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Items 1 to 11 of about 11
1. Beleford D, Liu Z, Rattan R, Quagliuolo L, Boccellino M, Baldi A, Maguire J, Staub J, Molina J, Shridhar V: Methylation induced gene silencing of HtrA3 in smoking-related lung cancer. Clin Cancer Res; 2010 Jan 15;16(2):398-409
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  • [Title] Methylation induced gene silencing of HtrA3 in smoking-related lung cancer.
  • Here, we investigate the role of serine protease HtrA3 in smoking-related lung cancer.
  • EXPERIMENTAL DESIGN: We assess HtrA3 methylation and its corresponding expression in the human bronchial cell line BEAS-2B following cigarette smoke carcinogen treatment, in lung cancer cell lines and in primary lung tumors from light, moderate, and heavy smokers.
  • RESULTS: We show for the first time that HtrA3 expression is reduced or completely lost in over 50% of lung cancer cell lines and primary lung tumors from heavy smokers.
  • Further, sequence analysis of bisulfite-modified DNA from lung cancer cell lines and from primary lung tumors showed an increased frequency of methylation within the first exon of HtrA3 with a corresponding loss of HtrA3 expression, particularly in tumors from smokers.
  • CONCLUSIONS: Collectively, these results suggest that cigarette smoke-induced methylation of HtrA3 could contribute to the etiology of chemoresistant disease in smoking-related lung cancer.
  • [MeSH-major] Carcinoma, Bronchogenic / etiology. DNA Methylation / physiology. Gene Silencing. Lung Neoplasms / etiology. Serine Endopeptidases / genetics. Smoking / adverse effects
  • [MeSH-minor] Adenocarcinoma / etiology. Adenocarcinoma / genetics. Animals. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Large Cell / etiology. Carcinoma, Large Cell / genetics. Carcinoma, Squamous Cell / etiology. Carcinoma, Squamous Cell / genetics. Cell Line, Tumor. Cells, Cultured. Cisplatin / administration & dosage. Drug Resistance, Neoplasm / genetics. Etoposide / administration & dosage. Humans. Mice. Mice, Inbred BALB C. Nitrosamines / adverse effects

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  • (PMID = 20068077.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nitrosamines; 64091-91-4 / 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone; 6PLQ3CP4P3 / Etoposide; EC 3.4.21.- / HTRA3 protein, human; EC 3.4.21.- / Serine Endopeptidases; Q20Q21Q62J / Cisplatin
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2. de La Motte Rouge T, Valent A, Ambrosetti D, Vielh P, Lacroix L: [Clinical and molecular predictors of response to EGFR tyrosine kinase inhibitors in non-small cell lung cancer]. Ann Pathol; 2007 Oct;27(5):353-63
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  • [Title] [Clinical and molecular predictors of response to EGFR tyrosine kinase inhibitors in non-small cell lung cancer].
  • [Transliterated title] Facteurs prédictifs de la réponse aux inhibiteurs de tyrosine kinase ciblant le récepteur à l'EGF dans le cancer bronchique.
  • This rate of response is related to non-smoker status, female gender, adenocarcinoma subtype, and Asian ethnicity.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Enzyme Inhibitors / therapeutic use. Lung Neoplasms / drug therapy. Receptor, Epidermal Growth Factor / antagonists & inhibitors
  • [MeSH-minor] Adenocarcinoma / classification. Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Carcinoma, Bronchogenic / drug therapy. Carcinoma, Bronchogenic / genetics. Carcinoma, Bronchogenic / pathology. Female. Gene Amplification. Humans. Male. Mutation


3. Fukami T, Nakajima M, Matsumoto I, Zen Y, Oda M, Yokoi T: Immunohistochemical analysis of CYP2A13 in various types of human lung cancers. Cancer Sci; 2010 Apr;101(4):1024-8
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  • The relevance of CYP2A13 in carcinogenicity and toxicity in the respiratory tract has been suggested, but the expression of CYP2A13 protein in lung cancer tissues remains to be determined.
  • [MeSH-minor] Adenocarcinoma / enzymology. Adenocarcinoma / metabolism. Adult. Aged. Aged, 80 and over. Animals. Biotransformation. Carcinoma, Bronchogenic / metabolism. Carcinoma, Large Cell / metabolism. Carcinoma, Non-Small-Cell Lung / metabolism. Carcinoma, Small Cell / metabolism. Carcinoma, Squamous Cell / metabolism. Female. Humans. Male. Mice. Middle Aged. Respiratory System / metabolism. Respiratory System / pathology

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  • (PMID = 20180810.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.14.14.1 / Aryl Hydrocarbon Hydroxylases; EC 1.14.14.1 / CYP2A13 protein, human
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4. Ko HW, Tsai YH, Yu CT, Huang CY, Chen CH: Good response to gefitinib for lung adenocarcinoma with hyperamylasemia: a case report. Chang Gung Med J; 2008 Nov-Dec;31(6):606-11
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  • [Title] Good response to gefitinib for lung adenocarcinoma with hyperamylasemia: a case report.
  • Hyperamylasemia in patients with bronchogenic carcinoma has been reported rarely.
  • Gefitinib, an oral tyrosine kinase inhibitor of epidermal growth factor receptor (EGFR) signaling, has shown activity for treating patients with refractory advanced non-small cell lung cancer (NSCLC).
  • This report describes a case of lung adenocarcinoma coexisting with hyperamylasemia in a 67-year-old man.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Agents / therapeutic use. Hyperamylasemia / etiology. Protein Kinase Inhibitors / therapeutic use. Quinazolines / therapeutic use. Receptor, Epidermal Growth Factor / antagonists & inhibitors
  • [MeSH-minor] Aged. Humans. Lung Neoplasms / drug therapy. Lung Neoplasms / enzymology. Male. Tomography, X-Ray Computed

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  • (PMID = 19241901.001).
  • [ISSN] 2072-0939
  • [Journal-full-title] Chang Gung medical journal
  • [ISO-abbreviation] Chang Gung Med J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China (Republic : 1949- )
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
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5. Boutemy M, Mispelaere D, Krzisch C, Jounieaux V: [Evaluation of combined chemotherapy with vinorelbine, ifosfamide and cisplatin in the treatment of metastatic non-small cell bronchial carcinoma]. Rev Mal Respir; 2005 Jun;22(3):413-9
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  • [Transliterated title] Evaluation de la chimiothérapie associant vinorelbine-ifosfamide-cisplatine dans le traitement des cancers bronchiques non à petites cellules métastatiques.
  • INTRODUCTION: In France, cancer of the bronchus is responsible for 25,000 deaths per year.
  • Non small cell lung cancer (NSCLC) represents 80% of bronchial carcinoma of which 40-50% are mefastatic at the time of diagnosis.
  • METHODS: We analysed retrospectively a cohort of 57 patients suffering from stage IV NSCLC treated with chemotherapy combining cisplatin (80 mg/rn2 on day 1), vinorelbine (25 mg/rn2 on days 1 and 8) and ifosfamide (3000 mg/in 2 on day 1), (NIP), repeated every 21 days.
  • CONCLUSION: Treatment of stage IV NSCLC with NIP chemotherapy is effective and improves the survival of these patients independently of other prognostic factors such as age, the presence of cerebral metastases, performance status, histological type, the number of metastatic sites or the serum LOH level.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Non-Small-Cell Lung / secondary. Lung Neoplasms / drug therapy
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / secondary. Adult. Aged. Brain Neoplasms / drug therapy. Brain Neoplasms / secondary. Carcinoma, Bronchogenic / drug therapy. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / secondary. Cisplatin / administration & dosage. Cisplatin / adverse effects. Cohort Studies. Female. Gastrointestinal Diseases / chemically induced. Hematologic Diseases / chemically induced. Humans. Ifosfamide / administration & dosage. Ifosfamide / adverse effects. Life Tables. Male. Middle Aged. Retrospective Studies. Smoking / adverse effects. Survival Analysis. Treatment Outcome. Vinblastine / administration & dosage. Vinblastine / adverse effects. Vinblastine / analogs & derivatives

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  • (PMID = 16227927.001).
  • [ISSN] 0761-8425
  • [Journal-full-title] Revue des maladies respiratoires
  • [ISO-abbreviation] Rev Mal Respir
  • [Language] fre
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 5V9KLZ54CY / Vinblastine; Q20Q21Q62J / Cisplatin; Q6C979R91Y / vinorelbine; UM20QQM95Y / Ifosfamide
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6. Mizutani H, Horiba M, Shindoh J, Kimura T, Son M, Ishikawa T: [Bronchiolo-alveolar cell carcinoma arising after active pulmonary tuberculosis' report of two cases]. Nihon Kokyuki Gakkai Zasshi; 2001 Feb;39(2):145-50
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  • We report on two patients diagnosed as having active pulmonary tuberculosis who later developed lung cancer.
  • In both cases, the lung cancer was detected during the treatment of pulmonary tuberculosis.
  • Although he was treated with isoniazid (INH), rifampicin (RFP), ethambutol (EB) and pyrazinamide (PZA), his general condition deteriorated, and the infiltrative shadows in the lung fields had expanded on subsequent chest radiography.
  • Despite medication with INH, RFP, EB and PZA, the infiltrative shadow in his chest radiograph increased in size.
  • Case 1 was diagnosed as lung cancer 10 months after being admission to the hospital, and Case 2, seven months after hospitalization.
  • Recent discussion concerning the simultaneous occurrence of pulmonary tuberculosis and bronchogenic carcinoma suggests a high frequency of coexistence of the two diseases.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / etiology. Lung Neoplasms / etiology. Tuberculosis, Pulmonary / complications

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  • (PMID = 11321828.001).
  • [ISSN] 1343-3490
  • [Journal-full-title] Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society
  • [ISO-abbreviation] Nihon Kokyuki Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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7. Wilderman MJ, Sun J, Jassar AS, Kapoor V, Khan M, Vachani A, Suzuki E, Kinniry PA, Sterman DH, Kaiser LR, Albelda SM: Intrapulmonary IFN-beta gene therapy using an adenoviral vector is highly effective in a murine orthotopic model of bronchogenic adenocarcinoma of the lung. Cancer Res; 2005 Sep 15;65(18):8379-87
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  • [Title] Intrapulmonary IFN-beta gene therapy using an adenoviral vector is highly effective in a murine orthotopic model of bronchogenic adenocarcinoma of the lung.
  • Given previous work showing that an adenoviral vector expressing IFN-beta (Ad.IFNbeta) was highly effective in eradicating i.p. mesothelioma tumors, the antitumor efficacy of this agent was evaluated in an orthotopic model of bronchogenic adenocarcinoma of the lung.
  • These studies, showing remarkable antitumor activity in this orthotopic lung cancer model, provide strong preclinical support for a trial of Ad.IFNbeta to treat human non-small cell lung cancer.
  • [MeSH-major] Carcinoma, Bronchogenic / genetics. Carcinoma, Bronchogenic / therapy. Genetic Therapy / methods. Interferon-beta / genetics. Lung Neoplasms / genetics. Lung Neoplasms / therapy
  • [MeSH-minor] Adenoviridae / genetics. Animals. Cell Line, Tumor. Female. Genes, ras / genetics. Male. Mice. Mice, Inbred C57BL. Mutation. T-Lymphocytes, Cytotoxic / immunology

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  • (PMID = 16166316.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA 66726
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 77238-31-4 / Interferon-beta
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8. Miller VA, Kris MG, Shah N, Patel J, Azzoli C, Gomez J, Krug LM, Pao W, Rizvi N, Pizzo B, Tyson L, Venkatraman E, Ben-Porat L, Memoli N, Zakowski M, Rusch V, Heelan RT: Bronchioloalveolar pathologic subtype and smoking history predict sensitivity to gefitinib in advanced non-small-cell lung cancer. J Clin Oncol; 2004 Mar 15;22(6):1103-9
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  • [Title] Bronchioloalveolar pathologic subtype and smoking history predict sensitivity to gefitinib in advanced non-small-cell lung cancer.
  • PURPOSE: Gefitinib, an inhibitor of the epidermal growth factor receptor tyrosine kinase, induces radiographic regressions and symptomatic improvement in patients with non-small-cell lung cancer (NSCLC).
  • Phase II trials suggested female sex and adenocarcinoma were associated with response.
  • Variables identified as significant in univariate analysis included adenocarcinoma versus other NSCLC (19% v 0%; P=.004), adenocarcinoma with bronchioloalveolar features versus other adenocarcinomas (38% v 14%; P<.001), never smoker status versus former/current (36% v 8%; P<.001), and Karnofsky performance status > or =80% versus < or =70% (22% v 8%; P=.03).
  • Multivariable analysis revealed the presence of adenocarcinoma with any bronchioloalveolar features (P=.004) and being a never smoker (P=.006) were independent predictors of response.
  • These observations may provide clues to mechanisms determining sensitivity to this agent and suggest that NSCLC has a different biology in patients who never smoked and those with bronchioloalveolar carcinoma.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Bronchogenic / drug therapy. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Quinazolines / pharmacology. Smoking


9. McGarry RC: Images in clinical medicine. Lung cancer presenting as an ankle metastasis. N Engl J Med; 2000 Jul 27;343(4):268
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  • [Title] Images in clinical medicine. Lung cancer presenting as an ankle metastasis.
  • [MeSH-major] Adenocarcinoma / secondary. Bone Neoplasms / secondary. Calcaneus / radionuclide imaging. Lung Neoplasms / pathology
  • [MeSH-minor] Carcinoma, Bronchogenic. Fatal Outcome. Humans. Magnetic Resonance Imaging. Male. Middle Aged

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  • (PMID = 10911009.001).
  • [ISSN] 0028-4793
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] UNITED STATES
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10. Girard N, Gérinière L, Blandin S, Perrot E, Souquet PJ: [French experience of gefitinib in non-small cell bronchial carcinoma]. Rev Mal Respir; 2004 Nov;21(5 Pt 1):934-42
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  • [Transliterated title] Expérience française du géfitinib dans le cancer bronchique non à petites cellules.
  • Multivariate analyses revealed that being a woman, a non-smoker and having an adenocarcinoma was associated with response rate.
  • Tumors included 25 adenocarcinoma, 4 squamous cell carcinoma, 7 large cell carcinoma, and 1 neuroendocrine carcinoma.
  • The 3 responders were all non-smoker women, with an histological type of adenocarcinoma.
  • We observed that responding patients had more adverse drugs-related reactions than stable or non-responding patients.
  • We suggest that being a woman, a never-smoker and having an adenocarcinoma may be clinical predictive factors of response to Gefitinib.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Bronchial Neoplasms / drug therapy. Carcinoma, Bronchogenic / drug therapy. Carcinoma, Non-Small-Cell Lung / drug therapy. Quinazolines / therapeutic use

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  • (PMID = 15622340.001).
  • [ISSN] 0761-8425
  • [Journal-full-title] Revue des maladies respiratoires
  • [ISO-abbreviation] Rev Mal Respir
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Quinazolines; 62229-50-9 / Epidermal Growth Factor; EC 2.7.10.1 / Protein-Tyrosine Kinases; S65743JHBS / gefitinib
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11. Lam DC, Girard L, Suen WS, Chung LP, Tin VP, Lam WK, Minna JD, Wong MP: Establishment and expression profiling of new lung cancer cell lines from Chinese smokers and lifetime never-smokers. J Thorac Oncol; 2006 Nov;1(9):932-42
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  • [Title] Establishment and expression profiling of new lung cancer cell lines from Chinese smokers and lifetime never-smokers.
  • BACKGROUND: Bronchogenic adenocarcinoma is the predominant histologic subtype of lung cancer, which ranks top in the cancer mortality in both men and women.
  • Female nonsmokers and adenocarcinoma have emerged as a distinct combination in patients with lung cancer in recent decades.
  • Lung cancer cell lines established from patients with known clinical characteristics such as gender and smoking habit would be useful for future research on lung cancer.
  • METHODS: Four new lung adenocarcinoma cell lines (HKULC 1-4) were established from Chinese patients with primary lung adenocarcinomas and with different clinical characteristics with respect to age, gender, smoking habits, tumor staging, and previous therapy.
  • RESULTS: The newly established HKULC lung adenocarcinoma cell lines were maintained for over 70 passages and demonstrated morphologic and immunohistochemical features and growth kinetics of tumor cell lines.
  • One of the four HKULC cell lines, HKULC 3 (derived from a female nonsmoking patient with lung adenocarcinoma), was found to have a deletion at exon 19 of the EGFR gene.
  • DISCUSSION: Four new lung adenocarcinoma cell lines were established from patients with different clinical characteristics.
  • These characterized cell lines and their gene expression profiles will provide resources for studies of lung cancer biology and in vitro chemotherapeutic drug study.
  • [MeSH-minor] Adenocarcinoma / ethnology. Adenocarcinoma / genetics. Adenocarcinoma / pathology. Adult. Aged. Animals. Cell Line, Tumor. China. Female. Gene Expression Regulation, Neoplastic. Humans. In Situ Hybridization. Male. Mice. Mice, Nude. Middle Aged. Mutation. Reference Values. Sensitivity and Specificity






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