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1. Choong NW, Mauer AM, Haraf DJ, Lester E, Hoffman PC, Kozloff M, Lin S, Dancey JE, Szeto L, Grushko T, Olopade OI, Salgia R, Vokes EE: Phase I trial of erlotinib-based multimodality therapy for inoperable stage III non-small cell lung cancer. J Thorac Oncol; 2008 Sep;3(9):1003-11
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  • [Title] Phase I trial of erlotinib-based multimodality therapy for inoperable stage III non-small cell lung cancer.
  • INTRODUCTION: This Phase I trial aimed to determine the maximum-tolerated-dose of erlotinib administered with two standard chemoradiotherapy regimens for non-small cell lung cancer.
  • METHODS: Unresectable stage III non-small cell lung cancer patients were enrolled in this 2-arm dose-escalation study.
  • PATIENT CHARACTERISTICS: performance status 0 to 24 patients, 1 to 10 patients, median age 63 years, adenocarcinoma 21% and female 14 patients.

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  • (PMID = 18758303.001).
  • [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 / T32 CA009566-15; United States / NCI NIH HHS / CA / P30 CA014599; United States / NCI NIH HHS / CA / P30 CA14599-32; United States / NCI NIH HHS / CA / CA009566-15; United States / NCI NIH HHS / CM / N01 CM007003; United States / NCI NIH HHS / CM / N01 CM-07003-74; United States / NCI NIH HHS / CA / T32 CA009566
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Quinazolines; 0 / Taxoids; 15H5577CQD / docetaxel; 6PLQ3CP4P3 / Etoposide; BG3F62OND5 / Carboplatin; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; Q20Q21Q62J / Cisplatin
  • [Other-IDs] NLM/ NIHMS154299; NLM/ PMC4535721
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2. Sequist LV, Martins RG, Spigel D, Grunberg SM, Spira A, Jänne PA, Joshi VA, McCollum D, Evans TL, Muzikansky A, Kuhlmann GL, Han M, Goldberg JS, Settleman J, Iafrate AJ, Engelman JA, Haber DA, Johnson BE, Lynch TJ: First-line gefitinib in patients with advanced non-small-cell lung cancer harboring somatic EGFR mutations. J Clin Oncol; 2008 May 20;26(15):2442-9
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  • [Title] First-line gefitinib in patients with advanced non-small-cell lung cancer harboring somatic EGFR mutations.
  • PURPOSE: Somatic mutations in the epidermal growth factor receptor (EGFR) correlate with increased response in patients with non-small-cell lung cancer (NSCLC) treated with EGFR tyrosine kinase inhibitors (TKIs).
  • Two patients with classic activating mutations exhibited de novo gefitinib resistance and had concurrent genetic anomalies usually associated with acquired TKI resistance, specifically the T790M EGFR mutation and MET amplification.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Mutation / genetics. Quinazolines / therapeutic use. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / genetics. Adenocarcinoma / secondary. Adult. Aged. Aged, 80 and over. Carcinoma, Large Cell / drug therapy. Carcinoma, Large Cell / genetics. Carcinoma, Large Cell / secondary. Central Nervous System Neoplasms / drug therapy. Central Nervous System Neoplasms / genetics. Central Nervous System Neoplasms / secondary. Disease-Free Survival. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Neoplasm Staging. Prospective Studies. Survival Rate. Treatment Outcome


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

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  • (PMID = 15743751.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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4. 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


5. Ma Y, Fiering S, Black C, Liu X, Yuan Z, Memoli VA, Robbins DJ, Bentley HA, Tsongalis GJ, Demidenko E, Freemantle SJ, Dmitrovsky E: Transgenic cyclin E triggers dysplasia and multiple pulmonary adenocarcinomas. Proc Natl Acad Sci U S A; 2007 Mar 6;104(10):4089-94
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  • Cyclin E is a critical G(1)-S cell cycle regulator aberrantly expressed in bronchial premalignancy and lung cancer.
  • Cyclin E expression negatively affects lung cancer prognosis.
  • Its role in lung carcinogenesis was explored.
  • Murine transgenic lines were engineered to mimic aberrant cyclin E expression in the lung.
  • Notably, high expression of degradation-resistant cyclin E frequently caused dysplasia and multiple lung adenocarcinomas.
  • Thus, recapitulation of aberrant cyclin E expression as seen in human premalignant and malignant lung lesions reproduces in the mouse frequent features of lung carcinogenesis, including CIN, Shh pathway activation, dysplasia, single or multiple lung cancers, or presence of metastases.
  • This article reports unique mouse lung cancer models that replicate many carcinogenic changes found in patients.
  • These models provide insights into the carcinogenesis process and implicate cyclin E as a therapeutic target in the lung.

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  • (PMID = 17360482.001).
  • [ISSN] 0027-8424
  • [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 / R01 CA 87546; United States / NCI NIH HHS / CA / R01 CA 111422; United States / NCI NIH HHS / CA / R01 CA111422; United States / NCI NIH HHS / CA / P30 CA023108; United States / NCI NIH HHS / CA / R01 CA087546
  • [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 / Cyclin E; 0 / Hedgehog Proteins; 0 / RNA, Small Interfering
  • [Other-IDs] NLM/ PMC1820713
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6. 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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7. Pinter F, Papay J, Almasi A, Sapi Z, Szabo E, Kanya M, Tamasi A, Jori B, Varkondi E, Moldvay J, Szondy K, Keri G, Dominici M, Conte P, Eckhardt S, Kopper L, Schwab R, Petak I: Epidermal growth factor receptor (EGFR) high gene copy number and activating mutations in lung adenocarcinomas are not consistently accompanied by positivity for EGFR protein by standard immunohistochemistry. J Mol Diagn; 2008 Mar;10(2):160-8
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  • [Title] Epidermal growth factor receptor (EGFR) high gene copy number and activating mutations in lung adenocarcinomas are not consistently accompanied by positivity for EGFR protein by standard immunohistochemistry.
  • The purpose of this study was to investigate whether detectable protein biomarker overexpression is a prerequisite for the presence of increased gene copy number or activating mutations and responsiveness to the epidermal growth factor receptor (EGFR) inhibitors gefitinib and erlotinib in patients with lung adenocarcinomas.
  • EGFR status was prospectively analyzed in tumor biopsy samples by three methods: protein expression (n = 117) by standardized immunohistochemistry (IHC), gene copy number (n = 97) by fluorescent in situ hybridization (FISH), and mutation analysis by sequencing (n = 126).
  • These results indicate that molecular diagnostic methods appear to be most important for the identification of lung adenocarcinoma patients who may benefit from EGFR inhibitor treatments.
  • [MeSH-major] Adenocarcinoma / genetics. Gene Dosage. Lung Neoplasms / genetics. Mutation / genetics. Receptor, Epidermal Growth Factor / genetics. Receptor, Epidermal Growth Factor / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Base Sequence. Biomarkers, Tumor. Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / pathology. DNA Mutational Analysis. Enzyme Inhibitors / pharmacology. Erlotinib Hydrochloride. Female. Genotype. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Middle Aged. Molecular Sequence Data. Quinazolines / pharmacology. Quinazolines / therapeutic use. Treatment Outcome

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  • (PMID = 18258923.001).
  • [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
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Enzyme Inhibitors; 0 / Quinazolines; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
  • [Other-IDs] NLM/ PMC2259471
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8. 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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9. 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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10. Kokura S, Yoshida N, Sakamoto N, Ishikawa T, Takagi T, Higashihara H, Nakabe N, Handa O, Naito Y, Yoshikawa T: The radical scavenger edaravone enhances the anti-tumor effects of CPT-11 in murine colon cancer by increasing apoptosis via inhibition of NF-kappaB. Cancer Lett; 2005 Nov 18;229(2):223-33
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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 / drug therapy. Adenocarcinoma / secondary. Animals. Apoptosis / drug effects. Blotting, Western. Camptothecin / administration & dosage. Camptothecin / analogs & derivatives. Camptothecin / metabolism. Caspase 3. Caspases / drug effects. Caspases / metabolism. Cell Line, Tumor. Disease Models, Animal. Electrophoretic Mobility Shift Assay. Free Radical Scavengers / administration & dosage. In Situ Nick-End Labeling. Lung Neoplasms / drug therapy. Lung Neoplasms / secondary. Male. Mice. Reactive Oxygen Species

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  • (PMID = 16095811.001).
  • [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 / Antineoplastic Agents; 0 / Free Radical Scavengers; 0 / NF-kappa B; 0 / Reactive Oxygen Species; 7673326042 / irinotecan; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; S798V6YJRP / phenylmethylpyrazolone; T3CHA1B51H / Antipyrine; XT3Z54Z28A / Camptothecin
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11. 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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12. Lee JW, Soung YH, Seo SH, Kim SY, Park CH, Wang YP, Park K, Nam SW, Park WS, Kim SH, Lee JY, Yoo NJ, Lee SH: Somatic mutations of ERBB2 kinase domain in gastric, colorectal, and breast carcinomas. Clin Cancer Res; 2006 Jan 1;12(1):57-61
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  • PURPOSE: Recent reports revealed that the kinase domain of the ERBB2 gene is somatically mutated in lung adenocarcinoma, suggesting the mutated ERBB2 gene as an oncogene in human cancers.
  • However, because previous reports focused the mutational search of ERBB2 primarily on lung cancers, the data on ERBB2 mutations in other types of human cancers have been largely unknown.
  • CONCLUSION: This study showed that in addition to lung adenocarcinomas, ERBB2 kinase domain mutation occurs in other common human cancers such as gastric, breast, and colorectal cancers, and suggested that alterations of ERBB2-mediated signaling pathway by ERBB2 mutations alone or together with K-RAS mutations may contribute to the development of human cancers.
  • [MeSH-minor] Aged. DNA Mutational Analysis. Female. Genes, ras / genetics. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Mutation. Phosphatidylinositol 3-Kinases / genetics. Polymerase Chain Reaction. Polymorphism, Single-Stranded Conformational. Proto-Oncogene Proteins B-raf / genetics. Receptor, Epidermal Growth Factor / genetics


13. 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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14. Balak MN, Gong Y, Riely GJ, Somwar R, Li AR, Zakowski MF, Chiang A, Yang G, Ouerfelli O, Kris MG, Ladanyi M, Miller VA, Pao W: Novel D761Y and common secondary T790M mutations in epidermal growth factor receptor-mutant lung adenocarcinomas with acquired resistance to kinase inhibitors. Clin Cancer Res; 2006 Nov 1;12(21):6494-501
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  • [Title] Novel D761Y and common secondary T790M mutations in epidermal growth factor receptor-mutant lung adenocarcinomas with acquired resistance to kinase inhibitors.
  • PURPOSE: In patients whose lung adenocarcinomas harbor epidermal growth factor receptor (EGFR) tyrosine kinase domain mutations, acquired resistance to the tyrosine kinase inhibitors (TKI) gefitinib (Iressa) and erlotinib (Tarceva) has been associated with a second-site EGFR mutation, which leads to substitution of methionine for threonine at position 790 (T790M).
  • [MeSH-major] Adenocarcinoma / genetics. Drug Resistance, Neoplasm / genetics. Lung Neoplasms / genetics. Protein Kinase Inhibitors / therapeutic use. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Amino Acid Sequence. Antineoplastic Agents / therapeutic use. DNA Mutational Analysis. Erlotinib Hydrochloride. Gene Dosage. Humans. In Situ Hybridization. Molecular Sequence Data. Mutation. Neoplasm Metastasis / genetics. Protein Structure, Tertiary. Quinazolines / therapeutic use. Reverse Transcriptase Polymerase Chain Reaction

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  • [CommentIn] Clin Cancer Res. 2007 Jun 1;13(11):3431; author reply 3431-2 [17545553.001]
  • (PMID = 17085664.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5T32CA009207; United States / NCI NIH HHS / CA / K08-CA097980; United States / NCI NIH HHS / CA / R21-CA115051
  • [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 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
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15. Boelens MC, van den Berg A, Vogelzang I, Wesseling J, Postma DS, Timens W, Groen HJ: Differential expression and distribution of epithelial adhesion molecules in non-small cell lung cancer and normal bronchus. J Clin Pathol; 2007 Jun;60(6):608-14
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  • [Title] Differential expression and distribution of epithelial adhesion molecules in non-small cell lung cancer and normal bronchus.
  • AIM: To screen for altered expression of epithelial adhesion genes in lung cancer development.
  • METHODS: Gene expression profiles were assessed with cDNA expression arrays in eight non-small cell lung cancer (NSCLC) and eight normal bronchi obtained from the same patient.
  • Immunohistochemistry (IHC) and RNA in situ hybridisation (ISH) were used to confirm the most prominently expressed adhesion molecules and to investigate their distribution at protein and mRNA levels.
  • RESULTS: 43 differentially expressed cancer-related genes were identified in adenocarcinoma, squamous cell carcinoma (SCC) and normal bronchus.
  • ITGA3 and ITGB4, showing predominantly cell-matrix staining, were up regulated in adenocarcinoma and SCC, respectively.
  • A possible association of strong presence and normal-distributed desmosomal molecules in SCC with the less frequent and late pattern of metastasis in SCC as compared with adenocarcinoma is suggested.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / metabolism. Cell Adhesion Molecules / metabolism. Lung Neoplasms / metabolism. Neoplasm Proteins / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Aged. Bronchi / metabolism. Carcinoma, Small Cell / metabolism. Desmosomes / metabolism. Female. Gene Expression Profiling / methods. Gene Expression Regulation, Neoplastic. Humans. Immunoenzyme Techniques. In Situ Hybridization. Integrins / metabolism. Male. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Up-Regulation

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  • (PMID = 16489176.001).
  • [ISSN] 0021-9746
  • [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 / Cell Adhesion Molecules; 0 / Integrins; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm
  • [Other-IDs] NLM/ PMC1955047
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16. Brantley-Sieders DM, Fang WB, Hicks DJ, Zhuang G, Shyr Y, Chen J: Impaired tumor microenvironment in EphA2-deficient mice inhibits tumor angiogenesis and metastatic progression. FASEB J; 2005 Nov;19(13):1884-6
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  • 4T1 metastatic mammary adenocarcinoma cells transplanted subcutaneously and orthotopically into EphA2-deficient female mice displayed decreased tumor volume, tumor cell survival, microvascular density, and lung metastasis relative to tumor-bearing littermate controls.
  • [MeSH-minor] Adenocarcinoma / metabolism. Animals. Antigens, CD31 / biosynthesis. Cell Line, Tumor. Cell Movement. Cell Survival. Cell Transplantation. Collagen / chemistry. Disease Progression. Drug Combinations. Endothelium, Vascular / pathology. Ephrin-A1 / metabolism. Female. In Situ Nick-End Labeling. Lac Operon. Laminin / chemistry. Ligands. Lung / pathology. Mice. Mice, Inbred BALB C. Mice, Nude. Mice, Transgenic. Microcirculation. Microscopy, Fluorescence. Models, Biological. Models, Statistical. Mutation. Neoplasm Metastasis. Neoplasm Transplantation. Neovascularization, Pathologic. Oxygen / metabolism. Phenotype. Proteoglycans / chemistry. Receptors, Eph Family / metabolism. rac1 GTP-Binding Protein / metabolism

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  • (PMID = 16166198.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA95004
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD31; 0 / Drug Combinations; 0 / Ephrin-A1; 0 / Laminin; 0 / Ligands; 0 / Proteoglycans; 119978-18-6 / matrigel; 9007-34-5 / Collagen; EC 2.7.10.1 / Receptor, EphA2; EC 2.7.10.1 / Receptors, Eph Family; EC 3.6.5.2 / rac1 GTP-Binding Protein; S88TT14065 / Oxygen
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17. Shen H, Gao W, Wu YJ, Qiu HR, Shu YQ: Multicolor fluorescence in situ hybridization and comparative genomic hybridization reveal molecular events in lung adenocarcinomas and squamous cell lung carcinomas. Biomed Pharmacother; 2009 Jul;63(6):396-403
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  • [Title] Multicolor fluorescence in situ hybridization and comparative genomic hybridization reveal molecular events in lung adenocarcinomas and squamous cell lung carcinomas.
  • We have used the molecular cytogenetic techniques of multicolor fluorescence in situ hybridization (M-FISH) and comparative genomic hybridization (CGH) to analyze two established lung cancer cell lines (A549, H520), 80 primary lung adenocarcinoma samples and 80 squamous cell lung carcinoma samples in order to identify common chromosomal aberrations.
  • In lung adenocarcinomas the most common gains were found in 16p13 (50%); while in squamous cell lung carcinomas the common gains were found in 17q21 (45%) and these alterations were observed to be associated with their specific pathological subtype.
  • In conclusion, the present study contributes to the molecular biological characterization in lung adenocarcinomas and squamous cell lung carcinomas and through evaluation of molecular events to the recently emergent focus on novel markers for lung cancer treatment.
  • [MeSH-major] Adenocarcinoma / genetics. Comparative Genomic Hybridization / methods. In Situ Hybridization, Fluorescence / methods. Lung Neoplasms / genetics
  • [MeSH-minor] Adult. Aged. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / pathology. Cell Line, Tumor. Chromosome Aberrations. Female. Humans. Male. Middle Aged. Translocation, Genetic / genetics

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  • (PMID = 18848758.001).
  • [ISSN] 1950-6007
  • [Journal-full-title] Biomedicine & pharmacotherapy = Biomédecine & pharmacothérapie
  • [ISO-abbreviation] Biomed. Pharmacother.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] France
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18. Dziadziuszko R, Merrick DT, Witta SE, Mendoza AD, Szostakiewicz B, Szymanowska A, Rzyman W, Dziadziuszko K, Jassem J, Bunn PA Jr, Varella-Garcia M, Hirsch FR: Insulin-like growth factor receptor 1 (IGF1R) gene copy number is associated with survival in operable non-small-cell lung cancer: a comparison between IGF1R fluorescent in situ hybridization, protein expression, and mRNA expression. J Clin Oncol; 2010 May 1;28(13):2174-80
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  • [Title] Insulin-like growth factor receptor 1 (IGF1R) gene copy number is associated with survival in operable non-small-cell lung cancer: a comparison between IGF1R fluorescent in situ hybridization, protein expression, and mRNA expression.
  • PURPOSE: The purpose of this study was to characterize insulin-like growth factor-1 receptor (IGF1R) protein expression, mRNA expression, and gene copy number in surgically resected non-small-cell lung cancers (NSCLC) in relation to epidermal growth factor receptor (EGFR) protein expression, patient characteristics, and prognosis.
  • IGF1R gene copy number was assessed by fluorescent in situ hybridization using customized probes (n = 181).
  • RESULTS: IGF1R IHC score was higher in squamous cell carcinomas versus other histologies (P < .001) and associated with stage (P = .03) but not survival (P = .46).
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Squamous Cell / genetics. Gene Dosage. Gene Expression Regulation, Neoplastic. In Situ Hybridization, Fluorescence. Lung Neoplasms / genetics. Pulmonary Surgical Procedures. RNA, Messenger / analysis. Receptor, IGF Type 1 / genetics
  • [MeSH-minor] Adenocarcinoma / chemistry. Adenocarcinoma / genetics. Adenocarcinoma / surgery. Adult. Aged. Aged, 80 and over. Aneuploidy. Carcinoma, Large Cell / chemistry. Carcinoma, Large Cell / genetics. Carcinoma, Large Cell / surgery. Disease-Free Survival. Female. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Middle Aged. Neoplasm Staging. Proportional Hazards Models. Receptor, Epidermal Growth Factor / genetics. Reverse Transcriptase Polymerase Chain Reaction. Risk Assessment. Risk Factors. Time Factors. Tissue Array Analysis. Treatment Outcome

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  • (PMID = 20351332.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA058187; United States / NCI NIH HHS / CA / P50 CA058187
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, IGF Type 1
  • [Other-IDs] NLM/ PMC2860435
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19. 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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20. Daniele L, Cassoni P, Bacillo E, Cappia S, Righi L, Volante M, Tondat F, Inghirami G, Sapino A, Scagliotti GV, Papotti M, Novello S: Epidermal growth factor receptor gene in primary tumor and metastatic sites from non-small cell lung cancer. J Thorac Oncol; 2009 Jun;4(6):684-8
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  • [Title] Epidermal growth factor receptor gene in primary tumor and metastatic sites from non-small cell lung cancer.
  • INTRODUCTION: The majority of patients with non-small cell lung cancer (NSCLC) develop distant metastases.
  • METHODS: Using fluorescence in situ hybridization (FISH) analysis, the EGFR gene status was evaluated in a series of 38 cerebral or adrenal metastases collected from two institutions and in the corresponding primary tumors.
  • [MeSH-major] Adrenal Gland Neoplasms / genetics. Brain Neoplasms / genetics. Carcinoma, Non-Small-Cell Lung / genetics. Lung Neoplasms / genetics. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / secondary. Aged. Aged, 80 and over. Carcinoma, Large Cell / genetics. Carcinoma, Large Cell / secondary. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / secondary. Chromosomes, Human, Pair 7 / genetics. DNA, Neoplasm / genetics. DNA, Neoplasm / metabolism. Female. Gene Expression Regulation, Neoplastic. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Prognosis. Small Cell Lung Carcinoma / genetics. Small Cell Lung Carcinoma / secondary. Survival Rate


21. 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


22. Takeuchi K, Choi YL, Soda M, Inamura K, Togashi Y, Hatano S, Enomoto M, Takada S, Yamashita Y, Satoh Y, Okumura S, Nakagawa K, Ishikawa Y, Mano H: Multiplex reverse transcription-PCR screening for EML4-ALK fusion transcripts. Clin Cancer Res; 2008 Oct 15;14(20):6618-24
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  • PURPOSE: EML4-ALK is a fusion-type protein tyrosine kinase that is generated by inv(2)(p21p23) in the genome of non-small cell lung cancer (NSCLC).
  • EXPERIMENTAL DESIGN: Primers were designed to detect all possible in-frame fusions of EML4 to exon 20 of ALK, and a single-tube multiplex RT-PCR assay was done with total RNA from 656 solid tumors of the lung (n = 364) and 10 other organs.
  • RESULTS: From consecutive lung adenocarcinoma cases (n = 253), we identified 11 specimens (4.35%) positive for fusion transcripts, 9 of which were positive for the previously identified variants 1, 2, and 3.
  • No fusion transcripts were detected for other types of lung cancer (n = 111) or for tumors from 10 other organs (n = 292).
  • Genomic rearrangements responsible for the fusion events in NSCLC cells were confirmed by genomic PCR analysis and fluorescence in situ hybridization.
  • CONCLUSIONS: These data reinforce the importance of accurate diagnosis of EML4-ALK-positive tumors for the optimization of treatment strategies.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Exons / genetics. Oncogene Proteins, Fusion / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / genetics. Carcinoma, Adenosquamous / diagnosis. Carcinoma, Adenosquamous / genetics. Carcinoma, Large Cell / diagnosis. Carcinoma, Large Cell / genetics. Carcinoma, Squamous Cell / diagnosis. Carcinoma, Squamous Cell / genetics. Cell Transformation, Neoplastic. Chromosome Inversion. DNA Primers / chemistry. Gene Rearrangement. Humans. Immunoenzyme Techniques. In Situ Hybridization, Fluorescence. Lung Neoplasms / diagnosis. Lung Neoplasms / genetics. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism

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  • (PMID = 18927303.001).
  • [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 / DNA Primers; 0 / EML4-ALK fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / RNA, Neoplasm
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23. 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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24. Yuan P, Kadara H, Behrens C, Tang X, Woods D, Solis LM, Huang J, Spinola M, Dong W, Yin G, Fujimoto J, Kim E, Xie Y, Girard L, Moran C, Hong WK, Minna JD, Wistuba II: Sex determining region Y-Box 2 (SOX2) is a potential cell-lineage gene highly expressed in the pathogenesis of squamous cell carcinomas of the lung. PLoS One; 2010 Feb 09;5(2):e9112
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  • [Title] Sex determining region Y-Box 2 (SOX2) is a potential cell-lineage gene highly expressed in the pathogenesis of squamous cell carcinomas of the lung.
  • BACKGROUND: Non-small cell lung cancer (NSCLC) represents the majority (85%) of lung cancers and is comprised mainly of adenocarcinomas and squamous cell carcinomas (SCCs).
  • The sequential pathogenesis of lung adenocarcinomas and SCCs occurs through dissimilar phases as the former tumors typically arise in the lung periphery whereas the latter normally arise near the central airway.
  • METHODOLOGY/PRINCIPAL FINDINGS: We assessed the expression of SOX2, an embryonic stem cell transcriptional factor that also plays important roles in the proliferation of basal tracheal cells and whose expression is restricted to the main and central airways and bronchioles of the developing and adult mouse lung, in NSCLC by various methodologies.
  • Here, we found that SOX2 mRNA levels, from various published datasets, were significantly elevated in lung SCCs compared to adenocarcinomas (all p<0.001).
  • Moreover, a previously characterized OCT4/SOX2/NANOG signature effectively separated lung SCCs from adenocarcinomas in two independent publicly available datasets which correlated with increased SOX2 mRNA in SCCs.
  • Immunohistochemical analysis of various histological lung tissue specimens demonstrated marked nuclear SOX2 protein expression in all normal bronchial epithelia, alveolar bronchiolization structures and premalignant lesions in SCC development (hyperplasia, dysplasia and carcinoma in situ) and absence of expression in all normal alveoli and atypical adenomatous hyperplasias.
  • Moreover, SOX2 protein expression was greatly higher in lung SCCs compared to adenocarcinomas following analyses in two independent large TMA sets (TMA set I, n = 287; TMA set II, n = 511 both p<0.001).
  • Furthermore, amplification of SOX2 DNA was detected in 20% of lung SCCs tested (n = 40) and in none of the adenocarcinomas (n = 17).
  • CONCLUSIONS/SIGNIFICANCE: Our findings highlight a cell-lineage gene expression pattern for the stem cell transcriptional factor SOX2 in the pathogenesis of lung SCCs and suggest a differential activation of stem cell-related pathways between squamous cell carcinomas and adenocarcinomas of the lung.

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  • (PMID = 20161759.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P50 CA070907; United States / NCI NIH HHS / CA / CA-16672; United States / NCI NIH HHS / CA / P50CA70907
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / NANOG protein, human; 0 / Octamer Transcription Factor-3; 0 / POU5F1 protein, human; 0 / SOX2 protein, human; 0 / SOXB1 Transcription Factors
  • [Other-IDs] NLM/ PMC2817751
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25. 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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26. 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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27. Bhargava R, Gerald WL, Li AR, Pan Q, Lal P, Ladanyi M, Chen B: EGFR gene amplification in breast cancer: correlation with epidermal growth factor receptor mRNA and protein expression and HER-2 status and absence of EGFR-activating mutations. Mod Pathol; 2005 Aug;18(8):1027-33
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  • We studied EGFR gene amplification by chromogenic in situ hybridization (CISH) and protein expression by immunohistochemistry in 175 breast carcinomas, using tissue microarrays.
  • HER-2 gene amplification by fluorescence in situ hybridization (FISH) and protein overexpression by immunohistochemistry were also studied.
  • Exons 19 and 21 of EGFR, the sites of hotspot mutations in lung adenocarcinomas, were screened in the 11 EGFR-amplified tumors but no mutations were found.
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adult. Aged. Aged, 80 and over. DNA Mutational Analysis / methods. Female. Gene Amplification. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. In Situ Hybridization / methods. In Situ Hybridization, Fluorescence. Lung Neoplasms / genetics. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Middle Aged. Mutation. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptor, ErbB-2 / genetics. Tissue Array Analysis


28. 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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29. Mino-Kenudson M, Chirieac LR, Law K, Hornick JL, Lindeman N, Mark EJ, Cohen DW, Johnson BE, Jänne PA, Iafrate AJ, Rodig SJ: A novel, highly sensitive antibody allows for the routine detection of ALK-rearranged lung adenocarcinomas by standard immunohistochemistry. Clin Cancer Res; 2010 Mar 1;16(5):1561-71
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  • [Title] A novel, highly sensitive antibody allows for the routine detection of ALK-rearranged lung adenocarcinomas by standard immunohistochemistry.
  • PURPOSE: Approximately 5% of lung adenocarcinomas harbor an EML4-ALK gene fusion and define a unique tumor group that may be responsive to targeted therapy.
  • However ALK-rearranged lung adenocarcinomas are difficult to detect by either standard fluorescence in situ hybridization or immunohistochemistry (IHC) assays.
  • In the present study, we used novel antibodies to compare ALK protein expression in genetically defined lung cancers and anaplastic large cell lymphomas.
  • RESULTS: ALK protein is invariably and exclusively expressed in ALK-rearranged lung adenocarcinomas but at much lower levels than in the prototypic ALK-rearranged tumor, anaplastic large cell lymphoma, and as a result, is often not detected by conventional IHC.
  • We further validate a novel IHC that shows excellent sensitivity and specificity (100% and 99%, respectively) for the detection of ALK-rearranged lung adenocarcinomas in biopsy specimens, with excellent interobserver agreement between pathologists (kappa statistic, 0.94).
  • CONCLUSIONS: Low levels of ALK protein expression is a characteristic feature of ALK-rearranged lung adenocarcinomas.
  • However, a novel, highly sensitive IHC assay reliably detects lung adenocarcinomas with ALK rearrangements and obviates the need for fluorescence in situ hybridization analysis for the majority of cases, and therefore could be routinely applicable in clinical practice to detect lung cancers that may be responsive to ALK inhibitors.

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  • (PMID = 20179225.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P20 CA090578; United States / NCI NIH HHS / CA / CA090578; United States / NCI NIH HHS / CA / CA136851-01A1; United States / NCI NIH HHS / CA / R01 CA136851-01A1; United States / NCI NIH HHS / CA / R01CA136851; United States / NCI NIH HHS / CA / P50 CA090578; United States / NCI NIH HHS / CA / R01 CA114465; United States / NCI NIH HHS / CA / R01 CA136851
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / EML4-ALK fusion protein, human; 0 / Oncogene Proteins, Fusion
  • [Other-IDs] NLM/ NIHMS170973; NLM/ PMC2831135
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30. Chung JH, Choe G, Jheon S, Sung SW, Kim TJ, Lee KW, Lee JH, Lee CT: Epidermal growth factor receptor mutation and pathologic-radiologic correlation between multiple lung nodules with ground-glass opacity differentiates multicentric origin from intrapulmonary spread. J Thorac Oncol; 2009 Dec;4(12):1490-5
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  • [Title] Epidermal growth factor receptor mutation and pathologic-radiologic correlation between multiple lung nodules with ground-glass opacity differentiates multicentric origin from intrapulmonary spread.
  • INTRODUCTION: No standard guidelines detailing recommendations for the selection and treatment for multiple lung nodules with ground-glass opacity (GGO) have been established.
  • For treatment decision, we analyzed epidermal growth factor receptor (EGFR)/K-ras somatic aberrations and pathologic-radiologic correlation in multiple lung nodules presented as GGO to differentiate multifocal lesions from intrapulmonary spread.
  • METHODS: Twenty-four patients with multiple lung nodules presented as GGO were identified to investigate somatic mutations of EGFR (exon 18-21) and K-ras (codons 2, 13, and 61).
  • RESULTS: High frequency of discordant EGFR mutations (17 of 24, 70.8%) could discriminate tumor clonality (18 of 24, 75%) of multiple lung neoplastic nodules presented as GGO.
  • These findings might be a clue to establish guidelines of the multiple neoplastic lung nodules with GGO.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / pathology. Carcinoma in Situ / pathology. Hyperplasia / pathology. Lung Neoplasms / pathology. Mutation / genetics. Precancerous Conditions / pathology. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / genetics. DNA, Neoplasm / genetics. Diagnosis, Differential. Female. Genotype. Humans. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging. Polymerase Chain Reaction. Prognosis. Proto-Oncogene Proteins / blood. Proto-Oncogene Proteins / genetics. Tomography, X-Ray Computed. ras Proteins / blood. ras Proteins / genetics

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  • (PMID = 19844187.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.6.5.2 / ras Proteins
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31. 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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32. 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


33. Rodig SJ, Mino-Kenudson M, Dacic S, Yeap BY, Shaw A, Barletta JA, Stubbs H, Law K, Lindeman N, Mark E, Janne PA, Lynch T, Johnson BE, Iafrate AJ, Chirieac LR: Unique clinicopathologic features characterize ALK-rearranged lung adenocarcinoma in the western population. Clin Cancer Res; 2009 Aug 15;15(16):5216-23
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  • [Title] Unique clinicopathologic features characterize ALK-rearranged lung adenocarcinoma in the western population.
  • PURPOSE: The anaplastic large cell kinase gene (ALK) is rearranged in approximately 5% of lung adenocarcinomas within the Asian population.
  • We evaluated the incidence and the characteristics of ALK-rearranged lung adenocarcinomas within the western population and the optimal diagnostic modality to detect ALK rearrangements in routine clinical practice.
  • EXPERIMENTAL DESIGN: We tested 358 lung adenocarcinomas from three institutions for ALK rearrangements by fluorescent in situ hybridization (FISH) and immunohistochemistry with and without tyramide amplification.
  • RESULTS: We identified 20 (5.6%) lung adenocarcinomas with ALK rearrangements within our cohort of western patients.
  • ALK rearrangement was associated with younger age (P = 0.0002), never smoking (P < 0.0001), advanced clinical stage (P = 0.0001), and a solid histology with signet-ring cells (P < 0.0001).
  • CONCLUSIONS: Lung adenocarcinomas with ALK rearrangements are uncommon in the western population and represent a distinct entity of carcinomas with unique characteristics.
  • For suspected cases, dual diagnostic testing, with FISH and immunohistochemistry, should be considered to accurately identify lung adenocarcinomas with ALK rearrangement.

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  • (PMID = 19671850.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA136851-02; United States / PHS HHS / / R01-135257; United States / PHS HHS / / R01-136851; United States / NCI NIH HHS / CA / P50 CA090578; United States / NCI NIH HHS / CA / R01 CA136851-02; United States / NCI NIH HHS / CA / R01 CA136851; United States / NCI NIH HHS / CA / 2P50 CA090578-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Other-IDs] NLM/ NIHMS198972; NLM/ PMC2865649
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34. 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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35. 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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36. 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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37. 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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38. 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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39. 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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40. 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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41. 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


42. 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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43. 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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44. 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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45. 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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  • [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
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46. 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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47. Zheng H, Abdel Aziz HO, Nakanishi Y, Masuda S, Saito H, Tsuneyama K, Takano Y: Oncogenic role of JC virus in lung cancer. J Pathol; 2007 Jul;212(3):306-15
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  • [Title] Oncogenic role of JC virus in lung cancer.
  • Here, JCV was examined by targeting its T-antigen in lung carcinomas (n=103) and normal lung tissues (n=18) by nested-PCR followed by Southern blot, real-time PCR, immunohistochemistry, in situ hybridization and in situ PCR.
  • Additionally, expression of Ki-67, caspase-3, beta-catenin, p53, and Rb was analysed by immunohistochemistry on tissue microarrays of lung carcinomas.
  • Normal lung tissue was positive significantly less frequently, and contained a lower copy number of JCV than lung carcinomas (p<0.05), and copies were lower in lung adenocarcinomas than in squamous, small or large cell carcinomas (p<0.05).
  • In situ PCR and immunolabelling revealed JCV positivity in the nuclei of lung carcinoma cells.
  • Age and UICC staging were independent prognostic factors for lung carcinoma patients.
  • These data suggest that JCV may be involved in lung carcinogenesis, especially in tumour types other than adenocarcinoma.
  • Lung carcinomas with higher JCV copy numbers display high proliferation and down-regulation of cell adhesion mediated by membrane beta-catenin.
  • [MeSH-major] Carcinoma / virology. JC Virus / pathogenicity. Lung Neoplasms / virology. Oncogenic Viruses
  • [MeSH-minor] Aged. Aged, 80 and over. Antigens, Viral, Tumor / genetics. Blotting, Southern / methods. Carcinoma, Large Cell / pathology. Carcinoma, Large Cell / virology. Carcinoma, Small Cell / pathology. Carcinoma, Small Cell / virology. Carcinoma, Squamous Cell / pathology. Carcinoma, Squamous Cell / virology. DNA, Viral / analysis. Female. Gene Expression Profiling. Humans. In Situ Hybridization. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Sequence Analysis, DNA

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  • [Copyright] Copyright (c) 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • (PMID = 17534844.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Viral, Tumor; 0 / DNA, Viral; 0 / RNA, Messenger
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48. Coffey JC, Wang JH, Bouchier-Hayes D, Cotter TG, Redmond HP: The targeting of phosphoinositide-3 kinase attenuates pulmonary metastatic tumor growth following laparotomy. Ann Surg; 2006 Feb;243(2):250-6
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  • METHODS: Balb/c mice underwent a tail vein injection of 1x10 metastatic murine mammary adenocarcinoma 4T1 cells.
  • Metastatic tumor burden was assessed using the lung/body weight ratio and a histologic metastatic index.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Adenocarcinoma / surgery. Chromones / pharmacology. Enzyme Inhibitors / pharmacology. Lung Neoplasms / drug therapy. Lung Neoplasms / pathology. Lung Neoplasms / surgery. Morpholines / pharmacology. Neoplasm Recurrence, Local / prevention & control. Neoplasms, Experimental / drug therapy. Neoplasms, Experimental / pathology. Neoplasms, Experimental / surgery. Phosphatidylinositol 3-Kinases / antagonists & inhibitors
  • [MeSH-minor] Animals. Apoptosis. Blotting, Western. Cell Division. In Situ Nick-End Labeling. Laparotomy. Mice. Mice, Inbred BALB C. Neoplasm Metastasis. Tumor Cells, Cultured

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  • (PMID = 16432359.001).
  • [ISSN] 0003-4932
  • [Journal-full-title] Annals of surgery
  • [ISO-abbreviation] Ann. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromones; 0 / Enzyme Inhibitors; 0 / Morpholines; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; EC 2.7.1.- / Phosphatidylinositol 3-Kinases
  • [Other-IDs] NLM/ PMC1448916
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49. Hirsch FR, Dziadziuszko R, Varella-Garcia M, Franklin WA, Gandara DR, Bunn PA Jr: First-generation epidermal growth factor receptor inhibitors in non-small cell lung cancer: clinical impact of the epidermal growth factor receptor fluorescence in situ hybridization assay. J Thorac Oncol; 2008 Jun;3(6 Suppl 2):S138-42
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  • [Title] First-generation epidermal growth factor receptor inhibitors in non-small cell lung cancer: clinical impact of the epidermal growth factor receptor fluorescence in situ hybridization assay.
  • Epidermal growth factor receptor (EGFR) inhibitors have been proven to improve survival in advanced non-small cell lung cancer patients, even after failure of previous chemotherapy.
  • Clinical and demographic factors, i.e., females, never-smokers, patients with Asian ethnicity, or histology of adenocarcinoma, seem all to be favorable factors for clinical outcome, but not sufficient for patient selection.
  • Increased EGFR gene copy number detected by fluorescence in situ hybridization has consistently been shown in several retrospective studies to be a good predictive "marker," especially for EGFR tyrosine kinase inhibitors.
  • The current review summarizes the clinical data based on the first generation EGFR inhibitors and discusses future strategies for exploring the role of EGFR fluorescence in situ hybridization as a selection marker for EGFR inhibitor therapy in non-small cell lung cancer.
  • [MeSH-major] Angiogenesis Inhibitors / administration & dosage. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Receptor, Epidermal Growth Factor / antagonists & inhibitors
  • [MeSH-minor] Biomarkers, Tumor / genetics. Female. Follow-Up Studies. Genetic Predisposition to Disease / epidemiology. Humans. In Situ Hybridization, Fluorescence. Male. Neoplasm Staging. Neovascularization, Pathologic / prevention & control. Risk Assessment. Survival Analysis. Treatment Outcome


50. Zen Y, Inoue D, Kitao A, Onodera M, Abo H, Miyayama S, Gabata T, Matsui O, Nakanuma Y: IgG4-related lung and pleural disease: a clinicopathologic study of 21 cases. Am J Surg Pathol; 2009 Dec;33(12):1886-93
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  • [Title] IgG4-related lung and pleural disease: a clinicopathologic study of 21 cases.
  • In this study, we examined clinical and pathologic features of, and follow-up data on, IgG4-related lung and pleural lesions.
  • Interestingly, 1 patient was found to have a primary adenocarcinoma against a background of IgG4-related lung disease during follow up.
  • [MeSH-major] Immunoglobulin G / analysis. Lung / immunology. Lung Diseases / immunology. Pleura / immunology. Pleural Diseases / immunology
  • [MeSH-minor] Adult. Aged. Biomarkers / analysis. Female. Humans. Immunohistochemistry. In Situ Hybridization. Male. Middle Aged. Steroids / therapeutic use. Time Factors. Treatment Outcome

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  • (PMID = 19898222.001).
  • [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; 0 / Immunoglobulin G; 0 / Steroids
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51. Weiss J, Sos ML, Seidel D, Peifer M, Zander T, Heuckmann JM, Ullrich RT, Menon R, Maier S, Soltermann A, Moch H, Wagener P, Fischer F, Heynck S, Koker M, Schöttle J, Leenders F, Gabler F, Dabow I, Querings S, Heukamp LC, Balke-Want H, Ansén S, Rauh D, Baessmann I, Altmüller J, Wainer Z, Conron M, Wright G, Russell P, Solomon B, Brambilla E, Brambilla C, Lorimier P, Sollberg S, Brustugun OT, Engel-Riedel W, Ludwig C, Petersen I, Sänger J, Clement J, Groen H, Timens W, Sietsma H, Thunnissen E, Smit E, Heideman D, Cappuzzo F, Ligorio C, Damiani S, Hallek M, Beroukhim R, Pao W, Klebl B, Baumann M, Buettner R, Ernestus K, Stoelben E, Wolf J, Nürnberg P, Perner S, Thomas RK: Frequent and focal FGFR1 amplification associates with therapeutically tractable FGFR1 dependency in squamous cell lung cancer. Sci Transl Med; 2010 Dec 15;2(62):62ra93
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  • [Title] Frequent and focal FGFR1 amplification associates with therapeutically tractable FGFR1 dependency in squamous cell lung cancer.
  • Lung cancer remains one of the leading causes of cancer-related death in developed countries.
  • Although lung adenocarcinomas with EGFR mutations or EML4-ALK fusions respond to treatment by epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) inhibition, respectively, squamous cell lung cancer currently lacks therapeutically exploitable genetic alterations.
  • We conducted a systematic search in a set of 232 lung cancer specimens for genetic alterations that were therapeutically amenable and then performed high-resolution gene copy number analyses.
  • We identified frequent and focal fibroblast growth factor receptor 1 (FGFR1) amplification in squamous cell lung cancer (n = 155), but not in other lung cancer subtypes, and, by fluorescence in situ hybridization, confirmed the presence of FGFR1 amplifications in an independent cohort of squamous cell lung cancer samples (22% of cases).
  • Using cell-based screening with the FGFR inhibitor PD173074 in a large (n = 83) panel of lung cancer cell lines, we demonstrated that this compound inhibited growth and induced apoptosis specifically in those lung cancer cells carrying amplified FGFR1.
  • Thus, focal FGFR1 amplification is common in squamous cell lung cancer and associated with tumor growth and survival, suggesting that FGFR inhibitors may be a viable therapeutic option in this cohort of patients.
  • [MeSH-major] Lung Neoplasms / genetics. Lung Neoplasms / metabolism. Receptor, Fibroblast Growth Factor, Type 1 / metabolism
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Animals. Apoptosis / genetics. Apoptosis / physiology. Blotting, Western. Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / metabolism. Cell Line. Enzyme Inhibitors / therapeutic use. Gene Expression Regulation, Neoplastic / genetics. Humans. Male. Mice. Mice, Nude. Pyrimidines / therapeutic use. RNA Interference. Xenograft Model Antitumor Assays

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  • (PMID = 21160078.001).
  • [ISSN] 1946-6242
  • [Journal-full-title] Science translational medicine
  • [ISO-abbreviation] Sci Transl Med
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE25016
  • [Grant] United States / NCI NIH HHS / CA / K08 CA097980; United States / NCI NIH HHS / CA / P01 CA129243; United States / NCI NIH HHS / CA / R01 CA121210
  • [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 / Enzyme Inhibitors; 0 / PD 173074; 0 / Pyrimidines; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1; Adenocarcinoma of lung
  • [Other-IDs] NLM/ NIHMS569992; NLM/ PMC3990281
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52. 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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53. 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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54. Shen H, Zhu Y, Wu YJ, Qiu HR, Shu YQ: Genomic alterations in lung adenocarcinomas detected by multicolor fluorescence in situ hybridization and comparative genomic hybridization. Cancer Genet Cytogenet; 2008 Mar;181(2):100-7
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  • [Title] Genomic alterations in lung adenocarcinomas detected by multicolor fluorescence in situ hybridization and comparative genomic hybridization.
  • We used two molecular cytogenetic techniques, multicolor fluorescence in situ hybridization (M-FISH) and comparative genomic hybridization (CGH), to analyze three established lung adenocarcinoma cell lines (A549, H1650, and SPC-A-1) and primary lung adenocarcinoma samples, to identify common chromosomal aberrations.
  • The most common gains were found in 16p13 (in 50% of samples), and 16p13 amplification was associated with relatively poor differentiation and late stage.
  • M-FISH and CGH can be a powerful tool in identification of genomic alterations in lung cancer, as well as in diagnosis.
  • The overrepresented regions may harbor potential candidate genes involved in lung adenocarcinoma pathogenesis.
  • [MeSH-major] Adenocarcinoma / genetics. Chromosome Aberrations. In Situ Hybridization, Fluorescence / methods. Lung Neoplasms / genetics. Nucleic Acid Hybridization
  • [MeSH-minor] Carcinoma, Non-Small-Cell Lung / diagnosis. Carcinoma, Non-Small-Cell Lung / genetics. Cell Line, Tumor. Color. Genome, Human. Humans. Karyotyping

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  • (PMID = 18295661.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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55. Angulo B, Suarez-Gauthier A, Lopez-Rios F, Medina PP, Conde E, Tang M, Soler G, Lopez-Encuentra A, Cigudosa JC, Sanchez-Cespedes M: Expression signatures in lung cancer reveal a profile for EGFR-mutant tumours and identify selective PIK3CA overexpression by gene amplification. J Pathol; 2008 Feb;214(3):347-56
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  • [Title] Expression signatures in lung cancer reveal a profile for EGFR-mutant tumours and identify selective PIK3CA overexpression by gene amplification.
  • Here, we aim to identify gene expression profiles and single markers that recapitulate the pathological and genetic background of non-small cell lung cancer (NSCLC).
  • We performed cDNA microarray analysis on a series of 69 NSCLCs, with known mutation status for important genes, and six normal lung tissues.
  • Unsupervised cluster analysis segregated normal lungs from lung tumours and lung tumours according to their histopathology and the presence of EGFR mutations.
  • Several transcripts were highly overexpressed (by approximately 20 times) in squamous cell carcinomas (SCCs) relative to adenocarcinomas (ACs) and confirmed by immunohistochemistry in an independent cohort of 75 lung tumours.
  • In conclusion, histopathological phenotypes and, likely, the presence of EGFR mutations confer lung tumours with a marked pattern of gene expression.
  • Moreover, our cDNA microarray analysis identified increased PIK3CA expression due to gene amplification in lung squamous cell carcinomas: this may represent a marker of sensitivity to therapy with PI3K inhibitors.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Gene Expression Profiling. Genetic Markers. Lung Neoplasms / genetics. Oligonucleotide Array Sequence Analysis
  • [MeSH-minor] Adenocarcinoma / genetics. Carcinoma, Squamous Cell / genetics. Case-Control Studies. Cluster Analysis. Gene Amplification. Genes, ras. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Mutation. Phosphatidylinositol 3-Kinases / genetics. Receptor, Epidermal Growth Factor / genetics

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  • [Copyright] Copyright (c) 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • (PMID = 17992665.001).
  • [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 / Genetic Markers; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.137 / PIK3CA protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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56. Gupta R, Dastane AM, McKenna R Jr, Marchevsky AM: The predictive value of epidermal growth factor receptor tests in patients with pulmonary adenocarcinoma: review of current "best evidence" with meta-analysis. Hum Pathol; 2009 Mar;40(3):356-65
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  • [Title] The predictive value of epidermal growth factor receptor tests in patients with pulmonary adenocarcinoma: review of current "best evidence" with meta-analysis.
  • Epidermal growth factor receptor signaling pathway plays an important role in pulmonary adenocarcinoma biology.
  • Several RCT and other studies have evaluated the value of various tests such as immunohistochemistry, polymerase chain reaction, and fluorescent in situ hybridization for epidermal growth factor receptor detection.
  • Estimated positive predictive values of immunohistochemistry, polymerase chain reaction, and fluorescent in situ hybridization range from 6.5% to 82%%, 7% to 100%, and 11% to 89%, respectively.
  • Meta-analysis of nearly 5000 cases in the literature estimates that all 3 tests significantly predict response to gefitinib in patients with lung cancer.
  • Further studies are needed to clarify the predictive value of epidermal growth factor receptor tests in patients with pulmonary adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / metabolism. Lung Neoplasms / metabolism. Receptor, Epidermal Growth Factor / metabolism

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  • (PMID = 18976796.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Quinazolines; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
  • [Number-of-references] 50
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57. Keith RL: Chemoprevention of lung cancer. Proc Am Thorac Soc; 2009 Apr 15;6(2):187-93
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  • [Title] Chemoprevention of lung cancer.
  • Lung cancer is the leading cause of cancer death in the United States, and the majority of diagnoses are made in former smokers.
  • While avoidance of tobacco abuse and smoking cessation clearly will have the greatest impact on lung cancer development, effective chemoprevention could prove to be more effective than treatment of established disease.
  • Chemoprevention is the use of dietary or pharmaceutical agents to reverse or inhibit the carcinogenic process and has been successfully applied to common malignancies other than lung.
  • Despite previous studies in lung cancer chemoprevention failing to identify effective agents, our ability to determine higher risk populations and the understanding of lung tumor and pre-malignant biology continues to advance.
  • The World Health Organization/International Association for the Study of Lung Cancer classification for lung cancer now recognizes distinct histologic lesions that can be reproducibly graded as precursors of non-small cell lung cancer.
  • For example, carcinogenesis in the bronchial epithelium starts with normal epithelium and progresses through hyperplasia, metaplasia, dysplasia, and carcinoma in situ to invasive squamous cell cancer.
  • Similar precursor lesions exist for adenocarcinoma, and these pre-malignant lesions are targeted by chemopreventive agents in current and future trials.
  • [MeSH-major] Chemoprevention / methods. Lung Neoplasms / prevention & control. Precancerous Conditions / drug therapy

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  • (PMID = 19349487.001).
  • [ISSN] 1546-3222
  • [Journal-full-title] Proceedings of the American Thoracic Society
  • [ISO-abbreviation] Proc Am Thorac Soc
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers
  • [Number-of-references] 86
  • [Other-IDs] NLM/ PMC2674227
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58. 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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59. 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]
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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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60. 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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61. 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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62. Reimer TA, Anagnostopoulos I, Erdmann B, Lehmann I, Stein H, Daniel P, Dörken B, Rehm A: Reevaluation of the 22-1-1 antibody and its putative antigen, EBAG9/RCAS1, as a tumor marker. BMC Cancer; 2005;5:47
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  • RESULTS: Here, we compared expression of the 22-1-1 and EBAG9-defined antigens in normal and neoplastic tissues in situ.
  • [MeSH-minor] Adenocarcinoma / metabolism. Antibodies, Monoclonal / chemistry. Antibodies, Monoclonal / metabolism. Antigens, Tumor-Associated, Carbohydrate / chemistry. Antineoplastic Agents / pharmacology. Apoptosis. Brefeldin A / pharmacology. Carcinoma / metabolism. Carcinoma, Squamous Cell / metabolism. Caspase 3. Caspase 7. Caspases / biosynthesis. Cell Line. Cell Line, Tumor. Cell Nucleus / metabolism. Colorectal Neoplasms / metabolism. Flow Cytometry. Golgi Apparatus / metabolism. Humans. Immunoblotting. Immunohistochemistry. Immunotherapy / methods. Lung Neoplasms / metabolism. Male. Microscopy, Confocal. Microscopy, Electron. Mouth Neoplasms / metabolism. Nocodazole / pharmacology. Polysaccharides / chemistry. Prostatic Neoplasms / metabolism. Protein Synthesis Inhibitors / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Stomach Neoplasms / metabolism. Subcellular Fractions. Tissue Distribution

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  • (PMID = 15904507.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 22-1-1 antigen; 0 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm; 0 / Antigens, Tumor-Associated, Carbohydrate; 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / EBAG9 protein, human; 0 / Polysaccharides; 0 / Protein Synthesis Inhibitors; 0 / Tn antigen; 20350-15-6 / Brefeldin A; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / CASP7 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 7; EC 3.4.22.- / Caspases; SH1WY3R615 / Nocodazole
  • [Other-IDs] NLM/ PMC1164403
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63. 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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  • [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


64. Sterlacci W, Fiegl M, Hilbe W, Jamnig H, Oberaigner W, Schmid T, Augustin F, Auberger J, Obermann EC, Tzankov A: Deregulation of p27 and cyclin D1/D3 control over mitosis is associated with unfavorable prognosis in non-small cell lung cancer, as determined in 405 operated patients. J Thorac Oncol; 2010 Sep;5(9):1325-36
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  • [Title] Deregulation of p27 and cyclin D1/D3 control over mitosis is associated with unfavorable prognosis in non-small cell lung cancer, as determined in 405 operated patients.
  • INTRODUCTION: A large group of interacting molecular factors, involved in epithelial-mesenchymal transition, epidermal growth factor receptor (EGFR) signaling, and G1 mitotic phase, are shown to play an important role in cancerogenesis and progression of non-small cell lung cancer (NSCLC).
  • In addition, the gene status of EGFR and cyclin D1 was examined by fluorescence in situ hybridization.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / metabolism. Cyclin D1 / metabolism. Cyclin D3 / metabolism. Intracellular Signaling Peptides and Proteins / metabolism. Lung Neoplasms / metabolism. Mitosis / physiology
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adult. Aged. Aged, 80 and over. Carcinoma, Large Cell / genetics. Carcinoma, Large Cell / metabolism. Carcinoma, Large Cell / pathology. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / pathology. Cyclin-Dependent Kinase Inhibitor p27. Female. Humans. Immunoenzyme Techniques. In Situ Hybridization, Fluorescence. Male. Middle Aged. Prognosis. Retrospective Studies. Survival Rate. Tissue Array Analysis. Young Adult


65. Moreira AL: Bronchioloalveolar Carcinoma and Minimally Invasive Adenocarcinoma. Surg Pathol Clin; 2010 Mar;3(1):1-26
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  • [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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66. 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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67. Hwang SK, Lim HT, Minai-Tehrani A, Lee ES, Park J, Park SB, Beck GR Jr, Cho MH: Repeated aerosol delivery of carboxyl-terminal modulator protein suppresses tumor in the lungs of K-rasLA1 mice. Am J Respir Crit Care Med; 2009 Jun 15;179(12):1131-40
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  • RATIONALE: Difficulties in achieving long-term survival of patients with lung cancer treated with conventional therapies suggest that novel approaches are required.
  • Recent advances in aerosol-mediated gene delivery have provided the possibility of an alternative for the safe and effective treatment of lung cancer.
  • OBJECTIVES: To investigate the repeated effect of carboxyl-terminal modulator protein (CTMP) on multistage lung tumorigenesis.
  • In this study, we addressed this question by studying the effects of lentivirus-based CTMP in the lungs of 9- and 13-week-old K-ras(LA1) mice, a model of lung cancer.
  • METHODS: An aerosol of lentivirus-based CTMP was delivered into 9- and 13-week-old K-ras(LA1) mice, a model of lung cancer, through a nose-only inhalation system twice a week for 4 weeks.
  • The effects of CTMP on lung cancer progression and Akt-related signals were evaluated.
  • MEASUREMENTS AND MAIN RESULTS: Long-term repeated delivery of CTMP effectively reduced tumor progression in the lungs at different stages of development.
  • CONCLUSIONS: Long-term repeated viral delivery of CTMP may provide a useful tool for designing lung tumor treatment.
  • [MeSH-major] Adenocarcinoma / therapy. Carrier Proteins / genetics. Gene Expression Regulation, Neoplastic. Gene Transfer Techniques. Lung Neoplasms / therapy. Neoplasms, Experimental / drug therapy
  • [MeSH-minor] Aerosols. Animals. Apoptosis. Blotting, Western. Cell Line, Tumor. Disease Progression. Genes, ras. In Situ Nick-End Labeling. Male. Mice. Mice, Inbred C57BL. Treatment Outcome

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  • (PMID = 19286625.001).
  • [ISSN] 1535-4970
  • [Journal-full-title] American journal of respiratory and critical care medicine
  • [ISO-abbreviation] Am. J. Respir. Crit. Care Med.
  • [Language] eng
  • [Grant] United States / NIAMS NIH HHS / AR / R01 AR056090
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aerosols; 0 / CTMP protein, mouse; 0 / Carrier Proteins
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68. Ludovini V, Gori S, Pistola L, Della Fazia MA, Piobbico D, Servillo G, Flacco A, Scuderi C, Crinò L: Long-lasting complete remission with tyrosine kinase inhibitor in bronchioloalveolar carcinoma with a so far unknown EGFR mutation. J Thorac Oncol; 2008 Apr;3(4):452-3
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  • [Title] Long-lasting complete remission with tyrosine kinase inhibitor in bronchioloalveolar carcinoma with a so far unknown EGFR mutation.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / drug therapy. Adenocarcinoma, Bronchiolo-Alveolar / genetics. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lung Neoplasms / drug therapy. Lung Neoplasms / genetics. Mutation / genetics. Protein-Tyrosine Kinases / antagonists & inhibitors. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Cisplatin / administration & dosage. Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Humans. Immunoenzyme Techniques. In Situ Hybridization, Fluorescence. Male. Middle Aged. Remission Induction. Tomography Scanners, X-Ray Computed

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  • (PMID = 18379371.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; Q20Q21Q62J / Cisplatin
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69. Ullrich RT, Zander T, Neumaier B, Koker M, Shimamura T, Waerzeggers Y, Borgman CL, Tawadros S, Li H, Sos ML, Backes H, Shapiro GI, Wolf J, Jacobs AH, Thomas RK, Winkeler A: Early detection of erlotinib treatment response in NSCLC by 3'-deoxy-3'-[F]-fluoro-L-thymidine ([F]FLT) positron emission tomography (PET). PLoS One; 2008;3(12):e3908
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  • BACKGROUND: Inhibition of the epidermal growth factor receptor (EGFR) has shown clinical success in patients with advanced non-small cell lung cancer (NSCLC).
  • Somatic mutations of EGFR were found in lung adenocarcinoma that lead to exquisite dependency on EGFR signaling; thus patients with EGFR-mutant tumors are at high chance of response to EGFR inhibitors.
  • METHODOLOGY/PRINCIPAL FINDINGS: We performed a systematic comparison of 3'-Deoxy-3'-[(18)F]-fluoro-L-thymidine ([(18)F]FLT) and 2-[(18)F]-fluoro-2-deoxy-D-glucose ([(18)F]FDG) positron emission tomography (PET) for their potential to identify response to EGFR inhibitors in a model of EGFR-dependent lung cancer early after treatment initiation.
  • CONCLUSIONS: [(18)F]FLT PET enables robust identification of erlotinib response in EGFR-dependent tumors at a very early stage.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / radionuclide imaging. Dideoxynucleosides. Lung Neoplasms / drug therapy. Lung Neoplasms / radionuclide imaging. Positron-Emission Tomography. Quinazolines / therapeutic use
  • [MeSH-minor] Animals. Cell Cycle. Cell Line, Tumor. Down-Regulation. Early Detection of Cancer. Erlotinib Hydrochloride. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Ki-67 Antigen / metabolism. Mice. Receptor, Epidermal Growth Factor / metabolism. Signal Transduction. Treatment Outcome. Xenograft Model Antitumor Assays

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  • (PMID = 19079597.001).
  • [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 / Dideoxynucleosides; 0 / Ki-67 Antigen; 0 / Quinazolines; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; PG53R0DWDQ / alovudine
  • [Other-IDs] NLM/ PMC2592703
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70. Varella-Garcia M, Mitsudomi T, Yatabe Y, Kosaka T, Nakajima E, Xavier AC, Skokan M, Zeng C, Franklin WA, Bunn PA Jr, Hirsch FR: EGFR and HER2 genomic gain in recurrent non-small cell lung cancer after surgery: impact on outcome to treatment with gefitinib and association with EGFR and KRAS mutations in a Japanese cohort. J Thorac Oncol; 2009 Mar;4(3):318-25
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  • [Title] EGFR and HER2 genomic gain in recurrent non-small cell lung cancer after surgery: impact on outcome to treatment with gefitinib and association with EGFR and KRAS mutations in a Japanese cohort.
  • BACKGROUND: Sensitivity to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) and frequency of activation mutations in EGFR is lower in Caucasian than Asian non small-cell lung cancer (NSCLC) patients.
  • Increased EGFR gene copy numbers evaluated by fluorescence in situ hybridization (FISH) has been reported as predictor of clinical benefit from EGFR-TKIs in Caucasian NSCLC patients.
  • The cohort included 48% females and 52% never-smokers; 73% had prior chemotherapy and 57% had stage III-IV at the time of surgery.
  • Adenocarcinoma was the most common histology (86%).
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Genes, ras. Lung Neoplasms / genetics. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / genetics. Quinazolines / therapeutic use. Receptor, Epidermal Growth Factor / metabolism
  • [MeSH-minor] Aged. Biomarkers, Tumor / genetics. Cohort Studies. Female. Genes, erbB-2. Genome. Humans. In Situ Hybridization, Fluorescence. Japan. Kaplan-Meier Estimate. Male. Middle Aged. Mutation. Probability. Prognosis. Retrospective Studies. Sensitivity and Specificity. Statistics, Nonparametric. Survival Analysis


71. Striebel JM, Dacic S, Yousem SA: Gross cystic disease fluid protein-(GCDFP-15): expression in primary lung adenocarcinoma. Am J Surg Pathol; 2008 Mar;32(3):426-32
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  • [Title] Gross cystic disease fluid protein-(GCDFP-15): expression in primary lung adenocarcinoma.
  • A total of 211 cases of primary lung adenocarcinoma were tested for expression of gross cystic disease fluid protein-15 (GCDFP-15) and only 11 cases (5.2%) were positive.
  • This report details the first 11 cases of pulmonary adenocarcinoma to express GCDFP-15 and their distinctive morphology with frequent mucin production and coexpression of thyroid transcription factor-1 and synaptophysin.
  • [MeSH-major] Adenocarcinoma / chemistry. Adenocarcinoma / pathology. Carrier Proteins / analysis. Glycoproteins / analysis. Lung Neoplasms / chemistry. Lung Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma, Papillary / chemistry. Adenocarcinoma, Papillary / pathology. Aged. Female. Histocytochemistry. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Mucins / analysis. Nuclear Proteins / analysis. Synaptophysin / analysis. Transcription Factors / analysis

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  • (PMID = 18300807.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Glycoproteins; 0 / Mucins; 0 / Nuclear Proteins; 0 / PIP protein, human; 0 / Synaptophysin; 0 / Transcription Factors; 0 / thyroid nuclear factor 1
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72. 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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73. 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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74. 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.
  • They were characterized by immunohistochemical and growth kinetic studies, tests for tumorigenicity in nude mice, epidermal growth factor receptor (EGFR) gene mutation analysis, and in situ hybridization, and gene expression profiling with Affymetrix GeneChip HG-U133A.
  • 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.
  • EGFR in situ hybridization showed no EGFR gene amplification in these cell lines.
  • 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-major] Gene Expression Profiling. Lung Neoplasms / genetics. Receptor, Epidermal Growth Factor / genetics. Smoking / adverse effects
  • [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


75. Fernández E, de Castro PL, Astudillo J, Fernández-Llamazares J, Bronchogenic Carcinoma Cooperative Group of the Spanish Society of Pneumology and Thoracic Surgery: Bronchial stump infiltration after lung cancer surgery. Retrospective study of a series of 2994 patients. Interact Cardiovasc Thorac Surg; 2009 Aug;9(2):182-6
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  • [Title] Bronchial stump infiltration after lung cancer surgery. Retrospective study of a series of 2994 patients.
  • The incidence of lung cancer has been increasing in developed countries since the mid-1990s.
  • The main objective of this study is to determine if bronquial stump infiltration can affect survival in patients with lung cancer.
  • For this purpose, we differentiate between carcinoma 'in situ' and invasive carcinoma.
  • We included patients suffering from non-small cell lung cancer who underwent thoracothomy as treatment.
  • Eight patients were excluded thus a total of 72 patients were included, 52 of them had carcinoma 'in situ' and 20 invasive carcinoma.
  • Patients with carcinoma 'in situ' had a median survival of 25 months as opposed to 21 months in patients with invasive carcinoma.
  • We did not observe statistical significance in survival between carcinoma 'in situ' and invasive carcinoma bronchial stump infiltration (P=0.094).
  • The only survival predictor variable is histology (adenocarcinoma), P=0.0001.
  • [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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  • [CommentIn] Interact Cardiovasc Thorac Surg. 2009 Aug;9(2):186 [19628536.001]
  • (PMID = 19470498.001).
  • [ISSN] 1569-9285
  • [Journal-full-title] Interactive cardiovascular and thoracic surgery
  • [ISO-abbreviation] Interact Cardiovasc Thorac Surg
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] England
  • [Investigator] Duque JL; López Encuentra A; Rami-Porta R; Astudillo J; Cantó Armengol A; Casanova J; Mariñan M; Cerezal J; Fernández de la Rota A; Arrabal R; Gimferrer JM; González Aragoneses F; Moreno Mata N; Freixinet J; Rodríguez-Suárez P; Llobregat Poyán N; Mañez N; Serra-Mitjans M; Martín de Nicolás JL; Novoa Valentín N; Rodríguez J; Torres García AJ; Gómez A; de la Torre M; Sánchez-Palencia Ramos A; Zafra JR; Varela Ugarte A; Gámez García P; Wah Pun Y
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76. Pelosi G, Fumagalli C, Trubia M, Sonzogni A, Rekhtman N, Maisonneuve P, Galetta D, Spaggiari L, Veronesi G, Scarpa A, Malpeli G, Viale G: Dual role of RASSF1 as a tumor suppressor and an oncogene in neuroendocrine tumors of the lung. Anticancer Res; 2010 Oct;30(10):4269-81
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  • [Title] Dual role of RASSF1 as a tumor suppressor and an oncogene in neuroendocrine tumors of the lung.
  • BACKGROUND: Little is known about the dual role of RAS-association domain family 1 (RASSF1) gene at 3p21.3 in neuroendocrine tumors (NET) of the lung.
  • MATERIALS AND METHODS: Twenty typical carcinoids (TC), 11 atypical carcinoids (ATC), 11 large cell neuroendocrine carcinomas (LCNEC) and 16 small cell lung carcinomas (SCLC) were analyzed for RASSF1 promoter methylation, mRNA and protein expression, and loss of 3p21.3 locus.
  • RESULTS: Promoter 1 was hypermethylated in NET but not in paired non-neoplastic lung tissues nor in 20 control NSCLC, with the degree of hypermethylation paralleling tumor grade.
  • [MeSH-major] Lung Neoplasms / genetics. Neuroendocrine Tumors / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Aged. Carcinoma, Small Cell / genetics. Carcinoma, Squamous Cell / genetics. DNA Methylation. Female. Genes, Tumor Suppressor. Humans. In Situ Hybridization, Fluorescence. Loss of Heterozygosity. Male. Middle Aged. Oncogenes. Promoter Regions, Genetic. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

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  • (PMID = 21036752.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / RASSF1 protein, human; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins
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77. 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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78. Anagnostou VK, Bepler G, Syrigos KN, Tanoue L, Gettinger S, Homer RJ, Boffa D, Detterbeck F, Rimm DL: High expression of mammalian target of rapamycin is associated with better outcome for patients with early stage lung adenocarcinoma. Clin Cancer Res; 2009 Jun 15;15(12):4157-64
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  • [Title] High expression of mammalian target of rapamycin is associated with better outcome for patients with early stage lung adenocarcinoma.
  • Despite the well known role of mTOR in carcinogenesis, its prognostic potential in lung cancer has not been investigated.
  • EXPERIMENTAL DESIGN: Automated quantitative analysis (AQUA), a fluorescent-based method for analysis of in situ protein expression, was used to assess mTOR expression in a training cohort of 167 lung cancer patients.
  • An independent cohort of 235 lung cancer patients (from a second institution) was used for validation.
  • Patients with high mTOR expression had a longer median overall survival compared with the low expressers (52.7 versus 38.5 months; log rank P = 0.06), which was more prominent in the adenocarcinoma group (55.7 versus 38.88 months; log rank P = 0.018).
  • Multivariate analysis revealed an independent lower risk of death for adenocarcinoma and adenocarcinoma stage IA patients with mTOR-expressing tumors (hazard ratio, 0.48; 95% confidence interval, 0.24-0.98; P = 0.04, and hazard ratio, 0.12; 95% confidence interval, 0.03-0.72; P = 0.019, respectively).
  • CONCLUSIONS: mTOR expression defines a subgroup of patients with a favorable outcome and may be useful for prognostic stratification of lung adenocarcinoma patients as well as incorporation of mTOR into clinical decisions.
  • [MeSH-major] Adenocarcinoma / pathology. Biomarkers, Tumor / biosynthesis. Lung Neoplasms / pathology. Protein Kinases / biosynthesis

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  • (PMID = 19509151.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases
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79. 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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80. 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


81. Tanaka R, Ishiyama T, Uchihara T, Inadome Y, Iijima T, Morishita Y, Kano J, Goya T, Noguchi M: Expression of the Bax inhibitor-1 gene in pulmonary adenocarcinoma. Cancer; 2006 Feb 1;106(3):648-53
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  • [Title] Expression of the Bax inhibitor-1 gene in pulmonary adenocarcinoma.
  • METHODS: Surgically resected lung specimens were obtained from 32 patients with peripheral adenocarcinomas, and BI-1 gene expression was examined and compared with expression of the p53, bcl-2 and Bax genes.
  • RESULTS: Fourteen of 32 tumors (43.8%) were positive for BI-1 gene expression by in situ hybridization.
  • Patients who had BI-1-positive adenocarcinoma showed a relatively favorable prognosis compared with patients who had BI-1-negative adenocarcinoma.
  • CONCLUSIONS: BI-1 gene expression was restricted to tumor cells with lepidic growth and was a prognostic factor for peripheral-type adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Apoptosis / genetics. Lung Neoplasms / genetics. Proteins / analysis

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  • [Copyright] Copyright (c) 2005 American Cancer Society.
  • (PMID = 16353209.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Membrane Proteins; 0 / Proteins; 0 / TMBIM6 protein, human
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82. 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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83. Maekawa S, Hishima T, Yamada Y, Ichikawa H, Natsui S, Shinohara M: [A case of primary urethral adenocarcinoma accompanied by vaginal wall infiltration in which the CA19-9 level was very high]. Hinyokika Kiyo; 2009 Aug;55(8):513-6
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  • [Title] [A case of primary urethral adenocarcinoma accompanied by vaginal wall infiltration in which the CA19-9 level was very high].
  • Computed tomography confirmed a urethral tumor, and transurethral biopsy confirmed adenocarcinoma.
  • However, the majority of the tumor was located in the bladder and urethra, a duct with intestinal metaplasia was present around the urethra, and carcinoma in situ was seen in the urethral mucosa.
  • Based on the above findings, the patient was diagnosed as having primary urethral adenocarcinoma.
  • Six months after surgery, the patient developed bone metastasis, followed by peritoneal and pleural dissemination, as well as multiple lung metastases.
  • [MeSH-major] Adenocarcinoma / pathology. Biomarkers, Tumor / blood. CA-19-9 Antigen / blood. Urethral Neoplasms / pathology. Vagina / pathology

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  • (PMID = 19764540.001).
  • [ISSN] 0018-1994
  • [Journal-full-title] Hinyokika kiyo. Acta urologica Japonica
  • [ISO-abbreviation] Hinyokika Kiyo
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CA-19-9 Antigen
  • [Number-of-references] 11
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84. Cutz JC, Guan J, Bayani J, Yoshimoto M, Xue H, Sutcliffe M, English J, Flint J, LeRiche J, Yee J, Squire JA, Gout PW, Lam S, Wang YZ: Establishment in severe combined immunodeficiency mice of subrenal capsule xenografts and transplantable tumor lines from a variety of primary human lung cancers: potential models for studying tumor progression-related changes. Clin Cancer Res; 2006 Jul 1;12(13):4043-54
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  • [Title] Establishment in severe combined immunodeficiency mice of subrenal capsule xenografts and transplantable tumor lines from a variety of primary human lung cancers: potential models for studying tumor progression-related changes.
  • PURPOSE: Lung cancer is a biologically diverse disease and relevant models reflecting its diversity would facilitate the improvement of existing therapies.
  • With a view to establishing such models, we developed and evaluated xenografts of a variety of human lung cancers.
  • EXPERIMENTAL DESIGN: Using nonobese diabetic/severe combined immunodeficiency mice, subrenal capsule xenografts were generated from primary lung cancer tissue, including moderately and poorly differentiated squamous cell carcinoma, adenocarcinoma, adenosquamous carcinoma, small cell carcinoma, large cell undifferentiated carcinoma, and carcinosarcoma.
  • Immunohistochemistry and fluorescence in situ hybridization confirmed the human origin of the tumor cells and development in xenografts of murine supportive stroma.
  • Four transplantable lines were developed from rapidly growing tumors (>5 generations), i.e., a small cell lung carcinoma, large cell undifferentiated carcinoma, pulmonary carcinosarcoma, and squamous cell carcinoma.
  • Analyses including spectral karyotyping, comparative genomic hybridization, and fluorescence in situ hybridization, revealed that the xenografts were genetically similar to the original tumors, showing chromosomal abnormalities consistent with karyotypic changes reported for lung cancer.
  • [MeSH-major] Cell Line, Tumor. Disease Models, Animal. Lung Neoplasms / pathology. Subrenal Capsule Assay


85. Yuan J, Ma J, Zheng H, Shi T, Sun W, Zhang Q, Lin D, Zhang K, He J, Mao Y, Gao X, Gao P, Han N, Fu G, Xiao T, Gao Y, Ma D, Cheng S: Overexpression of OLC1, cigarette smoke, and human lung tumorigenesis. J Natl Cancer Inst; 2008 Nov 19;100(22):1592-605
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  • [Title] Overexpression of OLC1, cigarette smoke, and human lung tumorigenesis.
  • BACKGROUND: Exposure to cigarette smoke is a major risk factor for lung cancer, but how it induces cancer is unclear.
  • The overexpressed in lung cancer 1 (OLC1) gene is one of 50 candidate lung cancer genes identified by suppression subtractive hybridization as having higher expression in squamous cell carcinoma (SCC) than normal lung epithelia.
  • METHODS: We used immunohistochemistry (IHC) to measure OLC1 protein levels in primary lung cancer samples from 559 patients and used fluorescence in situ hybridization to measure OLC1 copy number in primary SCC samples from 23 patients.
  • We assayed OLC1 protein levels by immunoblotting in H1299 human lung cancer cells, immortalized human bronchial epithelial cells, and primary cultured normal human bronchial epithelial cells that were treated with cigarette smoke condensate.
  • We assayed tumor formation in athymic mice using NIH3T3 mouse fibroblast cells transfected with OLC1 (eight mice) and analyzed apoptosis and colony formation of H1299 and H520 lung cancer cells transfected with scrambled (negative) or OLC1 small interfering RNAs (siRNAs) (s1).
  • RESULTS: OLC1 protein was overexpressed in 387 of 464 (83.4%) of primary lung cancers, as detected by IHC, and OLC1 was amplified in 14 of 23 (60%) of SCC samples.
  • CONCLUSIONS: OLC1 is a candidate oncogene in lung cancer whose expression may be regulated by exposure to cigarette smoke.
  • [MeSH-major] Adenocarcinoma / etiology. Carcinoma, Small Cell / etiology. Carcinoma, Squamous Cell / etiology. Lung Neoplasms / etiology. Oncogene Proteins / metabolism. Oncogenes. Tobacco Smoke Pollution / adverse effects
  • [MeSH-minor] Animals. Cell Proliferation. Cloning, Molecular. Flow Cytometry. Gene Expression Regulation, Neoplastic. Humans. Immunoblotting. In Situ Hybridization, Fluorescence. Mice. Mice, Nude. Molecular Sequence Data. NIH 3T3 Cells. Neoplastic Stem Cells. Plasmids. RNA Interference. Reverse Transcriptase Polymerase Chain Reaction. Risk Factors. Up-Regulation

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  • (PMID = 19001599.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AK057902
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / OLC1 protein, human; 0 / Oncogene Proteins; 0 / Tobacco Smoke Pollution
  • [Other-IDs] NLM/ PMC3299210
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86. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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87. Conde E, Angulo B, Tang M, Morente M, Torres-Lanzas J, Lopez-Encuentra A, Lopez-Rios F, Sanchez-Cespedes M: Molecular context of the EGFR mutations: evidence for the activation of mTOR/S6K signaling. Clin Cancer Res; 2006 Feb 1;12(3 Pt 1):710-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE: Activating somatic mutations in the epidermal growth factor receptor (EGFR) gene are present in a small subset of lung adenocarcinomas.
  • To further determine the genetic and molecular characteristics of tumors carrying EGFR gene mutations, we investigated the EGFR gene status in lung adenocarcinomas and evaluated its association with specific characteristics of the patients and tumors, such as mutations at KRAS and p53, EGFR and ErbB2 gene amplification, levels of EGFR and HER2 proteins, and levels of downstream effectors of EGFR, such as phospho-extracellular signal-regulated kinase and phospho-S6 proteins.
  • EXPERIMENTAL DESIGN: The mutational status of EGFR was determined by direct sequencing in 86 primary lung adenocarcinomas and 12 lung cancer cell lines, and was correlated with a number of variables relating to the tumor and patient.
  • A tissue microarray containing 37 lung tumors was constructed to determine, by fluorescence in situ hybridization analysis, the number of copies of EGFR and ErbB2 genes and, by immunohistochemistry, the levels of EGFR, HER2, phospho-ERK, and phospho-S6 proteins.
  • CONCLUSIONS: Our data agree with the accumulation of EGFR mutations in a subset of patients with lung cancer.
  • [MeSH-major] Adenocarcinoma / genetics. Lung Neoplasms / genetics. Protein Kinases / metabolism. Receptor, Epidermal Growth Factor / genetics. Ribosomal Protein S6 Kinases / metabolism. Signal Transduction


88. Liehr T, Mrasek K, Starke H, Claussen U, Schreiber G: Unusual small supernumerary marker chromosome (sSMC) 9 in a Klinefelter patient. Cytogenet Genome Res; 2005;111(2):179-81
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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 / surgery. Adult. Chromosome Mapping. Gene Duplication. Genetic Markers. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Lung Neoplasms / surgery. Male. Oligospermia / genetics

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  • (PMID = 16103662.001).
  • [ISSN] 1424-859X
  • [Journal-full-title] Cytogenetic and genome research
  • [ISO-abbreviation] Cytogenet. Genome Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Genetic Markers
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89. Yeh IT, Lenci RE, Qin Y, Buddavarapu K, Ligon AH, Leteurtre E, Do Cao C, Cardot-Bauters C, Pigny P, Dahia PL: A germline mutation of the KIF1B beta gene on 1p36 in a family with neural and nonneural tumors. Hum Genet; 2008 Oct;124(3):279-85
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  • Genetic studies including sequencing, copy number analysis and fluorescence in situ-hybridization (FISH) showed retention of both KIF1B beta alleles in all neural crest-derived tumors in this family, consistent with haploinsufficiency or methylation of the wild-type allele.
  • In contrast, the lung adenocarcinoma from one mutation carrier had somatic loss of the wild-type allele in agreement with a classical two-hit inactivation.
  • [MeSH-major] Adenocarcinoma / genetics. Chromosomes, Human, Pair 1. Germ-Line Mutation. Kinesin / genetics. Lung Neoplasms / genetics. Nervous System Neoplasms / metabolism. Neurons / metabolism. Pheochromocytoma / genetics

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  • (PMID = 18726616.001).
  • [ISSN] 1432-1203
  • [Journal-full-title] Human genetics
  • [ISO-abbreviation] Hum. Genet.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA541
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / KIF1B protein, human; EC 3.6.4.4 / Kinesin
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90. 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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91. Liao WT, Lin P, Cheng TS, Yu HS, Chang LW: Arsenic promotes centrosome abnormalities and cell colony formation in p53 compromised human lung cells. Toxicol Appl Pharmacol; 2007 Dec 1;225(2):162-70
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  • [Title] Arsenic promotes centrosome abnormalities and cell colony formation in p53 compromised human lung cells.
  • Epidemiological evidence indicated that residents, especially cigarette smokers, in arseniasis areas had significantly higher lung cancer risk than those living in non-arseniasis areas.
  • Thus, an interaction between arsenic and cigarette smoking in lung carcinogenesis was suspected. p53 dysfunction or mutation in lung epithelial cells was frequently observed in cigarette smokers.
  • Our present study was to explore the differential effects by arsenic on H1355 cells (human lung adenocarcinoma cell line with mutation in p53), BEAS-2B (immortalized lung epithelial cell with functional p53) and pifithrin-alpha-treated BEAS-2B cells (p53-inhibited cells).
  • [MeSH-major] Arsenites / toxicity. Centrosome / drug effects. Enzyme Inhibitors / toxicity. Lung / drug effects. Sodium Compounds / toxicity. Tumor Suppressor Protein p53 / physiology
  • [MeSH-minor] Adenocarcinoma / metabolism. Apoptosis / drug effects. Cell Cycle Proteins / drug effects. Cell Cycle Proteins / genetics. Cell Line. Cell Line, Tumor. Cell Survival / drug effects. Chromosome Aberrations / drug effects. Chromosome Segregation / drug effects. Cyclin-Dependent Kinase Inhibitor p21 / drug effects. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Dose-Response Relationship, Drug. Epithelial Cells / drug effects. Epithelial Cells / metabolism. Gene Expression Regulation / drug effects. Humans. In Situ Nick-End Labeling. Mutation. Nuclear Proteins / drug effects. Nuclear Proteins / genetics