONS: Study results indicated that AURKA provides potent antiapoptotic properties to gastrointestinal cells by regulating levels of p53 through the AKT/HDM2 axis.

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  • (PMID = 18311783.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA095103; United States / NCI NIH HHS / CA / R01 CA106176; United States / NCI NIH HHS / CA / CA 95103; United States / NCI NIH HHS / CA / R01CA106176
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Coloring Agents; 0 / Enzyme Inhibitors; 0 / Luminescent Agents; 0 / Tetrazolium Salts; 0 / Thiazoles; 0 / Tumor Suppressor Protein p53; 298-93-1 / thiazolyl blue; 9007-43-6 / Cytochromes c; EC 1.13.12.- / Luciferases; EC 2.7.11.1 / AURKA protein, human; EC 2.7.11.1 / Aurora Kinase A; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; XT3Z54Z28A / Camptothecin
  • [Other-IDs] NLM/ NIHMS576419; NLM/ PMC4030394
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23. 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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24. Reid-Nicholson M, Kavuri S, Ustun C, Crawford J, Nayak-Kapoor A, Ramalingam P: Plasmablastic lymphoma: Cytologic findings in 5 cases with unusual presentation. Cancer; 2008 Oct 25;114(5):333-41
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  • Two patients had the acquired immunodeficiency syndrome and 3 had second non-PBL related malignancies including endometrial carcinoma, lung adenocarcinoma, and small lymphocytic lymphoma.
  • However, although these findings may suggest PBL, a definitive diagnosis requires adjunctive studies including immunohistochemistry and flow cytometry.
  • [MeSH-minor] Acquired Immunodeficiency Syndrome / complications. Adult. Female. HIV Infections / complications. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Middle Aged. Neoplasms, Multiple Primary / pathology

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  • [Copyright] (c) 2008 American Cancer Society.
  • (PMID = 18683216.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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25. Liang ZY, Zeng X, Zhang J, Wu SF, Gao J, Liu TH: [Status of gene mutation and copy number of EGFR in 290 cases of non-small cell lung carcinoma]. Zhonghua Bing Li Xue Za Zhi; 2008 Oct;37(10):654-9
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  • [Title] [Status of gene mutation and copy number of EGFR in 290 cases of non-small cell lung carcinoma].
  • OBJECTIVE: To investigate EGFR mutations and gene copy number status in non-small cell lung carcinomas in the Chinese patients.
  • METHODS: Using formalin fixed and paraffin embedded tissue samples, EGFR mutations were investigated in 290 cases of non-small cell lung carcinomas by microdissection and scorpions amplification refractory mutation system.
  • Furthermore, the relationship between EGFR mutations and gene copy number, and the relationship between EGFR gene status and clinicopathological variables of non-small cell lung carcinoma were analyzed.
  • The mutation rates in adenocarcinoma, large cell carcinoma and squamous carcinoma were 48.4%, 16.7% and 0, respectively.
  • FISH positive rates in adenocarcinoma, large cell carcinoma and squamous carcinoma were 52.1%, 75.0% and 11.1%, respectively.
  • Therefore, EGFR mutations mainly occurred in the adenocarcinoma, and was significantly correlated with EGFR high copy number.
  • CONCLUSIONS: There are higher EGFR mutation rate and FISH positive rate in non-small cell lung carcinoma in Chinese patients.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Gene Dosage. Genes, erbB-1. Genetic Diseases, Inborn. Lung Neoplasms / genetics. Mutation. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Carcinoma, Squamous Cell / genetics. Female. Gene Amplification. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged

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  • (PMID = 19094482.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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26. 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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27. Matsuda Y, Yamakawa K, Saoo K, Hosokawa K, Yokohira M, Kuno T, Iwai J, Shirai T, Obika K, Kamataki T, Imaida K: CYP2A6 overexpression in human lung cancers correlates with a high malignant status. Oncol Rep; 2007 Jul;18(1):53-7
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  • [Title] CYP2A6 overexpression in human lung cancers correlates with a high malignant status.
  • CYP2A6 is a major phase I enzyme metabolizing tobacco-specific nitrosamines, implicated as risk factors for lung cancer.
  • In this study, immunohistochemistry and in situ hybridization (ISH) for CYP2A6 with human lung cancer tissues (n=31) obtained by surgical resection showed significantly higher immunoreactivity in the cases with lymph node metastasis.
  • The adenocarcinoma cases (n=23) with lymph node metastasis or large tumor size showed a high immunoreactivity for CYP2A6.
  • ISH for CYP2A6 revealed mRNA expression in both adenocarcinoma and squamous cell carcinoma cells.
  • The data suggest that CYP2A6 could have an important role in the development and proliferation of lung carcinomas.
  • [MeSH-major] Aryl Hydrocarbon Hydroxylases / metabolism. Lung Neoplasms / enzymology. Mixed Function Oxygenases / metabolism
  • [MeSH-minor] Adenocarcinoma / enzymology. Adenocarcinoma / secondary. Aged. Carcinoma, Large Cell / enzymology. Carcinoma, Large Cell / secondary. Carcinoma, Small Cell / enzymology. Carcinoma, Small Cell / secondary. Carcinoma, Squamous Cell / enzymology. Carcinoma, Squamous Cell / secondary. Cytochrome P-450 CYP2A6. Disease Progression. Female. Humans. Immunoenzyme Techniques. Lymphatic Metastasis / pathology. Male. Neoplasm Invasiveness / pathology. Neoplasm Staging. Prognosis

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  • (PMID = 17549345.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / CYP2A6 protein, human; EC 1.- / Mixed Function Oxygenases; EC 1.14.13.- / Cytochrome P-450 CYP2A6; EC 1.14.14.1 / Aryl Hydrocarbon Hydroxylases
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28. Sun M, Behrens C, Feng L, Ozburn N, Tang X, Yin G, Komaki R, Varella-Garcia M, Hong WK, Aldape KD, Wistuba II: HER family receptor abnormalities in lung cancer brain metastases and corresponding primary tumors. Clin Cancer Res; 2009 Aug 1;15(15):4829-37
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  • [Title] HER family receptor abnormalities in lung cancer brain metastases and corresponding primary tumors.
  • PURPOSE: To compare the characteristics of deregulation of HER receptors and their ligands between primary tumor and corresponding brain metastases of non-small cell lung carcinoma (NSCLC).
  • Analysis of EGFR copy number using fluorescence in situ hybridization and mutation by PCR-based sequencing was also done.
  • However, adenocarcinoma metastases (30%) showed higher frequency of EGFR amplification than corresponding primary tumors (10%).
  • CONCLUSIONS: Our findings suggest that NSCLC brain metastases have some significant differences in HER family receptor-related abnormalities from primary lung tumors.
  • [MeSH-major] Brain Neoplasms / metabolism. Carcinoma, Non-Small-Cell Lung / metabolism. Lung Neoplasms / metabolism. Receptor, Epidermal Growth Factor / metabolism. Receptor, ErbB-2 / metabolism. Receptor, ErbB-3 / metabolism


29. 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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  • [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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30. Sakuma Y, Matsukuma S, Yoshihara M, Nakamura Y, Nakayama H, Kameda Y, Tsuchiya E, Miyagi Y: Epidermal growth factor receptor gene mutations in atypical adenomatous hyperplasias of the lung. Mod Pathol; 2007 Sep;20(9):967-73
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  • [Title] Epidermal growth factor receptor gene mutations in atypical adenomatous hyperplasias of the lung.
  • Activating epidermal growth factor receptor (EGFR) gene mutations are frequently detected in lung adenocarcinomas, especially adenocarcinomas with a nonmucinous bronchioloalveolar carcinoma component.
  • EGFR-mutated lung adenocarcinomas respond well to EGFR tyrosine kinase inhibitors.
  • We previously found that most (88%) pure nonmucinous bronchioloalveolar carcinomas (adenocarcinoma in situ) already harbor EGFR mutations, indicating that the mutations are an early genetic event in the pathogenesis.
  • We examined 54 atypical adenomatous hyperplasias, precursor lesions of lung adenocarcinomas, obtained from 28 Japanese patients for the hotspot mutations of EGFR exons 19 and 21 and K-ras codon 12.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / genetics. Adenomatosis, Pulmonary / genetics. Gene Expression Regulation, Neoplastic. Lung Neoplasms / genetics. Mutation. Receptor, Epidermal Growth Factor / genetics

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  • (PMID = 17618248.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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31. González Manzano R, Martínez Navarro E, Eugenieva E, Fernández Morejón FJ, Farré J, Brugarolas A: A novel EGFR nonsense mutation in a non-small-cell lung cancer (NSCLC) patient who did not derive any clinical benefit with combination chemotherapy and erlotinib. Clin Transl Oncol; 2008 Jul;10(7):442-4
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  • [Title] A novel EGFR nonsense mutation in a non-small-cell lung cancer (NSCLC) patient who did not derive any clinical benefit with combination chemotherapy and erlotinib.
  • Most of the somatic epidermal growth factor receptor (EGFR) mutations described to date in non-smallcell lung cancer (NSCLC) patients are located in the kinase domain and are considered activating mutations.
  • Here we report a case of a previously undescribed EGFR nonsense mutation in a lung adenocarcinoma patient who did not derive any clinical benefit with combination chemotherapy and erlotinib.
  • To the best of our knowledge this is the second report in the literature describing an EGFR nonsense mutation in lung cancer patients.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Lung Neoplasms / genetics. Protein Kinase Inhibitors / therapeutic use. Quinazolines / therapeutic use. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Base Sequence. Codon, Nonsense. Erlotinib Hydrochloride. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Middle Aged

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  • (PMID = 18628075.001).
  • [ISSN] 1699-048X
  • [Journal-full-title] Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
  • [ISO-abbreviation] Clin Transl Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Codon, Nonsense; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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32. 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


33. Gabrecht T, Glanzmann T, Freitag L, Weber BC, van den Bergh H, Wagnières G: Optimized autofluorescence bronchoscopy using additional backscattered red light. J Biomed Opt; 2007 Nov-Dec;12(6):064016
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  • We have performed a clinical study involving 41 lung cancers using modified autofluorescence bronchoscopy systems.
  • [MeSH-major] Bronchial Neoplasms / diagnosis. Bronchoscopy / methods
  • [MeSH-minor] Adenocarcinoma / diagnosis. Bronchi / pathology. Bronchoscopes. Carcinoma in Situ / diagnosis. Carcinoma, Small Cell / diagnosis. Carcinoma, Squamous Cell / diagnosis. Fluorescence. Humans. Image Processing, Computer-Assisted. Light. Lung Neoplasms / diagnosis. Metaplasia / diagnosis. Predictive Value of Tests. Scattering, Radiation. Spectrometry, Fluorescence

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  • (PMID = 18163832.001).
  • [ISSN] 1083-3668
  • [Journal-full-title] Journal of biomedical optics
  • [ISO-abbreviation] J Biomed Opt
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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34. Finberg KE, Sequist LV, Joshi VA, Muzikansky A, Miller JM, Han M, Beheshti J, Chirieac LR, Mark EJ, Iafrate AJ: Mucinous differentiation correlates with absence of EGFR mutation and presence of KRAS mutation in lung adenocarcinomas with bronchioloalveolar features. J Mol Diagn; 2007 Jul;9(3):320-6
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  • [Title] Mucinous differentiation correlates with absence of EGFR mutation and presence of KRAS mutation in lung adenocarcinomas with bronchioloalveolar features.
  • Somatic mutations in the epidermal growth factor receptor gene (EGFR) are detected in a subset of lung adenocarcinomas, particularly bronchioloalveolar carcinoma (BAC) and adenocarcinoma with bronchioloalveolar features (AWBF), and correlate with clinical response to tyrosine kinase inhibitors (TKIs).
  • In contrast, lung adenocarcinomas refractory to TKIs often have activating mutations in KRAS but lack EGFR mutations.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / pathology. Adenocarcinoma, Mucinous / genetics. Adenocarcinoma, Mucinous / pathology. Genes, erbB-1. Genes, ras. Lung Neoplasms / genetics. Lung Neoplasms / pathology. Mutation
  • [MeSH-minor] Aged. Aged, 80 and over. Cell Differentiation / genetics. DNA Mutational Analysis. Disease Progression. Female. Gene Dosage. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Prognosis. Retrospective Studies

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  • (PMID = 17591931.001).
  • [ISSN] 1525-1578
  • [Journal-full-title] The Journal of molecular diagnostics : JMD
  • [ISO-abbreviation] J Mol Diagn
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1899415
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35. 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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36. Sihto H, Puputti M, Pulli L, Tynninen O, Koskinen W, Aaltonen LM, Tanner M, Böhling T, Visakorpi T, Bützow R, Knuuttila A, Nupponen NN, Joensuu H: Epidermal growth factor receptor domain II, IV, and kinase domain mutations in human solid tumors. J Mol Med (Berl); 2005 Dec;83(12):976-83
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  • Mutations that may predict response to adenosine 5'-triphosphate (ATP)-mimetic epidermal growth factor receptor (EGFR) inhibitors occur in the EGFR kinase domain in lung adenocarcinomas and bronchioloalveolar carcinomas (BACs).
  • Eight (11%) out of the 40 lung adenocarcinomas, or 33 BACs, investigated had exon 19 or 21 mutation in the kinase domain, but no mutations were found in other tumor types.
  • Most of the lung cancers with mutated EGFR had three to six copies of the mutated gene in fluorescence in situ hybridization.
  • We conclude that mutations of the EGFR kinase domain and the cysteine-rich extracellular domains are infrequent in most types of human cancer apart from lung adenocarcinoma.
  • Mutated EGFR is usually not amplified in lung cancer.
  • [MeSH-major] Glioblastoma / genetics. Lung Neoplasms / genetics. Mutation. Receptor Protein-Tyrosine Kinases / genetics. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Amino Acid Sequence. Carcinoma, Non-Small-Cell Lung / enzymology. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / pathology. Chromatography, High Pressure Liquid. Exons. Humans. In Situ Hybridization, Fluorescence. Molecular Sequence Data. Polymerase Chain Reaction. Protein Structure, Tertiary. Sequence Analysis, DNA

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  • (PMID = 16133419.001).
  • [ISSN] 0946-2716
  • [Journal-full-title] Journal of molecular medicine (Berlin, Germany)
  • [ISO-abbreviation] J. Mol. Med.
  • [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 Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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37. 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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38. Fulzele SV, Shaik MS, Chatterjee A, Singh M: Anti-cancer effect of celecoxib and aerosolized docetaxel against human non-small cell lung cancer cell line, A549. J Pharm Pharmacol; 2006 Mar;58(3):327-36
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  • [Title] Anti-cancer effect of celecoxib and aerosolized docetaxel against human non-small cell lung cancer cell line, A549.
  • Direct delivery of chemotherapeutic agents to the lung can increase both the drug concentration and exposure period to lung tumours.
  • The objective of this study was to formulate docetaxel (DOC) into a metered dose inhaler (MDI), assess its aerodynamic characteristics and to evaluate the effect of celecoxib (CXB), a cyclooxygenase-2 (COX-2) inhibitor, on the in-vitro cytotoxicity and apoptotic response of aerosolized DOC against human lung adenocarcinoma cell line A549.
  • A six-stage viable impactor was used to assess the in-vitro cytotoxicity of DOC-MDI alone or in combination with CXB.
  • Our results indicate the potential of inhalation delivery of DOC in the treatment of lung cancer.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Carcinoma, Non-Small-Cell Lung. Cyclooxygenase Inhibitors / pharmacology. Lung Neoplasms. Pyrazoles / pharmacology. Sulfonamides / pharmacology. Taxoids / pharmacology
  • [MeSH-minor] Aerosols. Apoptosis / drug effects. Caspase 3. Caspases / biosynthesis. Celecoxib. Cell Line, Tumor. Cyclooxygenase 2 / biosynthesis. Drug Synergism. Ethanol / chemistry. Humans. Hydrocarbons, Fluorinated / chemistry. In Situ Nick-End Labeling. Membrane Proteins / biosynthesis. Metered Dose Inhalers. PPAR gamma / biosynthesis. Particle Size. Polymerase Chain Reaction. RNA, Messenger / biosynthesis. Solubility

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  • (PMID = 16536899.001).
  • [ISSN] 0022-3573
  • [Journal-full-title] The Journal of pharmacy and pharmacology
  • [ISO-abbreviation] J. Pharm. Pharmacol.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / G12RR03020-11
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aerosols; 0 / Antineoplastic Agents, Phytogenic; 0 / Cyclooxygenase Inhibitors; 0 / Hydrocarbons, Fluorinated; 0 / Membrane Proteins; 0 / PPAR gamma; 0 / Pyrazoles; 0 / RNA, Messenger; 0 / Sulfonamides; 0 / Taxoids; 15H5577CQD / docetaxel; 3K9958V90M / Ethanol; 431-89-0 / HFA 134a; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; JCX84Q7J1L / Celecoxib
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39. 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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40. Udaka N, Miyagi Y, Ito T: Connexin expression in mouse lung tumor. Cancer Lett; 2007 Feb 8;246(1-2):224-9
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  • [Title] Connexin expression in mouse lung tumor.
  • In the present study, using reverse transcription-polymerase chain reaction (RT-PCR) and in situ RT-PCR, we examined expression of Connexins (Cx26, 32, 37, 40, 43 and 45) in the normal lung and lung tumors of mice to determine whether their expressions change during lung tumorigenesis.
  • Cx26, 32 and 40 were expressed similarly in the normal lung tissue and tumors with smaller size (0.5-1.5mm) though expression of Cx32 and 40 decreased in tumors with larger size (>2.5mm).
  • Cx37 and 45 were expressed in both normal lung and larger size tumors but no expression was seen in smaller size tumors.
  • Cx43 was similarly detectable in normal lung, smaller size tumor and larger size tumor, but western blotting showed that Cx43 was phosphorylated during lung tumorigenesis.
  • [MeSH-major] Connexins / genetics. Gene Expression Regulation, Neoplastic. Lung Neoplasms / genetics
  • [MeSH-minor] 4-Nitroquinoline-1-oxide. Adenocarcinoma / chemically induced. Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Animals. Blotting, Western. Connexin 43 / genetics. Connexin 43 / metabolism. Lung / chemistry. Lung / metabolism. Male. Mice. Mice, Inbred A. Phosphorylation. Quinolones. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 16580773.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / 4-nitroquinolone-1-oxide; 0 / Connexin 43; 0 / Connexins; 0 / Quinolones; 0 / RNA, Messenger; 0 / connexin 32; 0 / connexin 37; 0 / connexin 40; 0 / connexin 45; 127120-53-0 / connexin 26; 56-57-5 / 4-Nitroquinoline-1-oxide
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41. Kanomata N, Nakahara R, Oda T, Aoyagi Y, Ishii G, Yokose T, Hasebe T, Nagai K, Yokozaki H, Ochiai A: Expression and localization of mRNAs for matrix metalloproteinases and their inhibitors in mixed bronchioloalveolar carcinomas with invasive components. Mod Pathol; 2005 Jun;18(6):828-37
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  • Matrix metalloproteinases (MMPs) are believed to play an essential role in cancer invasion, although detailed differences between noninvasive and invasive lung carcinomas are still unclear.
  • To elucidate the expression and activity patterns of MMPs in noninvasive and invasive carcinoma of the lung, we performed in situ hybridization and real-time reverse transcription-polymerase chain reaction to detect messenger RNAs (mRNAs) of MMPs and their tissue inhibitors (TIMPs).
  • Gelatinase activity was examined by zymography and in situ zymography.
  • All the tumors were adenocarcinoma mixed bronchioloalveolar carcinomas according to the 1999 WHO classification.
  • MMP and TIMP2 mRNAs were detected by in situ hybridization in all samples, in both noninvasive and invasive carcinoma components.
  • Signals for MMP mRNAs were significantly higher in both noninvasive and invasive carcinomas than in tumor-free lung tissue.
  • Our data on mixed adenocarcinoma suggest that noninvasive carcinoma areas already express a molecular mechanism involving MMPs similar to that expressed by invasive carcinoma areas.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / pathology. Lung Neoplasms / pathology. Matrix Metalloproteinases / genetics. RNA, Messenger / metabolism. Tissue Inhibitor of Metalloproteinases / genetics
  • [MeSH-minor] Aged. Basement Membrane / metabolism. Basement Membrane / pathology. Collagen Type IV / analysis. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. In Situ Hybridization. Male. Middle Aged. Neoplasm Invasiveness. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15696122.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Collagen Type IV; 0 / RNA, Messenger; 0 / Tissue Inhibitor of Metalloproteinases; EC 3.4.24.- / Matrix Metalloproteinases
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42. Goyal A, Chen S: Bronchioloalveolar carcinoma is really carcinoma in situ. Arch Pathol Lab Med; 2008 Oct;132(10):1548
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  • [Title] Bronchioloalveolar carcinoma is really carcinoma in situ.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / diagnosis. Carcinoma in Situ / diagnosis. Lung Neoplasms / diagnosis
  • [MeSH-minor] Biopsy. Diagnosis, Differential. Humans. World Health Organization

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  • [CommentOn] Arch Pathol Lab Med. 2007 Jul;131(7):1027-32 [17616987.001]
  • (PMID = 18834206.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
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43. 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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44. Al-Kuraya K, Siraj AK, Bavi P, Al-Jommah N, Ezzat A, Sheikh S, Amr S, Al-Dayel F, Simon R, Guido S: High epidermal growth factor receptor amplification rate but low mutation frequency in Middle East lung cancer population. Hum Pathol; 2006 Apr;37(4):453-7
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  • [Title] High epidermal growth factor receptor amplification rate but low mutation frequency in Middle East lung cancer population.
  • Epidermal growth factor receptor (EGFR) exon 18-21 mutations were shown to be highly predictive of response to gefitinib (Iressa) therapy in lung cancer.
  • Studies on Western and Japanese lung cancers have indicated substantial differences in the EGFR mutation frequency between these populations.
  • To investigate the prevalence of EGFR in another distinct ethnic group, EGFR alterations were studied in 47 consecutive non small cell lung cancers from Saudi Arabia by immunohistochemistry, fluorescence in situ hybridization, and DNA sequencing.
  • Only 1 exon 18-21 mutation was seen among 34 lung cancers that could be successfully sequenced.
  • It is concluded that EGFR exon 18-21 mutations are rare in Middle East patients with lung cancer and occur in a similar range as in Western patients.
  • [MeSH-major] Adenocarcinoma / genetics. Carcinoma, Squamous Cell / genetics. Gene Amplification. Lung Neoplasms / genetics. Mutation. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Adult. Aged. Antineoplastic Agents / therapeutic use. Cohort Studies. DNA Mutational Analysis. DNA, Neoplasm / analysis. Female. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Middle Aged. Quinazolines / therapeutic use. Saudi Arabia. Tissue Array Analysis

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  • (PMID = 16564920.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA, Neoplasm; 0 / Quinazolines; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
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45. 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


46. 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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47. 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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48. 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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49. Strumylaite L, Bogusevicius A, Ryselis S, Pranys D, Poskiene L, Kregzdyte R, Abdrachmanovas O, Asadauskaite R: [Association between cadmium and breast cancer]. Medicina (Kaunas); 2008;44(6):415-20
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  • Cadmium is a known human lung carcinogen, although some studies indicate a link between cadmium exposure and human breast cancer.
  • [MeSH-major] Adenocarcinoma, Mucinous / chemistry. Breast / chemistry. Breast Neoplasms / chemistry. Cadmium / analysis. Carcinoma in Situ / chemistry. Carcinoma, Ductal, Breast / chemistry

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  • (PMID = 18660635.001).
  • [ISSN] 1648-9144
  • [Journal-full-title] Medicina (Kaunas, Lithuania)
  • [ISO-abbreviation] Medicina (Kaunas)
  • [Language] lit
  • [Publication-type] Comparative Study; English Abstract; Evaluation Studies; Journal Article
  • [Publication-country] Lithuania
  • [Chemical-registry-number] 0 / Receptors, Estrogen; 00BH33GNGH / Cadmium
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50. Savic S, Tapia C, Grilli B, Rufle A, Bihl MP, de Vito Barascud A, Herzog M, Terracciano L, Baty F, Bubendorf L: Comprehensive epidermal growth factor receptor gene analysis from cytological specimens of non-small-cell lung cancers. Br J Cancer; 2008 Jan 15;98(1):154-60
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  • [Title] Comprehensive epidermal growth factor receptor gene analysis from cytological specimens of non-small-cell lung cancers.
  • Epidermal growth factor receptor (EGFR) gene mutations and increased copy numbers are considered as predictors of response to EGFR tyrosine kinase inhibitors (EGFR-TKI) in non-small-cell lung cancer (NSCLC).
  • Lung cancer diagnosis is often based on cytology alone.
  • Eighty-four cytological specimens from NSCLCs were prospectively analysed for EGFR gene mutation in exons 18-21 and EGFR gene copy numbers were evaluated by fluorescence in situ hybridisation (FISH).
  • Fluorescence in situ hybridisation results of cytological specimens were compared to the FISH results on matching biopsies (n=33).
  • Initial diagnosis of NSCLC was solely based on cytology in 37 out of 84 (44.0%) patients.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Lung Neoplasms / genetics. Mutation / genetics. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / secondary. Biopsy. Carcinoma, Large Cell / genetics. Carcinoma, Large Cell / metabolism. Carcinoma, Large Cell / secondary. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / secondary. Exons / genetics. Feasibility Studies. Female. Gene Dosage. Humans. In Situ Hybridization, Fluorescence. Male. Neoplasm Recurrence, Local / genetics. Neoplasm Recurrence, Local / metabolism. Neoplasm Recurrence, Local / pathology. Neuroectodermal Tumors / genetics. Neuroectodermal Tumors / metabolism. Neuroectodermal Tumors / secondary. Prospective Studies. Survival Rate

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  • (PMID = 18087280.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Other-IDs] NLM/ PMC2359717
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51. 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


52. Song Y, Huang J, Wang JW: [Relationship between HER2/neu gene amplification and protein expression and prognosis in patients with advanced gastric carcinoma]. Chin J Cancer; 2010 Jan;29(1):76-81
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  • The HER2/neu status in 83 advanced gastric carcinomas was evaluated using immunohistochemistry (IHC) and fluorescence in situ hybridization (FISH).
  • [MeSH-major] Adenocarcinoma. Genes, erbB-2. Receptor, ErbB-2 / metabolism. Stomach Neoplasms
  • [MeSH-minor] Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Signet Ring Cell / drug therapy. Carcinoma, Signet Ring Cell / genetics. Carcinoma, Signet Ring Cell / metabolism. Carcinoma, Signet Ring Cell / pathology. Carcinoma, Signet Ring Cell / secondary. Female. Gene Amplification. Gene Expression Regulation, Neoplastic. Humans. Liver Neoplasms / secondary. Lung Neoplasms / secondary. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Staging. Survival Rate

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  • (PMID = 20038314.001).
  • [ISSN] 1000-467X
  • [Journal-full-title] Chinese journal of cancer
  • [ISO-abbreviation] Chin J Cancer
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, ErbB-2
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53. Shinmura K, Kageyama S, Tao H, Bunai T, Suzuki M, Kamo T, Takamochi K, Suzuki K, Tanahashi M, Niwa H, Ogawa H, Sugimura H: EML4-ALK fusion transcripts, but no NPM-, TPM3-, CLTC-, ATIC-, or TFG-ALK fusion transcripts, in non-small cell lung carcinomas. Lung Cancer; 2008 Aug;61(2):163-9
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  • [Title] EML4-ALK fusion transcripts, but no NPM-, TPM3-, CLTC-, ATIC-, or TFG-ALK fusion transcripts, in non-small cell lung carcinomas.
  • EML4-ALK gene fusions have recently been discovered in a subset of human lung carcinomas, and fusions of the ALK tyrosine kinase gene with the NPM, TPM3, CLTC, ATIC, and TFG genes have been found in hematological malignancies.
  • To elucidate the role of fusions between ALK and other genes in pulmonary carcinogenesis, we examined 77 non-small cell lung carcinomas (NSCLCs) for EML4-, NPM-, TPM3-, CLTC-, ATIC-, and TFG-ALK fusion transcripts by RT-PCR and subsequent sequencing analysis.
  • Both patients had a history of smoking, and histologically the carcinomas were adenocarcinoma.
  • In situ PCR of a paraffin block section showed that the carcinoma with expression of the variant 1 actually contained an EML4-ALK fusion gene.
  • [MeSH-major] Adenocarcinoma / genetics. Carcinoma, Non-Small-Cell Lung / genetics. Lung Neoplasms / genetics. Oncogene Proteins, Fusion / genetics


54. Tirabosco R, Lang-Lazdunski L, Diss TC, Amary MF, Rodriguez-Justo M, Landau D, Lorenzi W, Flanagan AM: Clear cell sarcoma of the mediastinum. Ann Diagn Pathol; 2009 Jun;13(3):197-200
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  • At thoracotomy, the mass was found tightly adherent to the esophageal wall and right lower lobe of the lung.
  • The diagnosis of clear cell sarcoma was supported by demonstrating the presence of an EWS gene rearrangement by fluorescence in situ hybridization.
  • We present the case and discuss the differential diagnosis.
  • [MeSH-minor] Adenocarcinoma / pathology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / analysis. Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Diagnosis, Differential. Female. Gastrointestinal Stromal Tumors / pathology. Gene Rearrangement. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Lymphatic Metastasis / pathology. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19433300.001).
  • [ISSN] 1532-8198
  • [Journal-full-title] Annals of diagnostic pathology
  • [ISO-abbreviation] Ann Diagn Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA-Binding Protein EWS
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55. 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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56. Liu YJ, Yan PS, Li J, Jia JF: Expression and significance of CD44s, CD44v6, and nm23 mRNA in human cancer. World J Gastroenterol; 2005 Nov 14;11(42):6601-6
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  • AIM: To investigate the relationship between the expression levels of nm23 mRNA, CD44s, and CD44v6, and oncogenesis, development and metastasis of human gastric adenocarcinoma, colorectal adenocarcinoma, intraductal carcinoma of breast, and lung cancer.
  • METHODS: Using tissue microarray by immuhistochemical (IHC) staining and in situ hybridization (ISH), we examined the expression levels of nm23 mRNA, CD44s, and CD44v6 in 62 specimens of human gastric adenocarcinoma and 62 specimens of colorectal adenocarcinoma; the expression of CD44s and CD44v6 in 120 specimens of intraductal carcinoma of breast and 20 specimens of normal breast tissue; the expression of nm23 mRNA in 72 specimens of human lung cancer and 23 specimens of normal tissue adjacent to cancer.
  • RESULTS: The expression of nm23 mRNA in the tissues of gastric and colorectal adenocarcinoma was not significantly different from that in the normal tissues adjacent to cancer (P>0.05), and was not associated with the invasion of tumor and the pathology grade of adenocarcinoma (P>0.05).
  • However, the expression of nm23 mRNA was correlated negatively to the lymph node metastasis of gastric and colorectal adenocarcinoma (r = -0.49, P<0.01; r = -4.93, P<0.01).
  • The expression of CD44s in the tissues of gastric and colorectal adenocarcinoma was significantly different from that in the normal tissues adjacent to cancer (P<0.05; P<0.01).
  • CD44v6 was expressed in the tissues of gastric and colorectal adenocarcinoma only, the expression of CD44v6 was significantly associated with the lymph node metastasis, invasion and pathological grade of the tumor (r = 0.47, P<0.01; r = 5.04, P<0.01).
  • [MeSH-minor] Antigens, Neoplasm / genetics. Antigens, Neoplasm / metabolism. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Breast Neoplasms / genetics. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Colorectal Neoplasms / genetics. Colorectal Neoplasms / metabolism. Colorectal Neoplasms / pathology. Female. Humans. Immunohistochemistry. In Situ Hybridization. Lung Neoplasms / genetics. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. NM23 Nucleoside Diphosphate Kinases. Neoplasm Metastasis. Nucleoside-Diphosphate Kinase. Protein Array Analysis. Stomach Neoplasms / genetics. Stomach Neoplasms / metabolism. Stomach Neoplasms / pathology

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  • (PMID = 16425351.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD44; 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / CD44v6 antigen; 0 / Glycoproteins; 0 / NM23 Nucleoside Diphosphate Kinases; 0 / RNA, Messenger; EC 2.7.4.6 / NME1 protein, human; EC 2.7.4.6 / Nucleoside-Diphosphate Kinase
  • [Other-IDs] NLM/ PMC4355751
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57. Boland JM, Erdogan S, Vasmatzis G, Yang P, Tillmans LS, Johnson MR, Wang X, Peterson LM, Halling KC, Oliveira AM, Aubry MC, Yi ES: Anaplastic lymphoma kinase immunoreactivity correlates with ALK gene rearrangement and transcriptional up-regulation in non-small cell lung carcinomas. Hum Pathol; 2009 Aug;40(8):1152-8
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  • [Title] Anaplastic lymphoma kinase immunoreactivity correlates with ALK gene rearrangement and transcriptional up-regulation in non-small cell lung carcinomas.
  • Recently, the fusion gene EML4-ALK was identified in non-small cell lung carcinoma, which could be a potential therapeutic target.
  • Florescence in situ hybridization for the ALK locus and reverse transcriptase-polymerase chain reaction for EML4-ALK were performed on tumors positive for anaplastic lymphoma kinase by immunohistochemistry.
  • The 6 cases positive for anaplastic lymphoma kinase by immunohistochemistry showed evidence of ALK locus rearrangement by florescence in situ hybridization but were negative for EGFR and KRAS mutation.
  • In conclusion, anaplastic lymphoma kinase immunoreactivity in non-small cell lung carcinomas was associated with transcriptional up-regulation, ALK locus rearrangement, and the presence of EML4-ALK fusion transcript.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Gene Expression Regulation, Neoplastic. Gene Rearrangement. Lung Neoplasms / genetics. Protein-Tyrosine Kinases / genetics. Up-Regulation / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Aged. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / pathology. Cohort Studies. Female. Gene Expression Profiling. Humans. In Situ Hybridization, Fluorescence. Male. Oncogene Proteins, Fusion / genetics. Receptor Protein-Tyrosine Kinases. Sequence Analysis, DNA. Transcription, Genetic

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  • [CommentIn] Hum Pathol. 2010 Apr;41(4):614-5; author reply 615-616 [20163822.001]
  • (PMID = 19386350.001).
  • [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 / EML4-ALK fusion protein, human; 0 / Oncogene Proteins, Fusion; 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
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58. 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


59. 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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60. 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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61. 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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  • [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


62. Manxhuka-Kerliu S, Telaku S, Ahmetaj H, Baruti A, Loxha S, Kerliu A: Colorectal cancer: prognostic values. Bosn J Basic Med Sci; 2009 Feb;9(1):19-24
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  • After lung cancer colorectal cancer (Cc) is ranked the second, as a cause of cancer-related death.
  • Adenocarcinoma was the most frequent histological type found in 85,90% of cases, in 60,94% of males and 39,06% of females; squamous cell carcinoma in 7,38%, in 63,63% of males and 36,36% of females; mucinous carcinoma in 4,68%, in 57,15% of males and 42,85% of females; while adenosquamous carcinoma, undifferentiated carcinoma and carcinoma in situ in 0,71% of cases each.
  • Dukes' stage and degree of differentiation provide independent prognostic information in Cc.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma, Mucinous / diagnosis. Carcinoma, Squamous Cell / diagnosis. Colorectal Neoplasms / diagnosis

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  • [Cites] Ann Surg Oncol. 1999 Jun;6(4):385-8 [10379860.001]
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  • (PMID = 19284390.001).
  • [ISSN] 1512-8601
  • [Journal-full-title] Bosnian journal of basic medical sciences
  • [ISO-abbreviation] Bosn J Basic Med Sci
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Bosnia and Herzegovina
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63. 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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64. Hirsch FR, Varella-Garcia M, McCoy J, West H, Xavier AC, Gumerlock P, Bunn PA Jr, Franklin WA, Crowley J, Gandara DR, Southwest Oncology Group: Increased epidermal growth factor receptor gene copy number detected by fluorescence in situ hybridization associates with increased sensitivity to gefitinib in patients with bronchioloalveolar carcinoma subtypes: a Southwest Oncology Group Study. J Clin Oncol; 2005 Oct 1;23(28):6838-45
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  • [Title] Increased epidermal growth factor receptor gene copy number detected by fluorescence in situ hybridization associates with increased sensitivity to gefitinib in patients with bronchioloalveolar carcinoma subtypes: a Southwest Oncology Group Study.
  • PATIENTS AND METHODS: EGFR and HER2 gene copy numbers were assessed by fluorescence in situ hybridization (FISH) in 81 patients treated with gefitinib 500 mg/d (Southwest Oncology Group protocol S0126) and were correlated to treatment outcome.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / genetics. Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / genetics. Gene Dosage. Lung Neoplasms / genetics. Quinazolines / therapeutic use
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / genetics. Adult. Aged. Aged, 80 and over. Female. Genes, erbB-2. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Patient Selection. Predictive Value of Tests. Receptor, Epidermal Growth Factor / genetics. Receptor, Epidermal Growth Factor / physiology. Survival Analysis. Treatment Outcome

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  • [CommentIn] J Clin Oncol. 2005 Oct 1;23(28):6813-6 [16145056.001]
  • [CommentIn] J Clin Oncol. 2006 Mar 1;24(7):1219-20; author reply 1220-1 [16505443.001]
  • (PMID = 15998906.001).
  • [ISSN] 0732-183X
  • [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 / CA32102; United States / NCI NIH HHS / CA / CA38926; United States / NCI NIH HHS / CA / P30-CA46934; United States / NCI NIH HHS / CA / P50 CA058187
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Quinazolines; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
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65. Wehle D, Yonescu R, Long PP, Gala N, Epstein J, Griffin CA: Fluorescence in situ hybridization of 12p in germ cell tumors using a bacterial artificial chromosome clone 12p probe on paraffin-embedded tissue: clinical test validation. Cancer Genet Cytogenet; 2008 Jun;183(2):99-104
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  • [Title] Fluorescence in situ hybridization of 12p in germ cell tumors using a bacterial artificial chromosome clone 12p probe on paraffin-embedded tissue: clinical test validation.
  • Most germ cell tumors have an isochromosome 12p (detected by metaphase cytogenetics), 12p overrepresentation (detected by fluorescence in situ hybridization [FISH]), or both.
  • Twenty-four paraffin-embedded blocks from 14 tumor cases (7 malignant mixed germ cell tumors, 2 dysgerminomas, 4 non-germ cell malignancies arising in germ cell tumors, and 1 mediastinal adenocarcinoma) and 18 normal controls were studied.
  • Negative controls included normal lymph node, lung, and mediastinal tissue.
  • Because germ cell tumors may metastasize with non-germ cell tumor morphology, interphase FISH may be helpful in distinguishing de novo malignancy from germ cell tumor recurrence in its various forms.
  • [MeSH-major] Chromosomes, Artificial, Bacterial. Chromosomes, Human, Pair 12. In Situ Hybridization, Fluorescence / methods. Neoplasms, Germ Cell and Embryonal / genetics

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  • [Copyright] (c) 2008 Elsevier Inc.
  • (PMID = 18503827.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Validation Studies
  • [Publication-country] United States
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66. Quignon F, Rozier L, Lachages AM, Bieth A, Simili M, Debatisse M: Sustained mitotic block elicits DNA breaks: one-step alteration of ploidy and chromosome integrity in mammalian cells. Oncogene; 2007 Jan 11;26(2):165-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-minor] Adenocarcinoma / pathology. Anaphase. Animals. Antineoplastic Agents / pharmacology. Cells, Cultured. Colonic Neoplasms / pathology. Cricetinae. Cricetulus. DNA Breaks, Double-Stranded. Fibroblasts / physiology. G0 Phase. G1 Phase / genetics. Gene Rearrangement. Humans. Immunoblotting. In Situ Hybridization, Fluorescence. Lung / physiology. Microtubules. Mitotic Index. Nocodazole / pharmacology. Spindle Apparatus

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  • (PMID = 16832348.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; SH1WY3R615 / Nocodazole
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67. Lantuéjoul S, Salameire D, Salon C, Brambilla E: Pulmonary preneoplasia--sequential molecular carcinogenetic events. Histopathology; 2009 Jan;54(1):43-54
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  • The three pulmonary preneoplastic changes recognized to date in the lung include bronchial squamous dysplasia and in situ carcinoma, preceding invasive squamous cell carcinoma and basaloid carcinoma, atypical adenomatous hyperplasia, a preneoplastic condition of bronchioloalveolar carcinoma, and diffuse idiopathic pulmonary neuroendocrine cell hyperplasia, a proposed precursor for carcinoid tumours.
  • Although the gradual accumulation of molecular alterations has been widely investigated in bronchial carcinogenesis, with the aim of determining new biomarkers for early lung cancer detection in high-risk patients and targeted chemoprevention, lung adenocarcinoma pathogenesis has been only recently highlighted, with the recent discovery of epidermal growth factor receptor mutation pathway in non-smokers.
  • This review focuses on the current status of molecular pathology in lung cancer and pulmonary preneoplastic conditions.
  • [MeSH-major] Lung Neoplasms / genetics. Lung Neoplasms / pathology. Precancerous Conditions / genetics. Precancerous Conditions / pathology
  • [MeSH-minor] Adenocarcinoma / pathology. Humans. Lung / pathology. Small Cell Lung Carcinoma / pathology

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  • (PMID = 19187179.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 90
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68. 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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69. Ludwick C, Gilks CB, Miller D, Yaziji H, Clement PB: Aggressive behavior of stage I ovarian mucinous tumors lacking extensive infiltrative invasion: a report of four cases and review of the literature. Int J Gynecol Pathol; 2005 Jul;24(3):205-17
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  • [Title] Aggressive behavior of stage I ovarian mucinous tumors lacking extensive infiltrative invasion: a report of four cases and review of the literature.
  • We present four cases of stage I ovarian mucinous tumors that lacked extensive infiltrative invasion but were associated with an unexpectedly aggressive behavior.
  • The tumors were all stage Ia, 17 to 37 centimeters in maximal dimension, and typically multicystic with solid areas.
  • On follow-up, each patient experienced recurrent disease 7 months to 4.5 years after diagnosis, including hematogenous spread to lung and/or bone and liver in three patients.
  • [MeSH-major] Adenocarcinoma, Mucinous / pathology. Carcinoma in Situ / pathology. Ovarian Neoplasms / pathology

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  • (PMID = 15968194.001).
  • [ISSN] 0277-1691
  • [Journal-full-title] International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists
  • [ISO-abbreviation] Int. J. Gynecol. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 26
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70. Al-Saad S, Al-Shibli K, Donnem T, Andersen S, Bremnes RM, Busund LT: Clinical significance of epidermal growth factor receptors in non-small cell lung cancer and a prognostic role for HER2 gene copy number in female patients. J Thorac Oncol; 2010 Oct;5(10):1536-43
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  • [Title] Clinical significance of epidermal growth factor receptors in non-small cell lung cancer and a prognostic role for HER2 gene copy number in female patients.
  • INTRODUCTION: To compare the efficacy of silver in situ hybridization (SISH) and immunohistochemistry (IHC) in detecting HER2 alterations and to investigate the prevalence and prognostic significance of Erb family members in non-small cell lung cancer (NSCLC).
  • METHODS: Stage I to IIIA tumors from 335 patients with NSCLC were immunohistochemically tested for protein expression of all Erb family members.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / metabolism. Gene Dosage. Genes, erbB-2 / genetics. Lung Neoplasms / genetics. Lung Neoplasms / metabolism. Receptor, ErbB-2 / metabolism
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / therapy. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Large Cell / genetics. Carcinoma, Large Cell / metabolism. Carcinoma, Large Cell / therapy. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / therapy. Chromosomes, Human, Pair 17 / genetics. Combined Modality Therapy. Female. Follow-Up Studies. Humans. Immunoenzyme Techniques. In Situ Hybridization, Fluorescence. Male. Middle Aged. Neoplasm Staging. Prognosis. Radiotherapy Dosage. Receptor, Epidermal Growth Factor / metabolism. Retrospective Studies. Tissue Array Analysis


71. 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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72. 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


73. Oshikiri T, Miyamoto M, Hiraoka K, Shichinohe T, Kawarada Y, Kato K, Suzuoki M, Nakakubo Y, Kondo S, Dosaka-Akita H, Kasahara N, Katoh H: Transcriptional targeting of adenovirus vectors with the squamous cell carcinoma-specific antigen-2 promoter for selective apoptosis induction in lung cancer. Cancer Gene Ther; 2006 Sep;13(9):856-63
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  • [Title] Transcriptional targeting of adenovirus vectors with the squamous cell carcinoma-specific antigen-2 promoter for selective apoptosis induction in lung cancer.
  • Squamous cell carcinoma antigens SCCA1 and SCCA2 are highly homologous serine proteinase inhibitors which have been widely utilized as serological markers for squamous cell cancers, but it has recently been demonstrated that only SCCA2 is truly specific for certain forms of lung cancer.
  • Using a construct containing the 5'-flanking region of the SCCA2 gene between -460 and +0 bp and the luciferase reporter gene, SCCA2 promoter activity was detected in SCCA2-producing SCC cell lines (LK-2, LC-1), but not in SCCA2-nonproducing lung adenocarcinoma cell lines (A549, ABC-1, and RERF-LC-MS) or normal cells (WI-38, SAEC, and NHEK-Adult).
  • Infection with a recombinant adenovirus vector, Ad-SCCA2-DsRed, resulted in cell-specific expression of the SCCA2 promoter-driven DsRed marker gene only in LK-2 and LC-1 cells.
  • Infection with Ad-SCCA2-KLAKLAK2 specifically reduced the growth of the two human lung SCC cell lines compared to the SCCA2 nonproducing cell lines both in vitro and in vivo, suggesting that the SCCA2 promoter had a tumor-specific effect.
  • These results suggest that transduction of SCCA2 promoter-controlled suicide genes by adenoviral vectors can confer transcriptionally targeted cytotoxicity in SCCA2-producing lung SCC cells, and represents a novel strategy for gene transfer specifically targeted to SCC in the lung.
  • [MeSH-major] Adenoviridae / genetics. Antigens, Neoplasm / genetics. Apoptosis / genetics. Carcinoma, Squamous Cell / therapy. Gene Targeting / methods. Genetic Therapy / methods. Genetic Vectors / genetics. Lung Neoplasms / therapy. Serpins / genetics
  • [MeSH-minor] Cell Line, Tumor. DNA Primers. Humans. In Situ Nick-End Labeling. Luciferases / genetics. Promoter Regions, Genetic / genetics. Reverse Transcriptase Polymerase Chain Reaction


74. Rusin M, Zajkowicz A, Butkiewicz D: Resveratrol induces senescence-like growth inhibition of U-2 OS cells associated with the instability of telomeric DNA and upregulation of BRCA1. Mech Ageing Dev; 2009 Aug;130(8):528-37
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  • We examined how resveratrol influenced the growth of human cancer cell lines of different origin: osteosarcoma (U-2 OS) and lung adenocarcinoma (A549) and how it modulated the expression as well as the localization of key proteins, involved in DNA repair and cell cycle regulation.
  • [MeSH-minor] Blotting, Southern. Cell Aging. Cell Line, Tumor. Humans. In Situ Hybridization, Fluorescence. Models, Biological. Serine / chemistry. Sirtuin 1. Sirtuins / metabolism. Up-Regulation


75. Peng KJ, Wang JH, Su WT, Wang XC, Yang FT, Nie WH: Characterization of two human lung adenocarcinoma cell lines by reciprocal chromosome painting. Dongwuxue Yanjiu; 2010 Apr;31(2):113-21
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  • [Title] Characterization of two human lung adenocarcinoma cell lines by reciprocal chromosome painting.
  • Lung cancer is a leading cause of cancer death worldwide.
  • Some lung cancer patients correlate with a gas of radon besides smoking.
  • To search for common chromosomal aberrations in lung cancer cell lines established from patients induced by different factors, a combined approach of chromosome sorting, forward and reverse chromosome painting was used to characterize karyotypes of two lung adenocarcinoma cell lines: A549 and GLC-82 with the latter line derived from a patient who has suffered long-term exposure to environmental radon gas pollution.
  • The chromosome painting results revealed that complex chromosomal rearrangements occurred in these two lung adenocarcinoma cell lines.
  • Furthermore, two apparently common breakpoints, HSA8q24 and 12q14 were found in these two lung cancer cell lines.

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  • (PMID = 20545000.001).
  • [ISSN] 2095-8137
  • [Journal-full-title] Dong wu xue yan jiu = Zoological research
  • [ISO-abbreviation] Zool. Res.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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76. Lu S, Zhang J, Zhou Z, Liao ML, He WZ, Zhou XY, Li ZM, Xiang JQ, Wang JJ, Chen HQ: Synergistic inhibitory activity of zoledronate and paclitaxel on bone metastasis in nude mice. Oncol Rep; 2008 Sep;20(3):581-7
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  • However, there is limited data on the effects of combination therapies on the development of bone metastasis in animal models of lung cancer.
  • The purpose of this study was to establish a human lung adenocarcinoma cell line with high bone metastatic potential in an immunodeficient mouse model and to evaluate the synergistic inhibitory activity of zoledronate and paclitaxel (P) on bone metastasis in nude mice.
  • A human lung adenocarcinoma cell line with high bone metastatic potential (SPC-A1-BM) was established by 10 rounds of in vivo selection.
  • Tumor growth was evaluated with bone scans, X-rays and in situ immunohistochemistry.
  • The results of this study indicated that zoledronate enhanced the efficacy of paclitaxel synergistically, by reducing the incidence of bone metastasis from lung cancer and prolonging survival in a mouse model of non-small cell lung cancer with a high potential for metastasis to bone.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Bone Density Conservation Agents / therapeutic use. Bone Neoplasms / drug therapy. Carcinoma, Non-Small-Cell Lung / drug therapy. Diphosphonates / therapeutic use. Imidazoles / therapeutic use. Paclitaxel / therapeutic use
  • [MeSH-minor] Animals. Collagen Type I / blood. Drug Therapy, Combination. Enzyme-Linked Immunosorbent Assay. Humans. Immunoenzyme Techniques. Incidence. Lung Neoplasms / drug therapy. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Mice. Mice, Nude. Peptides / blood. Proto-Oncogene Proteins c-bcl-2 / metabolism. Survival Rate. Tumor Cells, Cultured. Xenograft Model Antitumor Assays. bcl-2-Associated X Protein / metabolism. bcl-X Protein / metabolism

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  • (PMID = 18695909.001).
  • [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 / Antineoplastic Agents, Phytogenic; 0 / Bcl2l1 protein, mouse; 0 / Bone Density Conservation Agents; 0 / Collagen Type I; 0 / Diphosphonates; 0 / Imidazoles; 0 / Peptides; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein; 0 / bcl-X Protein; 0 / collagen type I trimeric cross-linked peptide; 6XC1PAD3KF / zoledronic acid; P88XT4IS4D / Paclitaxel
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77. 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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  • [Cites] J Natl Cancer Inst. 2005 May 4;97(9):643-55 [15870435.001]
  • [Cites] Br J Cancer. 2008 Jan 15;98(1):154-60 [18087280.001]
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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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78. 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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79. Castaño Z, Vergara-Irigaray N, Pajares MJ, Montuenga LM, Pio R: Expression of alpha CP-4 inhibits cell cycle progression and suppresses tumorigenicity of lung cancer cells. Int J Cancer; 2008 Apr 1;122(7):1512-20
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  • [Title] Expression of alpha CP-4 inhibits cell cycle progression and suppresses tumorigenicity of lung cancer cells.
  • The protein alpha CP-4 (also known as hnRNP E4) is an RNA binding protein encoded by a gene at 3p21, one of the most common altered regions in lung cancer.
  • It has been proposed that alpha CP-4 may function as a lung tumor suppressor.
  • Lack of alpha CP-4 expression is frequent in highly proliferative lung tumors and correlates with alpha CP-4 allele losses.
  • The aim of this study was to evaluate the effect of alpha CP-4 on the tumorigenic capacity of lung cancer cells. alpha CP-4 expression was induced by transient transfection or stable infection with recombinant retroviruses.
  • Induction of alpha CP-4 expression caused cell cycle arrest in G(2)/M in 3 out of the 7 lung cancer cell lines studied, while no effect on apoptosis was observed.
  • In conclusion, expression of alpha CP-4 can inhibit proliferation and tumorigenesis of lung cancer cells, both in vivo and in vitro, by delaying the progression of the cell cycle.
  • [MeSH-major] Apoptosis. Carcinoma, Non-Small-Cell Lung / metabolism. Cell Cycle. DNA Damage. Lung Neoplasms / metabolism. RNA-Binding Proteins / metabolism. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma, Bronchiolo-Alveolar / metabolism. Animals. Blotting, Western. Carcinoid Tumor / metabolism. Carcinoma, Large Cell / metabolism. Carcinoma, Squamous Cell / metabolism. Chromosomes, Human, Pair 3. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Mice. Mice, Nude. Retroviridae. Reverse Transcriptase Polymerase Chain Reaction. Transfection. Transplantation, Heterologous

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17973258.001).
  • [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 / PCBP4 protein, human; 0 / RNA-Binding Proteins; 0 / Tumor Suppressor Proteins
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80. 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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81. Metro G, Finocchiaro G, Toschi L, Bartolini S, Magrini E, Cancellieri A, Trisolini R, Castaldini L, Tallini G, Crino L, Cappuzzo F: Epidermal growth factor receptor (EGFR) targeted therapies in non-small cell lung cancer (NSCLC). Rev Recent Clin Trials; 2006 Jan;1(1):1-13
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epidermal growth factor receptor (EGFR) targeted therapies in non-small cell lung cancer (NSCLC).
  • The Epidermal Growth Factor Receptor (EGFR) family, including EGFR, HER2, HER3, and HER4, is implicated in the development and progression of cancer, and is expressed in many human epithelial malignancies, including Non-Small Cell Lung Cancer (NSCLC).
  • Among clinical characteristics, although female gender, and adenocarcinoma histology, showed to be significantly associated to TKI sensitivity, never smoking history is probably the most relevant factor.
  • Recent findings in gefitinib treated patients support HER2 analysis by fluorescence in situ hybridization as a complementary test for selection of patient candidate for EGFR targeted therapies.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / therapy. Lung Neoplasms / therapy. Receptor, Epidermal Growth Factor / antagonists & inhibitors
  • [MeSH-minor] Antibodies, Monoclonal / pharmacology. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Cetuximab. Erlotinib Hydrochloride. Female. Genes, ras. Humans. In Situ Hybridization, Fluorescence. Male. Quinazolines / pharmacology. Quinazolines / therapeutic use. Trastuzumab. Treatment Outcome


82. Moreira AL: Bronchioloalveolar Carcinoma and Minimally Invasive Adenocarcinoma. Surg Pathol Clin; 2010 Mar;3(1):1-26
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bronchioloalveolar Carcinoma and Minimally Invasive Adenocarcinoma.
  • The most recent WHO classification of lung cancer defines bronchioloalveolar carcinoma (BAC) as a noninvasive carcinoma or adenocarcinoma in situ.
  • As a result, the diagnosis of BAC has been used in association with small, solitary, and well-differentiated adenocarcinoma as well as tumors with advanced clinical stage.
  • At present, there is a growing consensus among specialists in thoracic oncology that BAC or adenocarcinoma in situ is a rare tumor, and the term should be restricted to adenocarcinomas that show a pure lepidic pattern of growth.
  • The concept of minimally invasive adenocarcinoma is developing in order to differentiate a pure BAC from an invasive adenocarcinoma that still carries an excellent prognosis.

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 26839025.001).
  • [ISSN] 1875-9181
  • [Journal-full-title] Surgical pathology clinics
  • [ISO-abbreviation] Surg Pathol Clin
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Adenocarcinoma / Bronchioloalveolar carcinoma / Carcinoma in situ / Lung
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83. 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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84. Jäger M, Schoberth A, Ruf P, Hess J, Lindhofer H: The trifunctional antibody ertumaxomab destroys tumor cells that express low levels of human epidermal growth factor receptor 2. Cancer Res; 2009 May 15;69(10):4270-6
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  • However, no approved anti-HER2/neu therapy is available for the majority of breast cancer patients, who express HER2/neu at low levels (with scores of 1+ or 2+/fluorescence in situ hybridization-negative).
  • [MeSH-minor] Adenocarcinoma / pathology. Antineoplastic Agents / toxicity. Cecal Neoplasms / pathology. Cell Line, Tumor. Cell Survival / drug effects. Female. Gene Expression Profiling. Humans. Ileal Neoplasms / pathology. Leukocytes, Mononuclear / cytology. Leukocytes, Mononuclear / drug effects. Lung Neoplasms / pathology

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  • (PMID = 19435924.001).
  • [ISSN] 1538-7445
  • [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 / Antibodies, Bispecific; 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / ertumaxomab; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, ErbB-2
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85. Shaw AT, Yeap BY, Mino-Kenudson M, Digumarthy SR, Costa DB, Heist RS, Solomon B, Stubbs H, Admane S, McDermott U, Settleman J, Kobayashi S, Mark EJ, Rodig SJ, Chirieac LR, Kwak EL, Lynch TJ, Iafrate AJ: Clinical features and outcome of patients with non-small-cell lung cancer who harbor EML4-ALK. J Clin Oncol; 2009 Sep 10;27(26):4247-53
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  • [Title] Clinical features and outcome of patients with non-small-cell lung cancer who harbor EML4-ALK.
  • PURPOSE: The EML4-ALK fusion oncogene represents a novel molecular target in a small subset of non-small-cell lung cancers (NSCLC).
  • PATIENTS AND METHODS: Patients with NSCLC were selected for genetic screening on the basis of two or more of the following characteristics: female sex, Asian ethnicity, never/light smoking history, and adenocarcinoma histology.
  • EML4-ALK was identified by using fluorescent in situ hybridization for ALK rearrangements and was confirmed by immunohistochemistry for ALK expression.


86. 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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87. 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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88. 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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89. Bozzetti C, Tiseo M, Lagrasta C, Nizzoli R, Guazzi A, Graiani G, Rindi G, Ardizzoni A: Is cytology reliable for epidermal growth factor receptor gene evaluation in non-small cell lung cancer? J Thorac Oncol; 2010 Apr;5(4):551-3
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  • [Title] Is cytology reliable for epidermal growth factor receptor gene evaluation in non-small cell lung cancer?
  • BACKGROUND: Epidermal growth factor receptor (EGFR) gene copy number has been proposed as predictor of response to epidermal growth factor receptor tyrosine kinase inhibitors in advanced non-small cell lung cancer (NSCLC).
  • METHODS: Cytologic and matched histologic samples from 33 primary non-small cell lung cancers were analyzed by fluorescence in situ hybridization (FISH) for epidermal growth factor receptor gene.
  • [MeSH-major] Adenocarcinoma / pathology. Carcinoma, Non-Small-Cell Lung / pathology. Carcinoma, Squamous Cell / pathology. Gene Dosage. In Situ Hybridization, Fluorescence. Lung Neoplasms / pathology. Receptor, Epidermal Growth Factor / genetics


90. Li L, Xiong YY, Liu L, Chen TX, Yao XF, Wang YW: [Relationships among expressions of hTERT, MDR1, MRP mRNA, and C-myc protein in non-small cell lung cancer]. Ai Zheng; 2005 Jan;24(1):53-7
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  • [Title] [Relationships among expressions of hTERT, MDR1, MRP mRNA, and C-myc protein in non-small cell lung cancer].
  • This study was to investigate relations among expressions of hTERT, MDR1, MRP mRNA, and C-myc protein in non-small cell lung cancer (NSCLC).
  • METHODS: Expressions of hTERT, MDR1, MRP mRNA in 113 cases of NSCLC tissues were detected by in situ hybridization, expression of C-myc protein was detected by SP immunohistochemistry, their correlations with clinicopathologic features of NSCLC were statistically analyzed.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / metabolism. DNA-Binding Proteins / biosynthesis. Lung Neoplasms / metabolism. Multidrug Resistance-Associated Proteins / biosynthesis. P-Glycoprotein / biosynthesis. Proto-Oncogene Proteins c-myc / biosynthesis. Telomerase / biosynthesis
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adult. Aged. Female. Genes, MDR. Humans. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Staging. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

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  • (PMID = 15642200.001).
  • [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 / DNA-Binding Proteins; 0 / Multidrug Resistance-Associated Proteins; 0 / P-Glycoprotein; 0 / Proto-Oncogene Proteins c-myc; 0 / RNA, Messenger; EC 2.7.7.49 / Telomerase
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91. Zhu H, Lam DC, Han KC, Tin VP, Suen WS, Wang E, Lam WK, Cai WW, Chung LP, Wong MP: High resolution analysis of genomic aberrations by metaphase and array comparative genomic hybridization identifies candidate tumour genes in lung cancer cell lines. Cancer Lett; 2007 Jan 8;245(1-2):303-14
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  • [Title] High resolution analysis of genomic aberrations by metaphase and array comparative genomic hybridization identifies candidate tumour genes in lung cancer cell lines.
  • In this study, metaphase and array comparative genomic hybridization showed good correlation of aberration profiles in lung adenocarcinoma cell lines from patients with different tobacco exposure.
  • [MeSH-major] Adenocarcinoma / genetics. Chromosome Aberrations. Genetic Predisposition to Disease / genetics. Lung Neoplasms / genetics. Nucleic Acid Hybridization / methods
  • [MeSH-minor] Aged. Female. Gene Dosage. Gene Expression Regulation, Neoplastic. Genome, Human. Humans. In Situ Hybridization, Fluorescence. Male. Metaphase / genetics. Microarray Analysis / methods. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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  • (PMID = 16517066.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
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92. Ceteci F, Ceteci S, Karreman C, Kramer BW, Asan E, Götz R, Rapp UR: Disruption of tumor cell adhesion promotes angiogenic switch and progression to micrometastasis in RAF-driven murine lung cancer. Cancer Cell; 2007 Aug;12(2):145-59
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  • [Title] Disruption of tumor cell adhesion promotes angiogenic switch and progression to micrometastasis in RAF-driven murine lung cancer.
  • Progression of non-small-cell lung cancer (NSCLC) to metastasis is poorly understood.
  • In vivo, lung tumor cells with disrupted E-cadherin expressed beta-catenin target genes normally found in other endodermal lineages suggesting that reprogramming may be involved in metastatic progression.
  • [MeSH-major] Adenocarcinoma / secondary. Cadherins / metabolism. Carcinoma, Non-Small-Cell Lung / secondary. Cell Adhesion. Lung Neoplasms / blood supply. Neovascularization, Pathologic / pathology. Proto-Oncogene Proteins c-raf / physiology
  • [MeSH-minor] Adenoma / etiology. Adenoma / pathology. Adherens Junctions. Animals. Apoptosis. Biomarkers / metabolism. Cells, Cultured. Disease Progression. Endoderm / metabolism. Endothelium, Vascular / cytology. Endothelium, Vascular / metabolism. Endothelium, Vascular / pathology. Fluorescent Antibody Technique. Genes, Dominant. Immunoblotting. Immunoprecipitation. In Situ Nick-End Labeling. Luciferases / metabolism. Mice. Mice, Knockout. Mice, Transgenic. Neoplasm Invasiveness. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Vascular Endothelial Growth Factor A / genetics. Vascular Endothelial Growth Factor A / metabolism. beta Catenin / genetics. beta Catenin / metabolism


93. Sasaki H, Endo K, Okuda K, Kawano O, Kitahara N, Tanaka H, Matsumura A, Iuchi K, Takada M, Kawahara M, Kawaguchi T, Yukiue H, Yokoyama T, Yano M, Fujii Y: Epidermal growth factor receptor gene amplification and gefitinib sensitivity in patients with recurrent lung cancer. J Cancer Res Clin Oncol; 2008 May;134(5):569-77
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  • [Title] Epidermal growth factor receptor gene amplification and gefitinib sensitivity in patients with recurrent lung cancer.
  • To evaluate the epidermal growth factor receptor (EGFR) protein expression, gene mutations and amplification as predictors of clinical outcome in patients with non-small-cell lung cancer (NSCLC) receiving gefitinib, we have performed fluorescence in situ hybridization (FISH) and immunohistochemistry (IHC).
  • We investigated the EGFR amplification and EGFR protein expression statuses in 27 surgically treated non-small-cell lung cancer (NSCLC) cases.
  • EGFR mutations were found from 15/27 lung cancer patients.
  • Smoking status (never smoker vs. smoker, P=0.0032), and pathological subtypes (adenocarcinoma vs. non-adenocarcinoma, P=0.0011), but not EGFR amplification (P=0.1278), were correlated with survival of lung cancers.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / genetics. Drug Resistance, Neoplasm / genetics. Genes, erbB-1. Lung Neoplasms / genetics. Quinazolines / therapeutic use
  • [MeSH-minor] Adult. Aged. Female. Gene Amplification. Gene Dosage. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Japan. Kaplan-Meier Estimate. Male. Middle Aged. Mutation. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / mortality. Retrospective Studies. Smoking / adverse effects

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  • (PMID = 17932690.001).
  • [ISSN] 0171-5216
  • [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 / Antineoplastic Agents; 0 / Quinazolines; S65743JHBS / gefitinib
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94. Calleja-Macias IE, Kalantari M, Bernard HU: Cholinergic signaling through nicotinic acetylcholine receptors stimulates the proliferation of cervical cancer cells: an explanation for the molecular role of tobacco smoking in cervical carcinogenesis? Int J Cancer; 2009 Mar 1;124(5):1090-6
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  • We have analyzed the expression of mRNAs encoding nicotinic acetylcholine receptors (nAChRs) in CaSki, SiHa and HeLa cell lines, which are derived from two squamous and one adenocarcinoma of the cervix, respectively.
  • The beta-1 subunit was detected membrane-associated in normal and neoplastic squamous epithelia of the cervix in situ, but appeared to be absent from the underlying mesenchyme and even from adjacent columnar epithelia.
  • This indicates that cholinergic signaling under normal physiological conditions and stimulated by nicotine in tobacco users affects epithelial homeostasis and neoplastic progression at the cervix in a way similar to the known effects on epithelia of the mouth, the airways and the lung.

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  • (PMID = 19048619.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA062203
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Subunits; 0 / Receptors, Nicotinic; 6M3C89ZY6R / Nicotine
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95. Tao Q, Fujimoto J, Men T, Ye X, Deng J, Lacroix L, Clifford JL, Mao L, Van Pelt CS, Lee JJ, Lotan D, Lotan R: Identification of the retinoic acid-inducible Gprc5a as a new lung tumor suppressor gene. J Natl Cancer Inst; 2007 Nov 21;99(22):1668-82
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  • [Title] Identification of the retinoic acid-inducible Gprc5a as a new lung tumor suppressor gene.
  • BACKGROUND: Lung cancers develop via multiple genetic and epigenetic changes, including inactivation of tumor suppressor genes.
  • We previously cloned human G protein-coupled receptor family C type 5A (GPRC5A), whose expression is suppressed in some human lung carcinoma cells, and its mouse homolog Gprc5a.
  • GPRC5A mRNA expression was analyzed by reverse transcription-polymerase chain reaction in surgical specimens of 18 human lung tumors and adjacent normal tissues and by analyzing previously published data from 186 lung tumor tissues of a variety of histologic types and 17 normal lung samples.
  • Human embryonic kidney, human non-small-cell lung cancer, and mouse lung adenocarcinoma cells were transfected with a GPRC5A expression vector or a control vector, and colony formation in semisolid medium was assayed.
  • RESULTS: Homozygous knockout mice developed many more lung tumors at 1-2 years of age (incidence: 76% adenomas and 17% adenocarcinomas) than heterozygous (11% adenomas) or wild-type (10% adenomas) mice.
  • Human GPRC5A mRNA levels were lower in most (11 of 18 [61%]) human lung tumors than in adjacent normal tissues.
  • The mean GPRC5A mRNA level in adenocarcinoma (n = 139), squamous cell carcinoma (n = 21), small-cell lung cancer (n = 6), and carcinoid (n = 20) tissues was 46.2% (P = .014), 7.5% (P<.001), 5.3% (P<.001), and 1.8% (P<.001), respectively, that in normal lung tissues (n = 17) GPRC5A transfection suppressed colony formation in semisolid medium of immortalized human embryonic kidney, human non-small-cell lung cancer, and mouse lung adenocarcinoma cells by 91%, 91%, and 68%, respectively, compared with vector controls (all P<.001).
  • CONCLUSIONS: Gprc5a functions as a tumor suppressor in mouse lung, and human GPRC5A may share this property.
  • The Gprc5a-deficient mouse is a novel model to study lung carcinogenesis and chemoprevention.
  • [MeSH-major] Adenocarcinoma / chemistry. Genes, Tumor Suppressor. Lung / chemistry. Lung Neoplasms / chemistry. Neoplastic Stem Cells / chemistry. Receptors, G-Protein-Coupled / genetics. Respiratory Mucosa / pathology
  • [MeSH-minor] Animals. Blotting, Northern. Carcinoma, Non-Small-Cell Lung / chemistry. Carcinoma, Small Cell / chemistry. Cell Line, Tumor. Cell Transformation, Neoplastic. Disease Models, Animal. Embryonic Stem Cells. Fluorescent Antibody Technique. Gene Expression Regulation, Neoplastic. Genes, ras. Genetic Predisposition to Disease. Homozygote. Humans. Immunoblotting. Immunohistochemistry. In Situ Hybridization. Mice. Mice, Knockout. Mutation. Neoplasm Proteins / genetics. Phenotype. Protein Array Analysis. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Transfection. Tumor Stem Cell Assay


96. Vainer G, Vainer-Mosse E, Pikarsky A, Shenoy SM, Oberman F, Yeffet A, Singer RH, Pikarsky E, Yisraeli JK: A role for VICKZ proteins in the progression of colorectal carcinomas: regulating lamellipodia formation. J Pathol; 2008 Aug;215(4):445-56
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  • In patients, VICKZ expression varies with tumour type, with over 60% of colon, lung, and ovarian tumours showing strong expression.
  • Indeed, in stage II CRC, the level of VICKZ expression in the primary lesion correlates with the degree of lymph node metastasis.

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  • [Copyright] Copyright (c) 2008 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
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  • (PMID = 18535985.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] ENG
  • [Grant] United States / NIAMS NIH HHS / AR / R01 AR041480-13; United States / NIGMS NIH HHS / GM / R01 GM084364-17; United States / NIAMS NIH HHS / AR / R01 AR041480-11; United States / NIAMS NIH HHS / AR / AR041480-06; United States / NIAMS NIH HHS / AR / AR041480-11; United States / NIGMS NIH HHS / GM / R01 GM084364-15A1; United States / NIAMS NIH HHS / AR / R01 AR041480-10A2; United States / NIAMS NIH HHS / AR / AR041480-10A2; United States / NIAMS NIH HHS / AR / AR041480-09; United States / NIAMS NIH HHS / AR / R01 AR041480; United States / NIGMS NIH HHS / GM / R01 GM084364-18; United States / NIAMS NIH HHS / AR / R01 AR041480-09; United States / NIAMS NIH HHS / AR / AR041480-08; United States / NIAMS NIH HHS / AR / R01 AR041480-06; United States / NIAMS NIH HHS / AR / R01 AR041480-14; United States / NIGMS NIH HHS / GM / R01 GM084364-16; United States / NIAMS NIH HHS / AR / R01 AR041480-08; United States / NIAMS NIH HHS / AR / R01 AR041480-11S1; United States / NIAMS NIH HHS / AR / R01 AR041480-12; United States / NIGMS NIH HHS / GM / R01 GM084364
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / ZBP1 protein, human
  • [Other-IDs] NLM/ NIHMS314194; NLM/ PMC3148580
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97. Antoine M: [Contribution of immunohistochemistry to the management of lung cancer: from morphology to diagnosis and treatment]. Rev Pneumol Clin; 2007 Jun;63(3):183-92
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  • [Title] [Contribution of immunohistochemistry to the management of lung cancer: from morphology to diagnosis and treatment].
  • [Transliterated title] Qu'apporte l'immunohistochimie à la prise en charge du cancer bronchique? De la morphologie au diagnostic et au traitement.
  • We detail here the contribution of IHC to the classification of lung cancer: small-cell lung cancer and other neuroendocrine tumors, basaloid carcinoma, large-cell carcinoma.
  • Using IHC techniques, pathologists can now determine with certainty that an intrathoracic adenocarcinoma is primary or secondary.
  • By demonstrating the presence of carcinomatous cells within the neighboring structures (pleura) or lymph nodes, IHC contributes to lung cancer staging, particularly when there are few of these elements morphologically difficult to distinguish.
  • IHC studies may also be requested in a forensic setting, for example to demonstrate that the lung cancer observed in a patient exposed to asbestosis is primary.
  • Other morphological techniques such as hybridization in situ or molecular biology techniques will further complete the histological diagnosis in the future.
  • [MeSH-major] Immunohistochemistry. Lung Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / pathology. Biomarkers, Tumor / analysis. Carcinoma, Large Cell / pathology. Carcinoma, Small Cell / pathology. Carcinoma, Squamous Cell / pathology. Carcinoma, Transitional Cell / pathology. Chorionic Gonadotropin, beta Subunit, Human / analysis. Forecasting. Humans. Lymph Nodes / pathology. Lymphoma / pathology. Mediastinal Neoplasms / pathology. Melanoma / pathology. Neoplasm Staging. Neuroendocrine Tumors / pathology. Pleural Neoplasms / pathology. Prognosis. Sarcoma / pathology. alpha-Fetoproteins / analysis

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  • (PMID = 17675942.001).
  • [ISSN] 0761-8417
  • [Journal-full-title] Revue de pneumologie clinique
  • [ISO-abbreviation] Rev Pneumol Clin
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Chorionic Gonadotropin, beta Subunit, Human; 0 / alpha-Fetoproteins
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98. Tonon G, Brennan C, Protopopov A, Maulik G, Feng B, Zhang Y, Khatry DB, You MJ, Aguirre AJ, Martin ES, Yang Z, Ji H, Chin L, Wong KK, Depinho RA: Common and contrasting genomic profiles among the major human lung cancer subtypes. Cold Spring Harb Symp Quant Biol; 2005;70:11-24
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  • [Title] Common and contrasting genomic profiles among the major human lung cancer subtypes.
  • Lung cancer is the leading cause of cancer mortality worldwide.
  • With the recent success of molecularly targeted therapies in this disease, a detailed knowledge of the spectrum of genetic lesions in lung cancer represents a critical step in the development of additional effective agents.
  • An integrated high-resolution survey of regional amplifications and deletions and gene expression profiling of non-small-cell lung cancers (NSCLC) identified 93 focal high-confidence copy number alterations (CNAs), with 21 spanning less than 0.5 Mb with a median of five genes.
  • Additionally, the comparison of the genomic profiles of the two major subtypes of NSCLC, adenocarcinoma (AC) and squamous cell carcinoma (SCC), showed an almost complete overlap with the exception of one amplified region on chromosome 3, specific for SCC.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Gene Expression Profiling. Lung Neoplasms / genetics
  • [MeSH-minor] Adenocarcinoma / classification. Adenocarcinoma / genetics. Carcinoma, Squamous Cell / classification. Carcinoma, Squamous Cell / genetics. Chromosomes, Human, Pair 3 / genetics. Cytogenetics. Gene Dosage. Humans. In Situ Hybridization, Fluorescence. Membrane Proteins / genetics. Oncogenes

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  • (PMID = 16869734.001).
  • [ISSN] 0091-7451
  • [Journal-full-title] Cold Spring Harbor symposia on quantitative biology
  • [ISO-abbreviation] Cold Spring Harb. Symp. Quant. Biol.
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / K08AG 2400401; United States / NCI NIH HHS / CA / R01 CA084628-12; United States / NCI NIH HHS / CA / R01 CA099041; United States / NCI NIH HHS / CA / U01 U01-CA084313-07; United States / NCI NIH HHS / CA / U01-CA084313-07
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CKAP4 protein, human; 0 / Membrane Proteins
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99. Dobashi Y, Watanabe H, Sato Y, Hirashima S, Yanagawa T, Matsubara H, Ooi A: Differential expression and pathological significance of autocrine motility factor/glucose-6-phosphate isomerase expression in human lung carcinomas. J Pathol; 2006 Dec;210(4):431-40
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  • [Title] Differential expression and pathological significance of autocrine motility factor/glucose-6-phosphate isomerase expression in human lung carcinomas.
  • To clarify the involvement of autocrine motility factor (AMF) in the phenotype and biological profiles of human lung carcinomas, we analysed protein and mRNA expression in a total of 180 cases.
  • Among non-small cell lung carcinomas (NSCLCs), AMF protein levels correlated inversely with tumour size, but tumours exhibiting lymph node metastasis showed higher mRNA expression.
  • In cultured lung carcinoma cells which comprised all histological subtypes, AMF was detected in the lysates of all ten cell lines.
  • Thus, a particular subset of lung carcinomas secrete AMF, which may promote cell motility via autocrine stimulation through its cognate receptor and cause the biological aggressiveness seen in SmCC and LCC.
  • In conclusion, AMF was detected in a major proportion of lung carcinomas, and may play a part not only in proliferation and/or progression of the tumours, but also, possibly, in the differentiation of SCC.
  • [MeSH-major] Glucose-6-Phosphate Isomerase / analysis. Lung Neoplasms / chemistry
  • [MeSH-minor] Adenocarcinoma / chemistry. Adenocarcinoma / pathology. Carcinoma, Large Cell / chemistry. Carcinoma, Large Cell / pathology. Carcinoma, Non-Small-Cell Lung / chemistry. Carcinoma, Non-Small-Cell Lung / pathology. Carcinoma, Small Cell / chemistry. Carcinoma, Small Cell / pathology. Carcinoma, Squamous Cell / chemistry. Carcinoma, Squamous Cell / pathology. Cell Differentiation. Cell Line, Tumor. Cysteine Proteinase Inhibitors / pharmacology. Female. Humans. Immunohistochemistry / methods. In Situ Hybridization / methods. Lymphatic Metastasis / pathology. Male. Neoplasm Proteins / analysis. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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  • (PMID = 17029220.001).
  • [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 / Cysteine Proteinase Inhibitors; 0 / Neoplasm Proteins; 0 / RNA, Messenger; EC 5.3.1.9 / Glucose-6-Phosphate Isomerase
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100. 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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