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1. Hansen LV, Skov BG, Ploug M, Pappot H: Tumour cell expression of C4.4A, a structural homologue of the urokinase receptor, correlates with poor prognosis in non-small cell lung cancer. Lung Cancer; 2007 Nov;58(2):260-6
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  • [Title] Tumour cell expression of C4.4A, a structural homologue of the urokinase receptor, correlates with poor prognosis in non-small cell lung cancer.
  • PURPOSE: C4.4A expression has been implicated in human cancer progression.
  • In the present study, we therefore explored the possible association between C4.4A expression and prognosis in patients with non-small cell lung cancer (NSCLC).
  • A remarkably strong correlation was noted between high expression of C4.4A in pulmonary adenocarcinoma and survival (p < 0.0001).
  • Although histological type is not a predictor of outcome in NSCLC, high C4.4A expression in adenocarcinoma is nevertheless a very strong predictor of poor disease outcome (risk ratio, 1.62; 95% confidence interval, 1.24-2.09; p = 0.001).
  • CONCLUSIONS: High tumour cell C4.4A expression is associated with shorter survival for NSCLC patients.
  • Patients with pulmonary adenocarcinoma have a particularly poor prognosis if this histological type is combined with high tumour cell C4.4A expression.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / diagnosis. Carcinoma, Non-Small-Cell Lung / metabolism. Cell Adhesion Molecules / metabolism. Lung Neoplasms / diagnosis. Lung Neoplasms / metabolism. Receptors, Cell Surface / chemistry. Structural Homology, Protein

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  • (PMID = 17706320.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / GPI-Linked Proteins; 0 / LYPD3 protein, human; 0 / PLAUR protein, human; 0 / Receptors, Cell Surface; 0 / Receptors, Urokinase Plasminogen Activator
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2. Director's Challenge Consortium for the Molecular Classification of Lung Adenocarcinoma, Shedden K, Taylor JM, Enkemann SA, Tsao MS, Yeatman TJ, Gerald WL, Eschrich S, Jurisica I, Giordano TJ, Misek DE, Chang AC, Zhu CQ, Strumpf D, Hanash S, Shepherd FA, Ding K, Seymour L, Naoki K, Pennell N, Weir B, Verhaak R, Ladd-Acosta C, Golub T, Gruidl M, Sharma A, Szoke J, Zakowski M, Rusch V, Kris M, Viale A, Motoi N, Travis W, Conley B, Seshan VE, Meyerson M, Kuick R, Dobbin KK, Lively T, Jacobson JW, Beer DG: Gene expression-based survival prediction in lung adenocarcinoma: a multi-site, blinded validation study. Nat Med; 2008 Aug;14(8):822-7
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  • [Title] Gene expression-based survival prediction in lung adenocarcinoma: a multi-site, blinded validation study.
  • Although prognostic gene expression signatures for survival in early-stage lung cancer have been proposed, for clinical application, it is critical to establish their performance across different subject populations and in different laboratories.
  • Here we report a large, training-testing, multi-site, blinded validation study to characterize the performance of several prognostic models based on gene expression for 442 lung adenocarcinomas.
  • The hypotheses proposed examined whether microarray measurements of gene expression either alone or combined with basic clinical covariates (stage, age, sex) could be used to predict overall survival in lung cancer subjects.
  • Most methods performed better with clinical data, supporting the combined use of clinical and molecular information when building prognostic models for early-stage lung cancer.
  • This study also provides the largest available set of microarray data with extensive pathological and clinical annotation for lung adenocarcinomas.

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  • (PMID = 18641660.001).
  • [ISSN] 1546-170X
  • [Journal-full-title] Nature medicine
  • [ISO-abbreviation] Nat. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA084995; United States / NCI NIH HHS / CA / R01 CA098522; United States / NCI NIH HHS / CA / U01 CA084999; United States / NCI NIH HHS / CA / CA084953-050003; United States / NCI NIH HHS / CA / CA84999; United States / PHS HHS / / 263-MQ-319746; United States / NCI NIH HHS / CA / CA85052; United States / NCI NIH HHS / CA / P30 CA046592; United States / NCI NIH HHS / CA / U01 CA085052; United States / NIDDK NIH HHS / DK / R01 DK046952-14; United States / NCI NIH HHS / CA / CA84953; United States / NCI NIH HHS / CA / CA085052-05; United States / PHS HHS / / 263-MQ-319735; United States / NCI NIH HHS / CA / CA84995; United States / NCI NIH HHS / CA / U01 CA085052-05; United States / NCI NIH HHS / CA / CA084995-05; United States / NCI NIH HHS / CA / U01 CA084999-05; United States / NCI NIH HHS / CA / CA46592; United States / NCI NIH HHS / CA / CA098522-05; United States / NCI NIH HHS / CA / U19 CA084953-050003; United States / PHS HHS / / 263-MQ-319740; United States / NCI NIH HHS / CA / CA084999-05; United States / NCI NIH HHS / CA / U01 CA084995-05; United States / NCI NIH HHS / CA / R01 CA098522-05; United States / NCI NIH HHS / CA / U19 CA084953; United States / NCI NIH HHS / CA / R01 CA154365; United States / PHS HHS / / 263-MQ-510430; United States / NIDDK NIH HHS / DK / R01 DK046952
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS96850; NLM/ PMC2667337
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3. Xu J, Yang Y, Ott J: Survival analysis of microarray expression data by transformation models. Comput Biol Chem; 2005 Apr;29(2):91-4
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  • Gene-expression profiles predict survival of patients with lung adenocarcinoma. Nat. Med.
  • [MeSH-minor] Adenocarcinoma / metabolism. Humans. Lung Neoplasms / metabolism. Proportional Hazards Models

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  • (PMID = 15833436.001).
  • [ISSN] 1476-9271
  • [Journal-full-title] Computational biology and chemistry
  • [ISO-abbreviation] Comput Biol Chem
  • [Language] eng
  • [Grant] United States / NHGRI NIH HHS / HG / HG00008
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
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4. Xu H, Wang G, Ma L, Qi F, Liu Y, Yu J, Dai S, Wang E: [Expression of STK15 and its significance in squamous cell carcinoma and adenocarcinoma of the lung]. Zhongguo Fei Ai Za Zhi; 2006 Jun 20;9(3):259-62
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  • [Title] [Expression of STK15 and its significance in squamous cell carcinoma and adenocarcinoma of the lung].
  • The overexpression of STK15 is significantly associated with carcinogenesis in many tumors, however, its expression and significance in human lung cancer are still unclear.
  • The aim of this study is to investigate the expression of STK15 in squamous cell carcinoma and adenocarcinoma of the lung and to analyze the correlation between STK15 expression and clinicopathological factors.
  • METHODS: The pattern of STK15 protein expression was detected in 44 squamous cell carcinomas, 36 adenocarcinomas and 20 paracancerous lung tissue samples by immunohistochemistry method using anti-STK15 antibody.
  • The relative quantity of STK15 protein expression was detected by Western blot, and STK15 mRNA expression was detected by RT-PCR in 40 fresh lung cancer samples and corresponding paracancerous lung tissues.
  • RESULTS: Positive expression rate of STK15 protein was 68.75% (55/80) in lung cancer tissues and 0% in paracancerous controls (P < 0.001).
  • STK15 expression was significantly related to differentiation grade of lung cancer (P=0.011), but not to histological classification, TNM stages or lymphatic metastasis (P > 0.05).
  • The relative expression levels of STK15 protein (P < 0.001 ) and STK15 mRNA (P < 0.001) in lung cancer tissues were both significantly higher than those of corresponding paracancerous lung tissues.
  • CONCLUSIONS: The expression of STK15 protein and STK15 mRNA is significantly higher in lung cancer tissues than that in paracancerous lung tissues.
  • The expression of STK15 correlates with differentiation of lung cancer.

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  • (PMID = 21172157.001).
  • [ISSN] 1009-3419
  • [Journal-full-title] Zhongguo fei ai za zhi = Chinese journal of lung cancer
  • [ISO-abbreviation] Zhongguo Fei Ai Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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5. Takeo M, Yamamoto M: [Synchronous double carcinoma of the left lung and esophagus; report of a case]. Kyobu Geka; 2008 Aug;61(9):808-11
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  • [Title] [Synchronous double carcinoma of the left lung and esophagus; report of a case].
  • Further examination revealed left lung tumor that was suspected of lung carcinoma.
  • On 41st postoperative day, after open biopsy for the left lung tumor, left upper lobectomy was performed.
  • Pathological diagnosis was moderately differentiated squamous cell carcinoma of the esophagus and well differentiated adenocarcinoma of the lung.
  • Synchronous double carcinoma of the lung and the esophagus is rare.
  • [MeSH-major] Adenocarcinoma / pathology. Carcinoma, Squamous Cell / pathology. Esophageal Neoplasms / pathology. Lung Neoplasms / pathology. Neoplasms, Multiple Primary / pathology

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  • (PMID = 18697465.001).
  • [ISSN] 0021-5252
  • [Journal-full-title] Kyobu geka. The Japanese journal of thoracic surgery
  • [ISO-abbreviation] Kyobu Geka
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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6. Takigawa N, Takeuchi M, Shibayama T, Yoshida I, Kawata N, Tada A, Ueoka H, Takahashi K: Successful treatment of a patient with synchronous advanced non-small cell lung cancer and acute myeloid leukemia by a combination of gefitinib, low-dose cytarabine and aclarubicin. Anticancer Res; 2005 May-Jun;25(3c):2579-82
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  • [Title] Successful treatment of a patient with synchronous advanced non-small cell lung cancer and acute myeloid leukemia by a combination of gefitinib, low-dose cytarabine and aclarubicin.
  • There are few reports describing simultaneous occurrence of acute leukemia and lung cancer.
  • We describe here an 83-year-old woman who simultaneously developed advanced adenocarcinoma of the lung and acute myeloid leukemia.
  • This combination could be safely administered in the elderly patient with poor performance status and was effective for both lung cancer and acute myeloid leukemia.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Frail Elderly. Leukemia, Myeloid / drug therapy. Lung Neoplasms / drug therapy. Neoplasms, Multiple Primary / drug therapy


7. Wang Z, Dai T, Zhan F, Zeng X, Yang Y: [The role of the K+ channel in the inhibition of the human lung adenocarcinoma cell proliferation by rmhTNF]. Zhongguo Fei Ai Za Zhi; 2006 Oct 20;9(5):399-404
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  • [Title] [The role of the K+ channel in the inhibition of the human lung adenocarcinoma cell proliferation by rmhTNF].
  • The aim of this study is to investigate the electrophysiological properties of human lung adenocarcinoma cell line A-549 and the role of K+ channel in inhibition of cell proliferation by the recombinant mutant human tumor necrosis factor (rmhTNF).
  • METHODS: Ionic currents were recorded using the whole-cell patch clamp recording technique.
  • The cell cycle and apoptosis rates of the carcinoma cells were measured by flow cytometric analysis (FCM).
  • RESULTS: Whole-cell patch clamp recording revealed a voltage-gated K+ current in A-549 cells, which could be blocked by the K+ channel blocker, TEA and CsCl.
  • The rmhTNF inhibited the cell cycle shifting from G1 phase to S phase and promoted apoptosis as determined by FCM analysis.
  • CONCLUSIONS: rmhTNF exerts its cytotoxic effects on A-549 cells through inhibiting cell cycle shifting and inducing apoptosis.
  • The K+ channels on the A-549 cell membrane can be blocked by rmhTNF partly, and the effect of inhibiting proliferation and activating apoptosis on A-549 cells is a result of depression of the K+ channel.

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  • (PMID = 21176458.001).
  • [ISSN] 1009-3419
  • [Journal-full-title] Zhongguo fei ai za zhi = Chinese journal of lung cancer
  • [ISO-abbreviation] Zhongguo Fei Ai Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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8. Tseng RC, Lee CC, Hsu HS, Tzao C, Wang YC: Distinct HIC1-SIRT1-p53 loop deregulation in lung squamous carcinoma and adenocarcinoma patients. Neoplasia; 2009 Aug;11(8):763-70
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  • [Title] Distinct HIC1-SIRT1-p53 loop deregulation in lung squamous carcinoma and adenocarcinoma patients.
  • A HIC1-SIRT1-p53 circular loop in which hypermethylation in cancer 1 (HIC1) represses the transcription of SIRT1 that deacetylates and inactivates p53 thus leading to HIC1 inactivation has been identified in cell and animal models.
  • However, the alteration and prognostic effects of HIC1-SIRT1-p53 circular loop have never been demonstrated in human cancer patients.
  • We examine the HIC1-SIRT1-p53 alterations in 118 lung cancer patients to define their etiological roles in tumorigenesis.
  • We found that patients with lung squamous cell carcinoma with low p53 acetylation and SIRT1 expression mostly showed low HIC1 expression, confirming deregulation of HIC1-SIRT1-p53 circular loop in the clinical model.
  • Interestingly, the expression of deleted in breast cancer 1 (DBC1), which blocks the interaction between SIRT1 deacetylase and p53, led to acetylated p53 in patients with lung adenocarcinoma.
  • Importantly, lung cancer patients with altered HIC1-SIRT1-p53 circular regulation showed poor prognosis.
  • Our data show the first valid clinical evidence of the deregulation of HIC1-SIRT1-p53 loop in lung tumorigenesis and prognosis.
  • Distinct status of p53 acetylation/deacetylation and HIC1 alteration mechanism result from different SIRT1-DBC1 control and epigenetic alteration in lung squamous cell carcinoma and lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Squamous Cell / genetics. Kruppel-Like Transcription Factors / genetics. Lung Neoplasms / genetics. Sirtuins / genetics. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 19649206.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / HIC1 protein, human; 0 / Kruppel-Like Transcription Factors; 0 / RNA, Messenger; 0 / Tumor Suppressor Protein p53; EC 3.5.1.- / SIRT1 protein, human; EC 3.5.1.- / Sirtuin 1; EC 3.5.1.- / Sirtuins
  • [Other-IDs] NLM/ PMC2713589
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9. Yamada C, Ozaki T, Ando K, Suenaga Y, Inoue K, Ito Y, Okoshi R, Kageyama H, Kimura H, Miyazaki M, Nakagawara A: RUNX3 modulates DNA damage-mediated phosphorylation of tumor suppressor p53 at Ser-15 and acts as a co-activator for p53. J Biol Chem; 2010 May 28;285(22):16693-703
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  • In response to ADR, RUNX3 was induced to accumulate in the cell nucleus and co-localized with p53.
  • From the clinical point of view, coordinated p53 mutation and decreased expression of RUNX3 in 105 human lung adenocarcinomas were significantly associated with the poor outcome of patients (p = 0.0203).
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / metabolism. Apoptosis. Cell Line, Tumor. Humans. Lung Neoplasms / diagnosis. Lung Neoplasms / metabolism. Models, Biological. Mutation. Phosphorylation. Prognosis. Subcellular Fractions / metabolism


10. Hong SH: Identification of CLP36 as a tumor antigen that induces an antibody response in pancreatic cancer. Cancer Res Treat; 2005 Feb;37(1):71-7
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  • [Title] Identification of CLP36 as a tumor antigen that induces an antibody response in pancreatic cancer.
  • PURPOSE: Pancreatic cancer has a poor prognosis, due in part to the lack of an effective approach for its early detection.
  • The identification of tumor antigens potentially provides a means for the early diagnosis.
  • The purpose of this study was to use a proteomic approach for the identification of proteins that commonly induce a humoral response in patients with pancreatic cancer.
  • MATERIALS AND METHODS: Proteins from the pancreatic adenocarcinoma cell line, BxPC3, were subjected to two-dimensional polyacrylamide gel electrophoresis, followed by Western blot analysis, where individual sera were tested for autoantibodies.
  • Sera from 36 patients with pancreatic adenocarcinoma, and 68 from control groups (14 from lung adenocarcinoma, 19 from colon adenocarcinoma and 35 from healthy subjects) were analyzed.
  • RESULTS: The autoantibody was detected against a protein, identified by mass spectrometry as CLP36, in 14 of the 36 sera (38.9%) from patients with a pancreatic adenocarcinoma, and 3 of the 68 controls (4.4%).
  • Immunohistochemical analysis of CLP36 in a tissue array demonstrated diffuse and consistent immunoreactivity in the pancreatic adenocarcinomas.
  • The levels of CLP36 mRNA were highest in the pancreatic cancer cell lines of the different cells analyzed.
  • CONCLUSION: CLP36 was identified as a tumor autoantigen inducing a humoral immune response in pancreatic adenocarcinomas.

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  • (PMID = 19956513.001).
  • [ISSN] 2005-9256
  • [Journal-full-title] Cancer research and treatment : official journal of Korean Cancer Association
  • [ISO-abbreviation] Cancer Res Treat
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2785414
  • [Keywords] NOTNLM ; Autoantigens / Pancreatic neoplasms / Proteomics / Two-dimensional gel electrophoresis
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11. Zhu NL, Li C, Huang HH, Sebald M, Londhe VA, Heisterkamp N, Warburton D, Bellusci S, Minoo P: TNF-alpha represses transcription of human Bone Morphogenetic Protein-4 in lung epithelial cells. Gene; 2007 May 15;393(1-2):70-80
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  • [Title] TNF-alpha represses transcription of human Bone Morphogenetic Protein-4 in lung epithelial cells.
  • TNF-alpha reduced Bmp4 mRNA in lung adenocarcinoma A549 cells and repressed transcriptional activity of the human Bmp4 promoter in a dose-dependent manner.
  • In vivo, TNF-alpha inhibited branching morphogenesis and LacZ gene expression in Bmp4-lacz transgenic lungs.
  • These findings provide a mechanistic paradigm for interactions between mediators of inflammation and morphogenesis with relevant implications for normal lung development and pathogenesis of disease.
  • [MeSH-major] Bone Morphogenetic Proteins / genetics. Epithelial Cells / drug effects. Epithelial Cells / metabolism. Lung / cytology. Lung / metabolism. Transcription, Genetic / drug effects. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Base Pairing / genetics. Base Sequence. Binding Sites. Bone Morphogenetic Protein 4. Cell Line, Tumor. Enhancer Elements, Genetic / genetics. Gene Expression Regulation, Neoplastic / drug effects. Humans. Mice. Molecular Sequence Data. NF-kappa B / metabolism. Promoter Regions, Genetic / genetics. Protein Binding / drug effects. RNA, Messenger / genetics. RNA, Messenger / metabolism. Sequence Deletion. Transcription Factor RelA / metabolism

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  • (PMID = 17350185.001).
  • [ISSN] 0378-1119
  • [Journal-full-title] Gene
  • [ISO-abbreviation] Gene
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / P01 HL060231; United States / NHLBI NIH HHS / HL / R01 HL056590; United States / NHLBI NIH HHS / HL / R01 HL107307
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / BMP4 protein, human; 0 / Bmp4 protein, mouse; 0 / Bone Morphogenetic Protein 4; 0 / Bone Morphogenetic Proteins; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / Transcription Factor RelA; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ NIHMS22407; NLM/ PMC1945170
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12. Russo P, Catassi A, Cesario A, Servent D: Development of novel therapeutic strategies for lung cancer: targeting the cholinergic system. Curr Med Chem; 2006;13(29):3493-512
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  • [Title] Development of novel therapeutic strategies for lung cancer: targeting the cholinergic system.
  • One of the earliest descriptions of non-neuronal ACh synthesis was by Morris who reported that ACh was synthesized in the placenta [1]; furthermore, Falugi et al. showed the presence of AChE in human fibrosarcoma cells [2].
  • Afterward, the expression of ACh, AChE, and cholinergic receptors in non-neuronal cells was reported in several studies [3-16].
  • Indeed, recent data reported that SCLC expresses a cholinergic autocrine loop that can regulate cell growth.
  • Such work demonstrates that SCLC cells have a cholinergic phenotype and that ACh exerts as an autocrine growth factor in human lung tumours [16].
  • Moreover, it has been recently reported that nicotine in lung adenocarcinoma A549 cells, potently induces Bad phosphorylation at serine (S)112, S136 and S155 in a mechanism involving activation of MAPKs, ERK1/2, PI3K/AKT and PKA through the linking to alpha7-receptors [9].
  • We have recently reported that human malignant pleural mesothelioma expresses a cholinergic system, involved in cell growth regulation.
  • The involvement of the non-neuronal cholinergic system in lung cancer and mesothelioma appears reasonable and opens up new translational research strategies.
  • [MeSH-major] Lung Neoplasms / drug therapy. Receptors, Cholinergic / metabolism
  • [MeSH-minor] Acetylcholine / physiology. Apoptosis / drug effects. Cell Proliferation / drug effects. Cholinergic Antagonists / pharmacology. Humans. Mesothelioma / drug therapy. Mesothelioma / pathology. Snake Venoms / pharmacology


13. Gilad O, Nabet BY, Ragland RL, Schoppy DW, Smith KD, Durham AC, Brown EJ: Combining ATR suppression with oncogenic Ras synergistically increases genomic instability, causing synthetic lethality or tumorigenesis in a dosage-dependent manner. Cancer Res; 2010 Dec 1;70(23):9693-702
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  • In addition, consistent with a deficiency in long-term genome maintenance, hypomorphic ATR pathway reduction to 16% of normal levels was synthetic lethal with oncogenic Ras expression in cultured cells.
  • Notably, elevated genomic instability and synthetic lethality following suppression of ATR were not due to accelerated cycling rates in Ras-transformed cells, indicating that these synergistic effects were generated on a per-cell-cycle basis.
  • In contrast to the synthetic lethal effects of hypomorphic ATR suppression, subtle reduction of ATR expression (haploinsufficiency) in combination with endogenous levels of K-ras(G12D) expression elevated the incidence of lung adenocarcinoma, spindle cell sarcoma, and thymic lymphoma in p53 heterozygous mice.
  • These results highlight the importance of the ATR pathway both as a barrier to malignant progression and as a potential target for cancer treatment.

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  • (PMID = 21098704.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / R01 AG027376; United States / NCI NIH HHS / CA / R25 CA101871; United States / NIA NIH HHS / AG / R01 AG027376-04S1; United States / NIA NIH HHS / AG / R01 AG027376-04; United States / NIA NIH HHS / AG / AG027376-04; United States / NIA NIH HHS / AG / AG027376-04S1; United States / NCI NIH HHS / CA / R25CA101871; United States / NIA NIH HHS / AG / R01AG027376
  • [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, Hormonal; 0 / Cell Cycle Proteins; 0 / Tumor Suppressor Protein p53; 094ZI81Y45 / Tamoxifen; EC 2.7.- / Protein Kinases; EC 2.7.1.- / Atr protein, mouse; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Checkpoint kinase 1; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  • [Other-IDs] NLM/ NIHMS247139; NLM/ PMC3057927
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14. Galgano MT, Hampton GM, Frierson HF Jr: Comprehensive analysis of HE4 expression in normal and malignant human tissues. Mod Pathol; 2006 Jun;19(6):847-53
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  • HE4 gene expression was highest in normal human trachea and salivary gland, and to a lesser extent, lung, prostate, pituitary gland, thyroid, and kidney.
  • However, adenocarcinomas of the lung, and occasional breast, transitional cell and pancreatic carcinomas had moderate or high levels of HE4 expression.
  • In addition to consistent positivity in ovarian carcinoma, some pulmonary, endometrial, and breast adenocarcinomas, mesotheliomas, and less often, gastrointestinal, renal and transitional cell carcinomas were also positive.
  • Knowledge of the expression patterns of HE4 in our survey is useful for application in histopathologic diagnosis, and should be taken into consideration in future studies that examine the role of HE4 as a serological tumor biomarker or as a target for gene-based therapy.

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  • (PMID = 16607372.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DEFB126 protein, human; 0 / Epididymal Secretory Proteins; 0 / beta-Defensins
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15. Huang N, Lu H, Chang L, Zhang H, Zhang H, Li G: [Resveratrol inhibits EGF-induced invasion of human lung adenocarcinoma A549 cells]. Zhongguo Fei Ai Za Zhi; 2010 Apr;13(4):287-91
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  • [Title] [Resveratrol inhibits EGF-induced invasion of human lung adenocarcinoma A549 cells].
  • BACKGROUND AND OBJECTIVE: Invasion and metastasis are the primary causes of death in patients with pulmonary carcinoma.
  • Then, the A549 cells were treated with EGF and non-cytotoxic concentration of Resveratrol.
  • [MeSH-major] Adenocarcinoma. Anticarcinogenic Agents / pharmacology. Epidermal Growth Factor / pharmacology. Lung Neoplasms. Stilbenes / pharmacology
  • [MeSH-minor] Blotting, Western. Cell Line, Tumor. Humans. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Signal Transduction / drug effects

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  • (PMID = 20677551.001).
  • [ISSN] 1009-3419
  • [Journal-full-title] Zhongguo fei ai za zhi = Chinese journal of lung cancer
  • [ISO-abbreviation] Zhongguo Fei Ai Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Stilbenes; 62229-50-9 / Epidermal Growth Factor; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; Q369O8926L / resveratrol
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16. Bhure UN, Lardinois D, Kalff V, Hany TF, Soltermann A, Seifert B, Steinert HC: Accuracy of CT parameters for assessment of tumour size and aggressiveness in lung adenocarcinoma with bronchoalveolar elements. Br J Radiol; 2010 Oct;83(994):841-9
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  • [Title] Accuracy of CT parameters for assessment of tumour size and aggressiveness in lung adenocarcinoma with bronchoalveolar elements.
  • Accurate determination of tumour size in lung adenocarcinoma with bronchoalveolar features (BAC) is important for the determination of TNM (tumour, nodes, metastasis) scores used in staging, prognosis and therapy response assessment.
  • However, tumour sizes derived using lung window (LW) CT or soft-tissue/mediastinal window (MW) CT often give different results.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma / radiography. Lung Neoplasms / pathology. Lung Neoplasms / radiography

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  • (PMID = 20846983.001).
  • [ISSN] 1748-880X
  • [Journal-full-title] The British journal of radiology
  • [ISO-abbreviation] Br J Radiol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC3473756
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17. Matsumoto S, Iwakawa R, Takahashi K, Kohno T, Nakanishi Y, Matsuno Y, Suzuki K, Nakamoto M, Shimizu E, Minna JD, Yokota J: Prevalence and specificity of LKB1 genetic alterations in lung cancers. Oncogene; 2007 Aug 30;26(40):5911-8
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  • [Title] Prevalence and specificity of LKB1 genetic alterations in lung cancers.
  • Germline LKB1 mutations cause Peutz-Jeghers syndrome, a hereditary disorder that predisposes to gastrointestinal hamartomatous polyposis and several types of malignant tumors.
  • Somatic LKB1 alterations are rare in sporadic cancers, however, a few reports showed the presence of somatic alterations in a considerable fraction of lung cancers.
  • To determine the prevalence and the specificity of LKB1 alterations in lung cancers, we examined a large number of lung cancer cell lines and lung adenocarcinoma (AdC) specimens for the alterations.
  • LKB1 genetic alterations were frequently detected in the cell lines (21/70, 30%), especially in non-small cell lung cancers (NSCLCs) (20/51, 39%), and were significantly more frequent in cell lines with KRAS mutations.
  • Point mutations were detected only in AdCs and large cell carcinomas, whereas homozygous deletions were detected in all histological types of lung cancer.
  • Among lung AdC specimens, LKB1 mutations were found in seven (8%) of 91 male smokers but in none of 64 females and/or nonsmokers, and were significantly more frequent in poorly differentiated tumors.
  • The difference in the frequency of LKB1 alterations between cell lines and tumor specimens was likely to be owing to masking of deletions by the contamination of noncancerous cells in the tumor specimens.
  • These results indicate that somatic LKB1 genetic alterations preferentially occur in a subset of poorly differentiated lung AdCs that appear to correlate with smoking males.

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  • (PMID = 17384680.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA070907; United States / NCI NIH HHS / CA / P50 CA 70907
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.1.- / STK11 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  • [Other-IDs] NLM/ NIHMS399396; NLM/ PMC3457639
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18. Kawakami T, Nabeshima K, Makimoto Y, Hamasaki M, Iwasaki A, Shirakusa T, Iwasaki H: Micropapillary pattern and grade of stromal invasion in pT1 adenocarcinoma of the lung: usefulness as prognostic factors. Mod Pathol; 2007 May;20(5):514-21
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  • [Title] Micropapillary pattern and grade of stromal invasion in pT1 adenocarcinoma of the lung: usefulness as prognostic factors.
  • Recently, the stromal invasion grading system was proposed for small adenocarcinomas of < or =2.0 cm.
  • In this study, we investigated whether stromal invasion grading system could be applied to and validated in pT1 adenocarcinomas as the TNM classification is the most universally used system.
  • The study included 120 cases of pT1 lung adenocarcinomas, of which 81 (68%) cases were stromal invasion grade 3.
  • Thus, the stromal invasion grading system is reproducible and correlates with prognosis even in pT1 lung adenocarcinomas.
  • [MeSH-major] Adenocarcinoma / pathology. Lung Neoplasms / pathology. Neoplasm Invasiveness / pathology. Neoplasm Staging / methods

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  • (PMID = 17334347.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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19. Panduri V, Liu G, Surapureddi S, Kondapalli J, Soberanes S, de Souza-Pinto NC, Bohr VA, Budinger GR, Schumacker PT, Weitzman SA, Kamp DW: Role of mitochondrial hOGG1 and aconitase in oxidant-induced lung epithelial cell apoptosis. Free Radic Biol Med; 2009 Sep 15;47(6):750-9
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  • [Title] Role of mitochondrial hOGG1 and aconitase in oxidant-induced lung epithelial cell apoptosis.
  • We report here that overexpression of mitochondria-targeted human alpha-hOgg1 (mt-hOgg1) in human lung adenocarcinoma cells with some alveolar epithelial cell characteristics (A549 cells) prevents oxidant-induced mitochondrial dysfunction and apoptosis by preserving mitochondrial aconitase.

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  • (PMID = 19524665.001).
  • [ISSN] 1873-4596
  • [Journal-full-title] Free radical biology & medicine
  • [ISO-abbreviation] Free Radic. Biol. Med.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL35440; United States / NIEHS NIH HHS / ES / R01 ES013995; United States / NHLBI NIH HHS / HL / K08 HL067835; United States / NIEHS NIH HHS / ES / R01 ES013995-03; United States / NHLBI NIH HHS / HL / R01 HL035440; United States / NHLBI NIH HHS / HL / HL67835-01
  • [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 / Mutant Proteins; EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / oxoguanine glycosylase 1, human; EC 3.4.22.- / Caspase 9; EC 4.2.1.3 / Aconitate Hydratase
  • [Other-IDs] NLM/ NIHMS130237; NLM/ PMC4331123
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20. Amos CI, Gorlov IP, Dong Q, Wu X, Zhang H, Lu EY, Scheet P, Greisinger AJ, Mills GB, Spitz MR: Nicotinic acetylcholine receptor region on chromosome 15q25 and lung cancer risk among African Americans: a case-control study. J Natl Cancer Inst; 2010 Aug 04;102(15):1199-205
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  • [Title] Nicotinic acetylcholine receptor region on chromosome 15q25 and lung cancer risk among African Americans: a case-control study.
  • Genome-wide association studies of white persons with lung cancer have identified a region of extensive linkage disequilibrium on chromosome 15q25.1 that appears to be associated with both risk for lung cancer and smoking dependence.
  • Because studying African American persons, who exhibit lower levels of linkage disequilibrium in this region, may identify additional loci that are associated with lung cancer, we genotyped 34 single-nucleotide polymorphisms (SNPs) in this region (including LOC123688, PSMA4, CHRNA5, CHRNA3, and CHRNB4 genes) in 467 African American patients with lung cancer and 388 frequency-matched African American control subjects.
  • Associations of SNPs in LOC123688 (rs10519203; odds ratio [OR] = 1.60, 95% confidence interval [CI] = 1.25 to 2.05, P = .00016), CHRNA5 (rs2036527; OR = 1.67, 95% CI = 1.26 to 2.21, P = .00031), and CHRNA3 (rs1051730; OR = 1.81, 95% CI = 1.26 to 2.59, P = .00137) genes with lung cancer risk reached Bonferroni-corrected levels of statistical significance (all statistical tests were two-sided).
  • The functional A variant of rs1696698 in CHRNA5 had the strongest association with lung cancer (OR = 1.98, 95% CI = 1.25 to 3.11, P = .003).
  • These SNPs were primarily associated with increased risk for lung adenocarcinoma histology and were only weakly associated with smoking phenotypes.
  • Thus, among African American persons, multiple loci in the region of chromosome 15q25.1 appear to be strongly associated with lung cancer risk.
  • [MeSH-major] African Americans / statistics & numerical data. Chromosomes, Human, Pair 15. Lung Neoplasms / epidemiology. Lung Neoplasms / genetics. Polymorphism, Single Nucleotide. Receptors, Nicotinic / genetics
  • [MeSH-minor] Adenocarcinoma / epidemiology. Adenocarcinoma / genetics. Adult. Aged. Case-Control Studies. Female. Genetic Predisposition to Disease. Humans. Logistic Models. Male. Middle Aged. Nerve Tissue Proteins / genetics. Proteasome Endopeptidase Complex / genetics. Risk Factors. Smoking / adverse effects. Texas / epidemiology

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  • (PMID = 20554942.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01CA127219; United States / NCI NIH HHS / CA / P30CA016772; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / T32 CA096520; United States / NCI NIH HHS / CA / CA141716; United States / NCI NIH HHS / CA / R01 CA127219-04; United States / NCI NIH HHS / CA / R01 CA127219; United States / NCI NIH HHS / CA / P50CA70907; United States / NCI NIH HHS / CA / P50 CA098258; United States / NCI NIH HHS / CA / R01CA55769; United States / NCI NIH HHS / CA / CA111646; United States / NCI NIH HHS / CA / P50 CA070907; United States / NCI NIH HHS / CA / R01CA133996
  • [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 / CHRNA5 protein, human; 0 / CHRNB4 protein, human; 0 / Nerve Tissue Proteins; 0 / Receptors, Nicotinic; 0 / nicotinic receptor subunit alpha3; EC 3.4.25.1 / Proteasome Endopeptidase Complex
  • [Other-IDs] NLM/ PMC2914761
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21. Chen MW, Ni L, Zhao XG, Niu XY: [The inhibition of 20(R)-ginsenoside Rg3 on the expressions of angiogenesis factors proteins in human lung adenocarcinoma cell line A549 and HUVEC304 cell]. Zhongguo Zhong Yao Za Zhi; 2005 Mar;30(5):357-60
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  • [Title] [The inhibition of 20(R)-ginsenoside Rg3 on the expressions of angiogenesis factors proteins in human lung adenocarcinoma cell line A549 and HUVEC304 cell].
  • OBJECTIVE: To study the effect of 20( R)-ginsenoside Rg3 on the expressions of angiogenesis factors proteins (VEGF,bFGF, MMP-2) in human lung adenocarcinoma cell line A549 and HUVEC304 cell.
  • METHOD: The cell lines of A549 and HUVEC304 were cultured with 20(R)- Rg3.
  • RESULT: The positive rate of VEGF protein in A549 cell decreased significantly as compared with the control group ( P = 0.03).
  • The gray scales of VEGF, Flt, KDT proteins in both A549 cell lines and HUVEC 304 cell lines decreased ( P = 0.05).
  • Gray scale of MMP-2 also decreased in A549 cell lines.
  • The result of differential expressions of genes of A549 cell lines showed that 14 genes were down-regulated and 10 genes were up-regulated.
  • CONCLUSION: The Chinese materia medica of 20( R)-Rg3 can inhibit the expression of angiogenesis factors proteins via several target genes in both tumour cell and vascular endothelial cell.
  • [MeSH-major] Ginsenosides / pharmacology. Lung Neoplasms. Matrix Metalloproteinase 2 / metabolism. Vascular Endothelial Growth Factor A / metabolism
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Cell Line, Tumor. Endothelial Cells / metabolism. Gene Expression Profiling. Humans. Neovascularization, Pathologic. Oligonucleotide Array Sequence Analysis. Panax / chemistry. Umbilical Veins / cytology

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  • (PMID = 15806969.001).
  • [ISSN] 1001-5302
  • [Journal-full-title] Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica
  • [ISO-abbreviation] Zhongguo Zhong Yao Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Ginsenosides; 0 / Vascular Endothelial Growth Factor A; 14197-60-5 / ginsenoside Rg3; EC 3.4.24.24 / Matrix Metalloproteinase 2
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22. Kerr KM, Galler JS, Hagen JA, Laird PW, Laird-Offringa IA: The role of DNA methylation in the development and progression of lung adenocarcinoma. Dis Markers; 2007;23(1-2):5-30
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  • [Title] The role of DNA methylation in the development and progression of lung adenocarcinoma.
  • Lung cancer, caused by smoking in approximately 87% of cases, is the leading cause of cancer death in the United States and Western Europe.
  • Adenocarcinoma is now the most common type of lung cancer in men and women in the United States, and the histological subtype most frequently seen in never-smokers and former smokers.
  • The increasing frequency of adenocarcinoma, which occurs more peripherally in the lung, is thought to be at least partially related to modifications in cigarette manufacturing that have led to a change in the depth of smoke inhalation.
  • The rising incidence of lung adenocarcinoma and its lethal nature underline the importance of understanding the development and progression of this disease.
  • Alterations in DNA methylation are recognized as key epigenetic changes in cancer, contributing to chromosomal instability through global hypomethylation, and aberrant gene expression through alterations in the methylation levels at promoter CpG islands.
  • The identification of sequential changes in DNA methylation during progression and metastasis of lung adenocarcinoma, and the elucidation of their interplay with genetic changes, will broaden our molecular understanding of this disease, providing insights that may be applicable to the development of targeted drugs, as well as powerful markers for early detection and patient classification.

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  • (PMID = 17325423.001).
  • [ISSN] 0278-0240
  • [Journal-full-title] Disease markers
  • [ISO-abbreviation] Dis. Markers
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21 CA102247
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 250
  • [Other-IDs] NLM/ PMC3851711
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23. Masala S, Konda D, Massari F, Simonetti G: Sacroplasty and iliac osteoplasty under combined CT and fluoroscopic guidance. Spine (Phila Pa 1976); 2006 Aug 15;31(18):E667-9
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  • MATERIALS AND METHODS: A 61-year-old man with medically intractable pain from osteolytic lesions of the sacral ala and left iliac alum from pulmonary adenocarcinoma underwent osteoplasty.
  • [MeSH-minor] Adenocarcinoma / secondary. Bone Cements / therapeutic use. Fluoroscopy. Humans. Lung Neoplasms / pathology. Male. Middle Aged. Pain / etiology. Pain / surgery. Polymethyl Methacrylate / therapeutic use. Treatment Outcome

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  • (PMID = 16915083.001).
  • [ISSN] 1528-1159
  • [Journal-full-title] Spine
  • [ISO-abbreviation] Spine
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bone Cements; 9011-14-7 / Polymethyl Methacrylate
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24. Kaira K, Ishizuka T, Yanagitani N, Sunaga N, Tsuchiya T, Hisada T, Mori M: Forearm muscle metastasis as an initial clinical manifestation of lung cancer. South Med J; 2009 Jan;102(1):79-81
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  • [Title] Forearm muscle metastasis as an initial clinical manifestation of lung cancer.
  • Skeletal muscle metastasis from lung cancer is rare, and the optimal treatment strategy is unknown.
  • A biopsy of the swollen muscle disclosed the presence of pulmonary adenocarcinoma.
  • Skeletal muscle metastasis as a mode of presentation of primary lung cancer is an unusual phenomenon.
  • [MeSH-major] Adenocarcinoma / secondary. Forearm. Lung Neoplasms / pathology. Muscle Neoplasms / secondary

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  • (PMID = 19077783.001).
  • [ISSN] 1541-8243
  • [Journal-full-title] Southern medical journal
  • [ISO-abbreviation] South. Med. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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25. Yamada G, Tanaka Y, Otsuka M, Saikai T, Watanabe A, Satoh M, Takahashi H: Metastatic malignant melanoma mimicking primary lung adenocarcinoma. Intern Med; 2006;45(21):1255-6
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  • [Title] Metastatic malignant melanoma mimicking primary lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / diagnosis. Lung Neoplasms / diagnosis. Melanoma / diagnosis. Melanoma / secondary. Skin Neoplasms / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Humans. Male. Middle Aged

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  • (PMID = 17139129.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
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26. Iwakiri S, Sonobe M, Nagai S, Hirata T, Wada H, Miyahara R: Expression status of folate receptor alpha is significantly correlated with prognosis in non-small-cell lung cancers. Ann Surg Oncol; 2008 Mar;15(3):889-99
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  • [Title] Expression status of folate receptor alpha is significantly correlated with prognosis in non-small-cell lung cancers.
  • BACKGROUND: To evaluate the prognostic value of folate receptor alpha (FOLR1) and/or reduced folate carrier (RFC1) expression, which are well-characterized folate transporters, in completely resected non-small-cell lung cancer (NSCLC).
  • RESULTS: In adenocarcinoma, the FOLR1 gene expression was downregulated in smokers and male patients (P = 0.006 and P < 0.001, respectively).
  • In squamous cell carcinoma, FOLR1 expression values in patients with pN1-3 was significantly higher than those with pN0 (P = 0.037).
  • CONCLUSIONS: Higher levels of FOLR1 appear to be associated with better prognoses for patients with lung adenocarcinomas.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Carrier Proteins / genetics. Lung Neoplasms / genetics. Receptors, Cell Surface / genetics

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  • (PMID = 18181001.001).
  • [ISSN] 1534-4681
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / FOLR1 protein, human; 0 / Folate Receptor 1; 0 / Folate Receptors, GPI-Anchored; 0 / Receptors, Cell Surface
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27. Fan T, Li R, Todd NW, Qiu Q, Fang HB, Wang H, Shen J, Zhao RY, Caraway NP, Katz RL, Stass SA, Jiang F: Up-regulation of 14-3-3zeta in lung cancer and its implication as prognostic and therapeutic target. Cancer Res; 2007 Aug 15;67(16):7901-6
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  • [Title] Up-regulation of 14-3-3zeta in lung cancer and its implication as prognostic and therapeutic target.
  • A functional genomic approach integrating microarray and proteomic analyses done in our laboratory has identified 14-3-3zeta as a putative oncogene whose activation was common and driven by its genomic amplification in lung adenocarcinomas.
  • 14-3-3zeta is believed to function in cell signaling, cycle control, and apoptotic death.
  • Following our initial finding, here, we analyzed its expression in lung tumor tissues obtained from 205 patients with various histologic and stage non-small cell lung cancers (NSCLC) using immunohistochemistry and then explored the effects of specific suppression of the gene in vitro and in a xenograft model using small interfering RNA.
  • The increased 14-3-3zeta expression was positively correlated with a more advanced pathologic stage and grade of NSCLCs (P = 0.001 and P = 0.006, respectively) and was associated with overall and cancer-specific survival rates of the patients (P = 0.022 and P = 0.018, respectively).
  • Down-regulation of 14-3-3zeta in lung cancer cells led to a dose-dependent increased sensitivity to cisplatin-induced cell death, which was associated with the inhibition of cell proliferation and increased G2-M arrest and apoptosis.
  • The result was further confirmed in the animal model, which showed that the A549 lung cancer cells with reduced 14-3-3zeta grew significantly slower than the wild-type A549 cells after cisplatin treatment (P = 0.008).
  • [MeSH-major] 14-3-3 Proteins / biosynthesis. Carcinoma, Non-Small-Cell Lung / metabolism. Lung Neoplasms / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Cisplatin / pharmacology. Down-Regulation. Female. Humans. Immunohistochemistry. Male. Mice. Mice, Nude. Middle Aged. Prognosis. RNA, Small Interfering / genetics. Transfection. Up-Regulation

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  • (PMID = 17699796.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-113707
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 14-3-3 Proteins; 0 / RNA, Small Interfering; Q20Q21Q62J / Cisplatin
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28. Bolognesi C, Martini F, Tognon M, Filiberti R, Neri M, Perrone E, Landini E, Canessa PA, Ivaldi GP, Betta P, Mutti L, Puntoni R: A molecular epidemiology case control study on pleural malignant mesothelioma. Cancer Epidemiol Biomarkers Prev; 2005 Jul;14(7):1741-6
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  • A biomonitoring study was carried out to evaluate the micronuclei frequency in PBLs of patients with pleural malignant mesothelioma with respect to lung cancer, healthy, and risk controls as a marker of cancer susceptibility in correlation with the presence of SV40.
  • A significant increased micronuclei frequency was observed in patients with malignant mesothelioma in comparison with all the other groups, the mean micronuclei frequency was double in patients with malignant mesothelioma compared with healthy controls, risk controls, and patients with lung adenocarcinoma (median 11.4 binucleated cells with micronuclei/1,000 binucleated cells versus 6.2, 6.1, and 5.1, respectively).
  • Our data indicate that human T lymphocyte samples carry DNA sequences coding for SV40 large T antigen at low prevalence, both in cancer cases and controls.
  • Evidence of cytogenetic damage revealed as micronuclei frequency in mesothelioma cancer patients could be related to exogenous and endogenous cofactors besides asbestos exposure.
  • [MeSH-major] Asbestos / adverse effects. Lung Neoplasms / genetics. Mesothelioma / etiology. Molecular Epidemiology. Pleural Neoplasms / etiology. Smoking / adverse effects

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  • (PMID = 16030111.001).
  • [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] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 1332-21-4 / Asbestos
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29. Schwab R, Peták I, Pintér F, Szabó E, Kánya M, Tamási A, Várkondi E, Almási A, Szokolóczi O, Pápay J, Moldvay J, Kéri G, Kopper L: [Epidermal growth factor receptor (EGFR): therapeutic target in the treatment of lung adenocarcinoma]. Orv Hetil; 2005 Nov 13;146(46):2335-42
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  • [Title] [Epidermal growth factor receptor (EGFR): therapeutic target in the treatment of lung adenocarcinoma].
  • Revolution in biotechnology made possible to identify those gene errors, which via their encoded proteins (mostly kinase enzymes) are key players in tumor development, growth and progression, and could be considered as molecular targets in tumor diagnosis and therapy.
  • Activity of EGFR (epidermal growth factor receptor), an outstanding representative of the regulatory cell surface receptors, can be inhibited by drugs proved for clinical use.
  • In the past year many groups observed that those lung adenocarcinoma cells, which contain activating mutation in the tyrosine kinase domain of EGFR show remarkable sensitivity to anti-EGFR compounds.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Agents / pharmacology. Lung Neoplasms / drug therapy. Receptor, Epidermal Growth Factor / drug effects

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  • (PMID = 16370245.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Number-of-references] 27
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30. Sabisz M, Skladanowski A: Cancer stem cells and escape from drug-induced premature senescence in human lung tumor cells: implications for drug resistance and in vitro drug screening models. Cell Cycle; 2009 Oct 1;8(19):3208-17
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  • [Title] Cancer stem cells and escape from drug-induced premature senescence in human lung tumor cells: implications for drug resistance and in vitro drug screening models.
  • In this study, using an in vitro human tumor model, we show that non-small lung adenocarcinoma A549 cells after treatment with DNA damaging antitumor drugs become permanently growth-arrested as a result of so-called drug-induced premature senescence (pseudo-senescence).
  • However, a small fraction of drug-treated cells escapes pseudo-senescence that leads to re-growth of tumor cell population after drug treatment.
  • We show that this re-growth is associated with the presence of cancer stem cells (CSCs) in lung tumor cell population.
  • We also document that re-growth of CSCs can be greatly delayed if lung tumor cells are treated with drug/caffeine combination that leads to the inhibition of the ATM/ATR pathway and decreased phosphorylation of PKB/Akt at Ser473.
  • We show that in non-treated A549 cells caffeine by itself induces a reversible growth arrest that is associated with increased fraction of so-called side population cells, containing CSCs.
  • These results point to the existence of an unknown, caffeine-sensitive mechanism that controls the number of CSCs in lung tumor cell population.
  • Full characterization of this mechanism may lead to the development of innovative cancer therapies, which are based on small molecular weight inhibitors of CSC differentiation and self-renewal, which mimic caffeine action.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cell Aging / drug effects. Lung Neoplasms / metabolism. Neoplastic Stem Cells / drug effects. Razoxane / pharmacology
  • [MeSH-minor] 3-Phosphoinositide-Dependent Protein Kinases. Ataxia Telangiectasia Mutated Proteins. Caffeine / pharmacology. Cell Cycle Proteins / metabolism. Cell Line, Tumor. DNA Damage. DNA-Binding Proteins / metabolism. Drug Resistance, Neoplasm. Humans. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Tumor Suppressor Proteins / metabolism

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  • (PMID = 19738435.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Tumor Suppressor Proteins; 3G6A5W338E / Caffeine; 5AR83PR647 / Razoxane; EC 2.7.11.1 / 3-Phosphoinositide-Dependent Protein Kinases; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / ATR protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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31. Langley RR, Fan D, Guo L, Zhang C, Lin Q, Brantley EC, McCarty JH, Fidler IJ: Generation of an immortalized astrocyte cell line from H-2Kb-tsA58 mice to study the role of astrocytes in brain metastasis. Int J Oncol; 2009 Oct;35(4):665-72
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  • [Title] Generation of an immortalized astrocyte cell line from H-2Kb-tsA58 mice to study the role of astrocytes in brain metastasis.
  • Astrocytes play a critical role in maintaining cerebral homeostasis and their dysregulation is thought to contribute to the pathogenesis of several diseases, including brain cancer and metastasis.
  • Similar to the human disease, we found that lung and melanoma metastases in the mouse brain are accompanied by a reactive gliosis.
  • To begin to study the biology of astrocytes and examine how these cells might contribute to metastasis formation and progression in the brain, we generated a conditionally immortal astrocyte cell line from H-2Kb-tsA58 mice.
  • Astrocytes grown in culture expressed glial fibrillary acid protein (GFAP), glutamate receptor 1, and the N-methyl-D-aspartate (NMDA) receptor.
  • Astrocytes grown under permissive conditions (33 degrees C) expressed SV40 large T antigen and had a doubling time of 36 h, whereas expression of SV40 large T antigen was negligible in astrocytes grown at 37 degrees C for 72 h, which coincided with a plateau in cell division.
  • In a co-culture assay with human lung adenocarcinoma cells (PC14-PE6), astrocytes activated programs in the tumor cells that signal for cell division and survival.
  • Hence, the immortalized cell line will be useful for studying the role of astrocytes in disease processes in the brain, such as metastasis.

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  • (PMID = 19724901.001).
  • [ISSN] 1791-2423
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / NS059876-02; United States / NCI NIH HHS / CA / P30 CA016672; United States / NINDS NIH HHS / NS / R01 NS059876-03; United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / CA902701; United States / NINDS NIH HHS / NS / R01 NS059876-02S2; United States / NINDS NIH HHS / NS / R01 NS059876-01A2; United States / NINDS NIH HHS / NS / R01 NS059876; United States / NINDS NIH HHS / NS / R01 NS059876-02; United States / NINDS NIH HHS / NS / R01 NS059876-02S1; United States / NINDS NIH HHS / NS / NS059876-03; United States / NINDS NIH HHS / NS / R01 NS059876-04; United States / NINDS NIH HHS / NS / NS059876-01A2
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antigens, Polyomavirus Transforming; 0 / CD68 antigen, human; 0 / CD68 protein, mouse; 0 / Excitatory Amino Acid Transporter 1; 0 / Excitatory Amino Acid Transporter 2; 0 / Glial Fibrillary Acidic Protein; 0 / H-2 Antigens; 0 / H-2Kb protein, mouse; 0 / Receptors, N-Methyl-D-Aspartate; 0 / Slc1a2 protein, mouse; 0 / Slc1a3 protein, mouse
  • [Other-IDs] NLM/ NIHMS208798; NLM/ PMC2882684
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32. Hiramatsu M, Ninomiya H, Inamura K, Nomura K, Takeuchi K, Satoh Y, Okumura S, Nakagawa K, Yamori T, Matsuura M, Morikawa T, Ishikawa Y: Activation status of receptor tyrosine kinase downstream pathways in primary lung adenocarcinoma with reference of KRAS and EGFR mutations. Lung Cancer; 2010 Oct;70(1):94-102
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  • [Title] Activation status of receptor tyrosine kinase downstream pathways in primary lung adenocarcinoma with reference of KRAS and EGFR mutations.
  • The activation status of signal transduction pathways involving receptor tyrosine kinases and its association with EGFR or KRAS mutations have been widely studied using cancer cell lines, although it is still uncertain in primary tumors.
  • To study the activation status of main components of growth factor-induced pathways, phosphorylated Akt (pAkt), extracellular signal-regulated kinases 1 and 2 (pERK) and other downstream proteins were immunohistochemically examined using surgical samples of 193 primary lung adenocarcinomas.
  • In lung adenocarcinoma, tumors with TTF-1 expression have distinct characteristics regarding mutations, signal protein activation and clinical issues.
  • Moreover, this property was revealed to be important in outcome estimation at any tumor stage, whereas Akt activation is abnormally affected according to the tumor stage regardless of their cell origin.
  • [MeSH-major] Adenocarcinoma / enzymology. Adenocarcinoma / genetics. Genes, erbB-1. Genes, ras. Lung Neoplasms / enzymology. Lung Neoplasms / genetics. Receptor Protein-Tyrosine Kinases / metabolism

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  • [Copyright] Copyright 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20117855.001).
  • [ISSN] 1872-8332
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; 0 / TTF1 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.6.5.2 / ras Proteins
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33. Suda T, Mizoguchi Y, Hasegawa S, Negi K, Hattori Y: Frozen-section diagnosis of small adenocarcinoma of the lung for intentional limited surgery. Surg Today; 2006;36(8):676-9
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  • [Title] Frozen-section diagnosis of small adenocarcinoma of the lung for intentional limited surgery.
  • PURPOSE: To determine if Noguchi's classification can be evaluated accurately by frozen-section diagnosis before limited surgery.
  • METHODS: We performed frozen-section diagnosis in 31 of 343 patients who underwent excision of primary lung cancer at our hospital between 1993 and 2004.
  • All 31 patients had pulmonary adenocarcinoma, with a tumor diameter of < or = 20 mm.
  • RESULTS: The overall rate of correct frozen-section diagnosis during surgery was 67.7%; being 100%, 41.7%, and 70% in the < or = 10 mm, 11-15 mm, and 16-20 mm groups, respectively.
  • CONCLUSION: Limited surgery for primary lung cancer can be performed when the tumor diameter is < or = 10 mm, by confirming it as either type A or B according to Noguchi's classification, using frozen-section diagnosis.
  • Thus, examination of frozen sections might be an important diagnostic procedure before intentional limited surgery for lung cancer.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma / surgery. Frozen Sections. Lung Neoplasms / pathology. Lung Neoplasms / surgery

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  • (PMID = 16865509.001).
  • [ISSN] 0941-1291
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
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34. Kim JE, Lee DH, Choi Y, Yoon DH, Kim SW, Suh C, Lee JS: Epidermal growth factor receptor tyrosine kinase inhibitors as a first-line therapy for never-smokers with adenocarcinoma of the lung having asymptomatic synchronous brain metastasis. Lung Cancer; 2009 Sep;65(3):351-4
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  • [Title] Epidermal growth factor receptor tyrosine kinase inhibitors as a first-line therapy for never-smokers with adenocarcinoma of the lung having asymptomatic synchronous brain metastasis.
  • Good and rapid response to epidermal growth factor tyrosine kinase inhibitor (EGFR TKI) treatment makes this an attractive option for never-smokers with adenocarcinoma of the lung.
  • Between January 2005 and August 2007, 23 Korean never-smoking patients with adenocarcinoma of the lung who had synchronous asymptomatic brain metastasis were consecutively treated with EGFR TKI therapy, either gefitinib 250 mg or erlotinib 150 mg once daily, as first-line treatment after giving informed consent, until disease progression, unacceptable toxicity or patient's refusal.
  • In conclusion, EGFR TKI treatment showed promising antitumor activity against both intracranial and extracranial tumors in chemotherapy-naïve never-smokers with adenocarcinoma of the lung.
  • [MeSH-major] Adenocarcinoma / drug therapy. Brain Neoplasms / drug therapy. Lung Neoplasms / drug therapy

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  • (PMID = 19157632.001).
  • [ISSN] 1872-8332
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Quinazolines; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
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35. Nakamura Y, Niki T, Goto A, Morikawa T, Miyazawa K, Nakajima J, Fukayama M: c-Met activation in lung adenocarcinoma tissues: an immunohistochemical analysis. Cancer Sci; 2007 Jul;98(7):1006-13
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  • [Title] c-Met activation in lung adenocarcinoma tissues: an immunohistochemical analysis.
  • c-Met is often overexpressed in non-small cell lung cancer, but it remains unsolved whether its overexpression leads to its activation.
  • We used an antibody specific to phospho-c-Met (Tyr1235) to investigate c-Met activation immunohistochemically in 130 surgically resected lung adenocarcinomas.
  • The data suggest that in lung adenocarcinoma tissue, c-Met activation may take place either ligand-dependently or ligand-independently via c-Met overexpression. c-Met activation may play special roles in the papillary subtype and in well differentiated lung adenocarcinomas.
  • [MeSH-major] Adenocarcinoma / enzymology. Hepatocyte Growth Factor / metabolism. Lung Neoplasms / enzymology. Proto-Oncogene Proteins c-met / metabolism
  • [MeSH-minor] Aged. Cell Differentiation. Enzyme Activation. Female. Humans. Immunohistochemistry. Male. Middle Aged. Phosphoproteins / metabolism. Phosphorylation. Survival Analysis


36. Chijiwa T, Abe Y, Inoue Y, Matsumoto H, Kawai K, Matsuyama M, Miyazaki N, Inoue H, Mukai M, Ueyama Y, Nakamura M: Cancerous, but not stromal, thrombospondin-2 contributes prognosis in pulmonary adenocarcinoma. Oncol Rep; 2009 Aug;22(2):279-83
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  • [Title] Cancerous, but not stromal, thrombospondin-2 contributes prognosis in pulmonary adenocarcinoma.
  • Thrombospondin (TSP)-2 is known to be an endogenous negative regulator of vascularization in human cancer.
  • However, it is unclear whether TSP-2 expression is related to neovascularization and prognosis in non-small cell lung cancer.
  • In this study, we quantitatively examined the expression of TSP-2 mRNA by real-time reverse transcription-polymerase chain reaction (RT-PCR) in 102 pulmonary adenocarcinomas.
  • The expression of TSP-2 mRNA in carcinoma was significantly higher than normal lung tissues (p<0.0001, Kruskal-Wallis test).
  • The TSP-2 expression levels of the stage II/III pulmonary carcinomas were significantly increased as compared to those of stage I (p=0.0136, Kruskal-Wallis test).
  • We examined TSP-2 protein localizations in the pulmonary adenocarcinoma overexpressing TSP-2 mRNA.
  • The TSP-2 localizations were categorized in two patterns: cancerous TSP-2 expression pattern (TSP-2 expression in the cancerous cells) and non-cancerous TSP-2 expression pattern (TSP-2 expression in the stromal lymphoid cells).
  • Pulmonary adenocarcinoma patients with cancerous TSP-2 expression pattern showed good prognosis (p=0.0322; Fisher's probability exact test).
  • Pulmonary adenocarcinoma patients with non-cancerous TSP-2 expression pattern showed poor prognosis (p=0.0220; Fisher's probability exact test).
  • Non-cancerous TSP-2 expressions may reflect secondary reactions in the cancerous stroma.
  • The stromal TSP-2 expression is not enough to suppress growth of pulmonary adenocarcinoma, while the cancerous TSP-2 expression directly inhibits growth of the carcinoma.
  • [MeSH-major] Adenocarcinoma / mortality. Lung Neoplasms / mortality. Thrombospondins / physiology

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  • (PMID = 19578767.001).
  • [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 / RNA, Messenger; 0 / Thrombospondins; 0 / thrombospondin 2
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37. Guo F, Li Y, Liu Y, Wang J, Li Y, Li G: Inhibition of metastasis-associated lung adenocarcinoma transcript 1 in CaSki human cervical cancer cells suppresses cell proliferation and invasion. Acta Biochim Biophys Sin (Shanghai); 2010 Mar 15;42(3):224-9
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  • [Title] Inhibition of metastasis-associated lung adenocarcinoma transcript 1 in CaSki human cervical cancer cells suppresses cell proliferation and invasion.
  • Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is suggested to be a long (~7 kb) non-coding RNA.
  • To investigate the role of MALAT1 in human cervical cancer progression, we designed and used short hairpin RNA to inhibit MALAT1 expression in CaSki cells and validated its effect on cell proliferation and invasion.
  • Our data demonstrated that MALAT1 was involved in cervical cancer cell growth, cell cycle progression, and invasion through the regulation of gene expression, such as caspase-3, -8, Bax, Bcl-2, and BclxL, suggesting that MALAT1 could have important implications in cervical cancer biology.
  • Our findings illustrate the biological significance of MALAT1 in cervical cancer progression and provide novel evidence that MALAT1 may serve as a therapeutic target in the prevention of human cervical cancer.
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation. Female. Gene Silencing. Humans. Neoplasm Invasiveness


38. Yano Y, Satoh H, Fukumoto K, Kumadaki I, Ichikawa T, Yamada K, Hagiwara K, Yano T: Induction of cytotoxicity in human lung adenocarcinoma cells by 6-O-carboxypropyl-alpha-tocotrienol, a redox-silent derivative of alpha-tocotrienol. Int J Cancer; 2005 Jul 10;115(5):839-46
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  • [Title] Induction of cytotoxicity in human lung adenocarcinoma cells by 6-O-carboxypropyl-alpha-tocotrienol, a redox-silent derivative of alpha-tocotrienol.
  • We estimated the possibility of T3E as a new anticancer agent against lung adenocarcinoma showing poor prognosis based on the mutation of ras gene.
  • T3E showed cytotoxicity against A549 cells, a human lung adenocarcinoma cell line with a ras gene mutation, in a dose-dependent manner (0-40 microM), whereas T3 and a redox-silent analogue of alpha-tocopherol (T), 6-O-carboxypropyl-alpha-tocopherol (TE), showed much less cytotoxicity in cells within 40 microM.
  • T3E cytotoxicity was based on the accumulation of cells in the G1-phase of the cell-cycle and the subsequent induction of apoptosis.
  • Similar to this event, 24-hr treatment of A549 cells with 40 microM T3E caused the inhibition of Ras farnesylation, and a marked decrease in the levels of cyclin D required for G1/S progression in the cell-cycle and Bcl-xL, a key anti-apoptotic molecule.
  • In conclusion, a redox-silent analogue of T3, T3E may be a new candidate as an anticancer agent against lung adenocarcinoma showing poor prognosis based on the mutation of ras genes.
  • [MeSH-major] Adenocarcinoma / pathology. Antioxidants / pharmacology. Lung Neoplasms / pathology. Tocotrienols / pharmacology
  • [MeSH-minor] Cell Cycle / drug effects. Cell Death. Cyclin D. Cyclins / metabolism. Humans. Oxidation-Reduction. Prognosis. Tumor Cells, Cultured. ras Proteins / metabolism

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 15723336.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 6-O-carboxypropyl-alpha-tocotrienol; 0 / Antioxidants; 0 / Cyclin D; 0 / Cyclins; 0 / Tocotrienols; EC 3.6.5.2 / ras Proteins
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39. Zang YS, Xiu QY, Fang Z, Li B, Xia TB: Case report: dramatic recovery of lung adenocarcinoma-associated dermatomyositis with targeted lung cancer therapy alone. Oncologist; 2008 Jan;13(1):79-81
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  • [Title] Case report: dramatic recovery of lung adenocarcinoma-associated dermatomyositis with targeted lung cancer therapy alone.
  • This case report details the sudden onset of severe dermatomyositis (DM) symptoms followed by rapid progression of adenocarcinoma of the lung and an obvious diminution of the primary tumor with the administration of lung cancer targeted drug therapy alone, followed by nearly complete disappearance of the DM symptoms, with no conspicuous improvement in the DM symptoms when using corticosteroids.
  • [MeSH-major] Adenocarcinoma / drug therapy. Dermatomyositis / drug therapy. Glucocorticoids / therapeutic use. Lung Neoplasms / drug therapy. Paraneoplastic Syndromes / drug therapy

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  • (PMID = 18245014.001).
  • [ISSN] 1083-7159
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Glucocorticoids; 0 / Quinazolines; S65743JHBS / gefitinib
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40. Hasegawa Y, Tomita K, Watanabe M, Yamasaki A, Sano H, Hitsuda Y, Shimizu E: Dexamethasone inhibits phosphorylation of histone H3 at serine 10. Biochem Biophys Res Commun; 2005 Nov 4;336(4):1049-55
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  • Here, we investigated the ability of dexamethasone (Dex) to inhibit p-Ser10 expression in response to tumor necrosis factor (TNF-alpha) in the human lung adenocarcinoma cell line A549 and the SV-40-transformed human airway epithelial cell line BEAS-2B.
  • Flow cytometric analysis at a single-cell level in A549 cells indicated that TNF-alpha treatment caused early induction of p-Ser10 at 15 min, which was inhibited significantly by pretreatment with 10(-5) M Dex.
  • [MeSH-minor] Cell Line, Transformed. Cell Line, Tumor. Cell Nucleus / drug effects. Cell Nucleus / metabolism. Cytoplasmic Granules / drug effects. Cytoplasmic Granules / metabolism. Humans. Phosphorylation. RNA Polymerase II / metabolism. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 16165091.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Histones; 0 / Tumor Necrosis Factor-alpha; 452VLY9402 / Serine; 7S5I7G3JQL / Dexamethasone; EC 2.7.7.- / RNA Polymerase II
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41. Kobayashi K, Yano S, Kato K, Tatsukawa T, Ikeda T, Tokushima T: [Case with double primary cancers occurring synchronously in both the lung and jejunum diagnosed according to TTF-1 expression]. Nihon Kokyuki Gakkai Zasshi; 2005 Feb;43(2):84-8
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  • [Title] [Case with double primary cancers occurring synchronously in both the lung and jejunum diagnosed according to TTF-1 expression].
  • A 47-year-old man was diagnosed as having adenocarcinoma of the lung (T4N0M0) in August 2002.
  • Pathological examination of the lesion demonstrated adenocarcinoma.
  • The differential diagnosis between small intestine metastasis and primary small intestine cancer was difficult.
  • As adenocarcinoma of the jejunum was negative for TTF-1 in immunohistochemical staining and adenocarcinoma of the lung was positive, we diagnosed this patient as having primary jejunal cancer.
  • We report this rare case of double cancer involving the lung and jejunum.
  • [MeSH-major] Adenocarcinoma / diagnosis. Biomarkers, Tumor / analysis. Intestine, Small. Jejunal Neoplasms / diagnosis. Lung Neoplasms / diagnosis. Neoplasms, Multiple Primary / diagnosis. Nuclear Proteins / analysis. Transcription Factors / analysis
  • [MeSH-minor] Diagnosis, Differential. Humans. Immunohistochemistry. Male. Middle Aged

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  • (PMID = 15770938.001).
  • [ISSN] 1343-3490
  • [Journal-full-title] Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society
  • [ISO-abbreviation] Nihon Kokyuki Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / thyroid nuclear factor 1
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42. Licchesi JD, Westra WH, Hooker CM, Machida EO, Baylin SB, Herman JG: Epigenetic alteration of Wnt pathway antagonists in progressive glandular neoplasia of the lung. Carcinogenesis; 2008 May;29(5):895-904
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  • [Title] Epigenetic alteration of Wnt pathway antagonists in progressive glandular neoplasia of the lung.
  • BACKGROUND: Atypical adenomatous hyperplasia (AAH) is now recognized as a precursor lesion from which lung adenocarcinomas arise and thus represents an ideal target for studying the early genetic and epigenetic alterations associated with lung tumorigenesis such as alterations of the Wnt pathway.
  • METHODS: We assessed the level of Wnt signaling activity in lung cancer cell lines by determining the level of active beta-catenin and determined the level of expression of Wnt antagonists APC, DKK1, DKK3, LKB1, SFRP1, 2, 4, 5, WIF1 and RUNX3 using reverse transcription-polymerase chain reaction.
  • Using multiplex nested methylation-specific polymerase chain reaction, we analyzed promoter region methylation of these genes in resected lung tissue in the histopathologic sequence of glandular neoplasia (normal lung parenchyma, low-grade and high-grade AAH, adenocarcinoma).
  • RESULTS: The majority of non-small cell lung cancer cell lines (11 of 16, 69%) have evidence of active Wnt signaling and silencing of Wnt antagonists correlated with promoter hypermethylation.
  • Promoter region methylation of Wnt antagonists was common in primary lung adenocarcinoma and there was a significant increase in the frequency of methylation for Wnt antagonist genes and the number of genes methylated with each stage of tumorigenesis (test for rend P <or= 0.01).
  • Additionally, odds ratios for promoter hypermethylation of individual or multiple Wnt antagonist genes and adenocarcinomas were statistically significantly elevated and ranged between 3.64 and 48.17.
  • CONCLUSION: These results show that gene silencing of Wnt antagonists by promoter hypermethylation occurs during the earliest stages of glandular neoplasia of the lung and accumulates with progression toward malignancy.

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  • (PMID = 18308762.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA058184
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 3 Subunit; 0 / DMAP1 protein, human; 0 / DNA, Neoplasm; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; 0 / RNA, Neoplasm; 0 / Repressor Proteins; 0 / Wnt Proteins; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ PMC3312609
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43. Martin RC, Li Y, Liu Q, Barker DF, Doll MA, Hein DW: Manganese superoxide dismutase expression as a function of genotype and lung cancer pathology. Cancer Invest; 2010 Oct;28(8):813-9
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  • [Title] Manganese superoxide dismutase expression as a function of genotype and lung cancer pathology.
  • METHODS: One hundred lung cancer specimens and matched normal lung parenchyma from the same patient were evaluated for MnSOD expression.
  • CONCLUSION: MnSOD expression is significantly reduced in lung adenocarcinoma and squamous cell carcinoma compared to the matched normal lung tissue.

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  • (PMID = 20690800.001).
  • [ISSN] 1532-4192
  • [Journal-full-title] Cancer investigation
  • [ISO-abbreviation] Cancer Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA034627-23; United States / NCI NIH HHS / CA / R01 CA034627; United States / NCI NIH HHS / CA / R01 CA034627-23; United States / NCI NIH HHS / CA / R01-CA034627
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.15.1.1 / Superoxide Dismutase
  • [Other-IDs] NLM/ NIHMS321748; NLM/ PMC3196322
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44. Ishihara T, Takeuchi T, Nishimori I, Adachi Y, Minakuchi T, Fujita J, Sonobe H, Ohtsuki Y, Onishi S: Carbonic anhydrase-related protein VIII increases invasiveness of non-small cell lung adenocarcinoma. Virchows Arch; 2006 Jun;448(6):830-7
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  • [Title] Carbonic anhydrase-related protein VIII increases invasiveness of non-small cell lung adenocarcinoma.
  • Carbonic anhydrase-related protein VIII (CA-RP VIII) is believed to be an oncofetal antigen and is overexpressed in colorectal and non-small cell lung cancer.
  • However, the pathobiological properties of CA-RP VIII in lung cancer remain unclear.
  • In the present study, we examined ultrastructural changes caused by exogenous CA-RP VIII expression in a well-differentiated lung adenocarcinoma cell line, PC-9.
  • We subsequently examined CA-RP VIII expression in atypical adenomatous hyperplasia and early-stage lung adenocarcinoma (Stage Ia).
  • Significant expression of CA-RP VIII was observed in invasive lung adenocarcinoma but not in noninvasive adenocarcinoma.
  • Interestingly, CA-RP VIII was strongly expressed in signet-ring cell cancer and invasive mucinous adenocarcinoma components.
  • The present findings suggest that CA-RP VIII expression in lung adenocarcinoma is related to cancer cell invasion.
  • [MeSH-major] Carbonic Anhydrases / genetics. Carcinoma, Non-Small-Cell Lung / ultrastructure. Gene Expression Regulation, Neoplastic. Lung Neoplasms / ultrastructure. Nerve Tissue Proteins / genetics
  • [MeSH-minor] Adenoma / genetics. Adenoma / ultrastructure. Biomarkers, Tumor. Cell Line, Tumor. Cell Movement. Gene Expression. Humans. Hyperplasia. Immunohistochemistry. Microscopy, Electron, Transmission. Mucins / metabolism. Neoplasm Invasiveness. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction. Vacuoles / ultrastructure

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  • (PMID = 16609906.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CA8 protein, human; 0 / Car8 protein, mouse; 0 / Mucins; 0 / Nerve Tissue Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 4.2.1.1 / Carbonic Anhydrases
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45. Wong ET, Wu JK, Mahadevan A: Gefitinib and high-dose fractionated radiotherapy for carcinomatous encephalitis from non-small cell lung carcinoma. Biologics; 2007 Sep;1(3):321-4
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  • [Title] Gefitinib and high-dose fractionated radiotherapy for carcinomatous encephalitis from non-small cell lung carcinoma.
  • Carcinomatous encephalitis is a rapidly fatal form of metastasis caused by miliary spread of systemic cancer into the brain parenchyma.
  • We report a patient with rapid neurologic deterioration from carcinomatous encephalitis from lung adenocarcinoma.
  • Gefitinib and high-dose fractionated radiotherapy may have synergistic activity in patients with carcinomatous encephalitis from non-small cell lung cancer having favorable prognostic factors.

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  • (PMID = 19707341.001).
  • [ISSN] 1177-5475
  • [Journal-full-title] Biologics : targets & therapy
  • [ISO-abbreviation] Biologics
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC2721320
  • [Keywords] NOTNLM ; Gefitinib / brain metastases / radiation
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46. Hornick JL, Lauwers GY, Odze RD: Immunohistochemistry can help distinguish metastatic pancreatic adenocarcinomas from bile duct adenomas and hamartomas of the liver. Am J Surg Pathol; 2005 Mar;29(3):381-9
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  • [Title] Immunohistochemistry can help distinguish metastatic pancreatic adenocarcinomas from bile duct adenomas and hamartomas of the liver.
  • Not uncommonly, bile duct adenomas (BDAs) and hamartomas (BDHs) of the liver may be difficult to distinguish from metastatic well-differentiated ductal adenocarcinoma of the pancreas.
  • The primary purpose of this study was to determine if a panel of immunohistochemical stains can help distinguish BDA or BDH from metastatic pancreatic adenocarcinoma in the liver.
  • Routinely processed tissue sections from 25 BDA, 10 BDH, 25 metastatic pancreatic adenocarcinomas to the liver and 6 cases each of metastatic colorectal, breast, and lung adenocarcinomas were immunohistochemically stained for CK7, CK8/CK18, CK19, CK20, p53, p63, TAG-72, monoclonal CEA (mCEA), polyclonal CEA (pCEA), HER-2/neu, AMACR (alpha-methylacyl-CoA racemase), Dpc4 (Smad4), and mesothelin.
  • Significantly more (P < 0.05) metastatic pancreatic adenocarcinomas were positive for CK20 (76%), p53 (60%), TAG-72 (88%), mCEA (92%), HER2/neu (40%), and mesothelin (64%) and showed loss of Dpc4 (44%), in comparison to BDA (CK20, 40%; p53, 0%; TAG-72, 0%; mCEA, 0%; HER2/neu, 12%; mesothelin, 0%; loss of Dpc4, 0%) or BDH (CK20, 10%; p53, 0%; TAG-72, 0%; mCEA, 10%; HER2/neu, 0%; mesothelin, 0%; loss of Dpc4, 0%).
  • Of these antibodies, p53, TAG-72, mCEA, loss of Dpc4, and mesothelin had the highest specificity for pancreatic adenocarcinoma, with mCEA having the highest sensitivity (92%).
  • Although none of the BDA or BDH was positive for either p63 or AMACR, two of the metastatic pancreatic adenocarcinomas (8%) were positive for each of these peptides (P > 0.05).
  • For nonpancreatic adenocarcinomas, mCEA showed a reasonably high sensitivity and 100% specificity in the differential diagnosis versus BDA.
  • Immunohistochemical expression of p53, TAG-72, mCEA, mesothelin, and loss of Dpc4 can help distinguish metastatic pancreatic adenocarcinoma in the liver from BDA or BDH.
  • Although p63 and AMACR are also specific for pancreatic adenocarcinoma, their low sensitivity limits their use in clinical practice.
  • [MeSH-major] Adenocarcinoma / secondary. Adenoma / pathology. Bile Duct Neoplasms / pathology. Hamartoma / pathology. Liver Diseases / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Diagnosis, Differential. Humans. Immunoenzyme Techniques


47. Tang F, Zhao LT, Jiang Y, Ba de N, Cui LX, He W: Activity of recombinant human interleukin-15 against tumor recurrence and metastasis in mice. Cell Mol Immunol; 2008 Jun;5(3):189-96
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  • The results showed that tumor nodule formation was retarded and tumor growth was inhibited in the subcutaneous tumor model of LA795 lung adenocarcinoma after treatment with rhIL-15, and the survival rate of T739 tumor-bearing mice treated with rhIL-15 was much higher than that of mice treated with either saline or with the same dose of rhIL-2.
  • In some rhIL-15 treated mice, the tumor cells inoculated subcutaneously were eradicated and there was no tumor formation even 138 days after tumor cell inoculation.
  • The tumor-free mice were rechallenged with live tumor cells and no tumor reoccurred in the following two months in all of these mice, indicating that long-lasting antitumor systemic immunity developed.
  • It was also shown that tumor recurrence and metastasis were inhibited markedly after treatment with rhIL-15, but not with the same dose of rhIL-2, in both subcutaneously and intravenously disseminated tumor models of LA795 lung adenocarcinoma.
  • Simultaneously, the CTL and NK cell activities of the splenocytes obtained from tumor-bearing mice that had been treated with either rhIL-15 or rhIL-2 were both markedly enhanced.
  • However, the enhancement of CTL and NK cell activities was more significant in rhIL-15 treated mice than that in rhIL-2 treated mice.
  • This suggests that the anti-tumor effect of rhIL-15 in vivo was achieved by enhancing the CTL and NK cell activities in tumor immune response.
  • [MeSH-major] Adenocarcinoma / drug therapy. Interleukin-15 / immunology. Interleukin-15 / therapeutic use. Neoplasm Metastasis / prevention & control. Neoplasm Recurrence, Local / prevention & control
  • [MeSH-minor] Animals. Cell Line, Tumor. Humans. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary. Lung Neoplasms / drug therapy. Lung Neoplasms / secondary. Male. Mice. Mice, Inbred Strains. Neoplasm Transplantation. Random Allocation. Recombinant Proteins / immunology. Recombinant Proteins / metabolism. Recombinant Proteins / therapeutic use

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  • (PMID = 18582400.001).
  • [ISSN] 1672-7681
  • [Journal-full-title] Cellular & molecular immunology
  • [ISO-abbreviation] Cell. Mol. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Interleukin-15; 0 / Recombinant Proteins
  • [Other-IDs] NLM/ PMC4651289
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48. Heeger S: Targeted therapy of the epidermal growth factor receptor in the treatment of pancreatic cancer. Recent Results Cancer Res; 2008;177:131-6
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  • [Title] Targeted therapy of the epidermal growth factor receptor in the treatment of pancreatic cancer.
  • The so-called "small molecule" tyrosine kinase inhibitor erlotinib has gained marketing authorization in the United States for advanced adenocarcinoma of the lung and for pancreatic cancer, whereas the antibody cetuximab is registered for metastatic colorectal cancer and cancers of the head and neck.
  • Ongoing studies are evaluating the impact of EGFR-targeting therapy in the treatment of locally advanced and metastatic pancreatic cancer.

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  • (PMID = 18084955.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Number-of-references] 28
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49. Takano A, Ishikawa N, Nishino R, Masuda K, Yasui W, Inai K, Nishimura H, Ito H, Nakayama H, Miyagi Y, Tsuchiya E, Kohno N, Nakamura Y, Daigo Y: Identification of nectin-4 oncoprotein as a diagnostic and therapeutic target for lung cancer. Cancer Res; 2009 Aug 15;69(16):6694-703
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  • [Title] Identification of nectin-4 oncoprotein as a diagnostic and therapeutic target for lung cancer.
  • Gene expression profile analysis of lung cancers revealed the transactivation of an immunoglobulin-like molecule Nectin-4 in the majority of non-small cell lung cancers (NSCLC).
  • A combined ELISA for both Nectin-4 and CEA increased sensitivity and classified 65.0% of lung adenocarcinomas as positive with false-positive rate of 4.6%.
  • The use of both Nectin-4 and CYFRA21-1 classified 68.3% of lung squamous cell carcinomas as positive with false-positive rate of 6.1%.
  • Treatment of lung cancer cells with small interfering RNAs against Nectin-4 suppressed its expression and cell growth.
  • Nectin-4 might play a significant role in lung carcinogenesis, and it should be a new candidate serum and tissue biomarker, as well as a therapeutic target.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / diagnosis. Carcinoma, Non-Small-Cell Lung / drug therapy. Cell Adhesion Molecules / physiology. Lung Neoplasms / diagnosis. Lung Neoplasms / drug therapy


50. Tsai JR, Chong IW, Chen YH, Yang MJ, Sheu CC, Chang HC, Hwang JJ, Hung JY, Lin SR: Differential expression profile of MAGE family in non-small-cell lung cancer. Lung Cancer; 2007 May;56(2):185-92
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  • [Title] Differential expression profile of MAGE family in non-small-cell lung cancer.
  • The expression of the melanoma-associated antigen (MAGE) genes consists of variables in all tumor types, such as lung cancer, which are relevant to be silent in all normal tissues except germ cells.
  • They are considered as tumor-specific antigens, and are ideal targets for cancer immunotherapy.
  • A complete MAGE genes differential expression profile analysis of lung cancer can provide this study not only various target genes for immunotherapy, but also valuable markers for further diagnosis and prognosis.
  • This research has constructed a membrane array, which was consisted 32 MAGE genes, to detect whether the differential expression profile occurred in 52 pairs of non-small-cell lung cancer (NSCLC) samples.
  • MAGE-B, -C, -D, and subgroup -B6, -D4 have showed prominences in lung adenocarcinoma.
  • High-frequent expression of MAGE-D, and subgroup -A2, -D2 has also been discovered in non-metastasis group (p<0.05).
  • [MeSH-major] Antigens, Neoplasm / genetics. Carcinoma, Non-Small-Cell Lung / genetics. Gene Expression. Lung Neoplasms / genetics. Neoplasm Proteins / genetics

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  • (PMID = 17208331.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Neoplasm Proteins
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51. Kim IA, Kim IH, Kim HJ, Chie EK, Kim JS: HDAC inhibitor-mediated radiosensitization in human carcinoma cells: a general phenomenon? J Radiat Res; 2010;51(3):257-63
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  • Regarding a potential application of HDI as a radiosensitizer in the treatment of solid tumors, an important question is whether treatment efficacy would be influenced by intrinsic differences between cancer cells, such as different histologic origin and status of ATM or p53.
  • First we have observed the in vitro radiosensitization by Trichostatin A (TSA) on the broad spectrum of human tumor cell lines having different histologic origin such as HCT116 adenocarcinoma of colon, A549 adenocarcinoma of lung, HN-3 squamous cell carcinoma of head/neck, and HeLa squamous carcinoma of uterine cervix, using clonogenic assay.
  • Next, we have systematically assessed the radiosensitization on the cell lines having different ATM or p53 status.
  • We found that pretreatment of HDI consistently resulted in radiosensitization of all cell lines tested, though the sensitizer enhancement ratio of individual cell lines was variable.
  • The data presented here indicate that HDI enhances the radiation induced cell killing in the various cancer cells having intrinsic differences and may serve as a general strategy for enhancing tumor cell radiosensitivity.
  • [MeSH-minor] Cell Line, Tumor. Dose-Response Relationship, Radiation. Genes, p53. HeLa Cells. Humans. Hydroxamic Acids / pharmacology. Male. Radiation Tolerance. Radiation-Sensitizing Agents / pharmacology. Time Factors

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  • (PMID = 20505264.001).
  • [ISSN] 1349-9157
  • [Journal-full-title] Journal of radiation research
  • [ISO-abbreviation] J. Radiat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Radiation-Sensitizing Agents; 3X2S926L3Z / trichostatin A
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52. Lu ZJ, Song QF, Jiang SS, Song Q, Wang W, Zhang GH, Kan B, Chen LJ, Yang JL, Luo F, Qian ZY, Wei YQ, Gou LT: Identification of ATP synthase beta subunit (ATPB) on the cell surface as a non-small cell lung cancer (NSCLC) associated antigen. BMC Cancer; 2009;9:16
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  • [Title] Identification of ATP synthase beta subunit (ATPB) on the cell surface as a non-small cell lung cancer (NSCLC) associated antigen.
  • BACKGROUND: Antibody-based immunotherapy has achieved some success for cancer.
  • It is essential to identify more immunogenic antigens (especially cellular membrane markers) for tumor diagnosis and therapy.
  • METHODS: The membrane proteins of lung adenocarcinoma cell line A549 were used to immunize the BALB/c mice.
  • MTT cell proliferation assay was carried out to evaluate the inhibitory effect of McAb4E7 on A549 cells.
  • Flow cytometric assay, immunohistochemistry, western blot and proteomic technologies based on 2-DE and mass spectrometry were employed to detect and identify the corresponding antigen of McAb4E7.
  • Furthermore, immunohistochemistry showed that the antigen of McAb4E7 mainly aberrantly expressed in tumor cellular membrane in non-small cell lung cancer (NSCLC), but not in small cell lung cancer (SCLC).
  • The rate of ectopic expressed ATPB in the cellular membrane in lung adenocarcinoma, squamous carcinoma and their adjacent nontumourous lung tissues was 71.88%, 66.67% and 25.81% respectively.
  • CONCLUSION: In the present study, we identified that the ectopic ATPB in tumor cellular membrane was the non-small cell lung cancer (NSCLC) associated antigen.
  • [MeSH-major] Biomarkers, Tumor / analysis. Carcinoma, Non-Small-Cell Lung / enzymology. Lung Neoplasms / enzymology. Mitochondrial Proton-Translocating ATPases / analysis

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  • (PMID = 19144153.001).
  • [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 / Antibodies, Monoclonal; 0 / Biomarkers, Tumor; EC 3.6.3.- / Mitochondrial Proton-Translocating ATPases; EC 3.6.3.14 / ATP5B protein, human
  • [Other-IDs] NLM/ PMC2654462
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53. Guo NL, Wan YW, Tosun K, Lin H, Msiska Z, Flynn DC, Remick SC, Vallyathan V, Dowlati A, Shi X, Castranova V, Beer DG, Qian Y: Confirmation of gene expression-based prediction of survival in non-small cell lung cancer. Clin Cancer Res; 2008 Dec 15;14(24):8213-20
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  • [Title] Confirmation of gene expression-based prediction of survival in non-small cell lung cancer.
  • PURPOSE: It is a critical challenge to determine the risk of recurrence in early stage non-small cell lung cancer (NSCLC) patients.
  • EXPERIMENTAL DESIGN: Multiple published microarray data sets were used to evaluate our previously identified lung cancer prognostic gene signature.
  • Expression of the signature genes was further validated with real-time reverse transcription-PCR and Western blot assays of snap-frozen lung cancer tumor tissues.
  • The expression of the signature genes was validated with real-time reverse transcription-PCR analysis of lung cancer tumor specimens.
  • Protein expression of two signature genes, TAL2 and ILF3, was confirmed in lung adenocarcinoma tumors by using Western blot analysis.
  • These two biomarkers showed correlated mRNA and protein overexpression in lung cancer development and progression.

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  • (PMID = 19088038.001).
  • [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 / CA084953-050003; United States / NCRR NIH HHS / RR / P20 RR016440; United States / NCRR NIH HHS / RR / P20 RR16440-03; United States / NCI NIH HHS / CA / R01 CA060731; United States / NCI NIH HHS / CA / 5R01CA060731-13; United States / NLM NIH HHS / LM / R01 LM009500; United States / NLM NIH HHS / LM / LM009500-01A2; United States / NCI NIH HHS / CA / U19 CA084953-050003; United States / NCRR NIH HHS / RR / RR016440-08; United States / NLM NIH HHS / LM / R01 LM009500-01A2; United States / NCRR NIH HHS / RR / P20 RR016440-08; United States / NCI NIH HHS / CA / U19 CA084953; United States / NCI NIH HHS / CA / R01 CA154365
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS78586; NLM/ PMC2605664
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54. Xu Y, Liu H, Chen J, Zhou Q: Acquired resistance of lung adenocarcinoma to EGFR-tyrosine kinase inhibitors gefitinib and erlotinib. Cancer Biol Ther; 2010 Apr 15;9(8):572-82
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  • [Title] Acquired resistance of lung adenocarcinoma to EGFR-tyrosine kinase inhibitors gefitinib and erlotinib.
  • Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), such as gefitinib and erlotinib, are the first targeted therapy drugs approved for the treatment of advanced non-small-cell lung cancer (NSCLC).
  • Interestingly, treatment with these small molecule, reversible EGFR-TKIs leads to more positive response rates in patients with adenocarcinoma, in females, Asians, and patients with no history of smoking.
  • However, despite the dramatic initial response to TKIs, most lung cancer patients relapse and subsequently become resistant to the drug, a process termed acquired resistance.
  • [MeSH-major] Adenocarcinoma / drug therapy. Lung Neoplasms / drug therapy. Protein Kinase Inhibitors / pharmacology. Protein-Tyrosine Kinases / antagonists & inhibitors. Quinazolines / pharmacology. Receptor, Epidermal Growth Factor / antagonists & inhibitors

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  • (PMID = 20404520.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Quinazolines; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
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55. Ntalli NG, Cottiglia F, Bueno CA, Alché LE, Leonti M, Vargiu S, Bifulco E, Menkissoglu-Spiroudi U, Caboni P: Cytotoxic tirucallane triterpenoids from Melia azedarach fruits. Molecules; 2010 Sep;15(9):5866-77
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  • The cytotoxicity of the isolated compounds toward the human lung adenocarcinoma epithelial cell line A549 was determined, while no activity was observed against the phytonematode Meloidogyne incognita.
  • [MeSH-minor] Adenocarcinoma / pathology. Animals. Cell Line, Tumor. Epithelial Cells / drug effects. Fruit / chemistry. Humans. Lung Neoplasms / pathology. Molecular Structure. Plant Extracts / isolation & purification. Plant Extracts / toxicity. Tylenchoidea / drug effects

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  • (PMID = 20802401.001).
  • [ISSN] 1420-3049
  • [Journal-full-title] Molecules (Basel, Switzerland)
  • [ISO-abbreviation] Molecules
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Cytotoxins; 0 / Plant Extracts; 0 / Triterpenes; 0 / tirucallane; Adenocarcinoma of lung
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56. Cao X, Bennett RL, May WS: c-Myc and caspase-2 are involved in activating Bax during cytotoxic drug-induced apoptosis. J Biol Chem; 2008 May 23;283(21):14490-6
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  • To test whether c-Myc and caspase-2 cooperate to activate Bax and thereby mediate intrinsic apoptosis, small interfering RNA was used to efficiently knock down the expression of c-Myc, caspase-2, and Apaf-1, an activating component in the apoptosome, in two human cancer cell lines, lung adenocarcinoma A-549 and osteosarcoma U2-OS cells.

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  • (PMID = 18375382.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL054083; United States / NCI NIH HHS / CA / CA 44649
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / APAF1 protein, human; 0 / Apoptotic Protease-Activating Factor 1; 0 / BAX protein, human; 0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / RNA, Small Interfering; 0 / bcl-2-Associated X Protein; 9007-43-6 / Cytochromes c; EC 3.4.22.- / CASP2 protein, human; EC 3.4.22.- / Caspase 2; EC 3.4.22.- / Cysteine Endopeptidases; Q20Q21Q62J / Cisplatin
  • [Other-IDs] NLM/ PMC2386933
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57. Parra ER, Park JY, Saito DM, Takagaki TY, Rodrigues OR, Capelozzi VL: Prognostic index expression of cyclin-D1, cerbB-2 and VEGF: metastases vs corresponding primary cancers and metastatic vs non-metastatic adenocarcinomas. Histol Histopathol; 2008 08;23(8):987-93
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  • [Title] Prognostic index expression of cyclin-D1, cerbB-2 and VEGF: metastases vs corresponding primary cancers and metastatic vs non-metastatic adenocarcinomas.
  • The prognostic relevance of different molecular markers in lung cancer is a crucial issue still worth investigating, and the specimens collected and analyzed represent a valuable source of material.
  • Cyclin-D1, c-erbB-2 and vascular endothelial growth factor (VEGF) have shown to be promising as prognosticators in human cancer.
  • In this study, we sought to examine the importance of Cyclin-D1, c-erbB-2 and VEGF, and to study the quantitative relationship among these factors and disease progression in metastases vs corresponding primary cancer, and metastatic vs non metastatic cancers.
  • MATERIAL AND METHODS: We used immunohistochemistry and morphometric analysis to evaluate the amount of tumour staining for Cyclin-D1, c-erbB-2 and VEGF in 52 patients with surgically excised adenocarcinoma of the lung, and the outcome for our study was survival time until death from hematogenic metastases.
  • Non-metastatic cancers also presented significantly lower Cyclin-D1 and c-erbB-2 expression than metastatic cancers (p<0.01 and p<0.01, respectively).
  • Equally significant was the difference between higher c-erbB-2 expression by metastatic cancers compared to non-metastatic cancers (p=0.02).
  • CONCLUSION: Different tumour cell profiles in metastases, corresponding primary cancers, and non-metastatic cancers were found, thus suggesting that different cell clones control the invasive and non-invasive behaviour of the cancers.
  • [MeSH-major] Adenocarcinoma / metabolism. Cyclins / metabolism. Lung Neoplasms / metabolism. Receptor, ErbB-2 / metabolism. Vascular Endothelial Growth Factor A / metabolism


58. Kim Y, Kim HS, Cui ZY, Lee HS, Ahn JS, Park CK, Park K, Ahn MJ: Clinicopathological implications of EpCAM expression in adenocarcinoma of the lung. Anticancer Res; 2009 May;29(5):1817-22
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  • [Title] Clinicopathological implications of EpCAM expression in adenocarcinoma of the lung.
  • BACKGROUND: The frequency of epithelial cell adhesion molecule (EpCAM) expression was investigated in non-small cell lung cancer (NSCLC) cells and human tissues, and its clinicopathological significance in adenocarcinoma of the lung was evaluated.
  • EpCAM protein expression was evaluated in 234 adenocarcinoma tissues using immunohistochemistry.
  • EpCAM overexpression was detected in 120/234 (51.3%) surgically resected adenocarcinoma tissues.
  • EpCAM overexpression occurred significantly more frequently in adenocarcinoma than in bronchioloalveolar carcinoma (p=0.02).
  • CONCLUSION: These findings suggest EpCAM plays a role in the carcinogenesis of adenocarcinoma of the lung and might provide a promising molecule for targeted therapy in NSCLC.
  • [MeSH-major] Adenocarcinoma / metabolism. Antigens, Neoplasm / metabolism. Cell Adhesion Molecules / metabolism. Lung Neoplasms / metabolism
  • [MeSH-minor] Base Sequence. Cell Line, Tumor. DNA Primers. Flow Cytometry. Humans. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19443410.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cell Adhesion Molecules; 0 / DNA Primers; 0 / EPCAM protein, human
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59. Aokage K, Ishii G, Yoshida J, Hishida T, Nishimura M, Nagai K, Ochiai A: Histological progression of small intrapulmonary metastatic tumor from primary lung adenocarcinoma. Pathol Int; 2010 Dec;60(12):765-73
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  • [Title] Histological progression of small intrapulmonary metastatic tumor from primary lung adenocarcinoma.
  • Histological typing based on the World Health Organization classification (bronchioloalveolar carcinoma, acinar, papillary, and solid subtype) was used to evaluate 234 metastases from the primary lung adenocarcinomas of 139 patients.
  • These findings suggest that implanted cancer cells display lepidic growth in the early metastatic phase and recapitulate the morphological heterogeneity of the original tumor as the metastasis enlarges.
  • [MeSH-major] Adenocarcinoma / secondary. Lung Neoplasms / pathology. Lung Neoplasms / secondary. Neoplasm Metastasis / pathology

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  • [Copyright] © 2010 The Authors. Pathology International © 2010 Japanese Society of Pathology and Blackwell Publishing Asia Pty Ltd.
  • (PMID = 21091834.001).
  • [ISSN] 1440-1827
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
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60. Reinmuth N, Jauch A, Xu EC, Muley T, Granzow M, Hoffmann H, Dienemann H, Herpel E, Schnabel PA, Herth FJ, Gottschling S, Lahm H, Steins M, Thomas M, Meister M: Correlation of EGFR mutations with chromosomal alterations and expression of EGFR, ErbB3 and VEGF in tumor samples of lung adenocarcinoma patients. Lung Cancer; 2008 Nov;62(2):193-201
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  • [Title] Correlation of EGFR mutations with chromosomal alterations and expression of EGFR, ErbB3 and VEGF in tumor samples of lung adenocarcinoma patients.
  • INTRODUCTION: Mutations in the tyrosine kinase domain of the epidermal growth factor receptor (EGFR) are frequently detected in lung adenocarcinomas with bronchioloalveolar (BAC) differentiation and have been associated with increased response to small molecule EGFR inhibitors in some clinical studies.
  • METHODS: By DNA sequencing, 120 patients with lung adenocarcinomas (70 tumors with BAC components) were screened for EGFR mutations within exons 18-21.
  • Tumors with BAC components carried more frequently EGFR mutations compared to adenocarcinomas without BAC histology (17/70=24% vs 3/50=6.0%; p=0.012).
  • CONCLUSION: EGFR gene mutations are frequently seen in lung adenocarcinomas with BAC differentiation and can be linked to chromosomal imbalances and increased VEGF expression.
  • [MeSH-major] Adenocarcinoma / genetics. Lung Neoplasms / genetics. Receptor, Epidermal Growth Factor / genetics. Receptor, ErbB-3 / biosynthesis. Vascular Endothelial Growth Factor A / biosynthesis

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  • (PMID = 18450321.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-3
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61. Khan O, Tong WP, Karlin NJ: Metastatic lung adenocarcinoma in a 20-year-old patient. Curr Oncol; 2010 Feb;17(1):56-8
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  • [Title] Metastatic lung adenocarcinoma in a 20-year-old patient.
  • Lung cancer is rare disease in patients under 25 years of age.
  • He was treated for pneumonia after a chest radiograph showed total opacification of the right lung.
  • Tissue immunostaining confirmed a non-small-cell lung cancer.
  • In this paper, we hope to illustrate the unique challenges in diagnosing and treating young patients with metastatic lung cancer.

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  • (PMID = 20179804.001).
  • [ISSN] 1718-7729
  • [Journal-full-title] Current oncology (Toronto, Ont.)
  • [ISO-abbreviation] Curr Oncol
  • [Language] eng
  • [Publication-type] Journal Article
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  • [Other-IDs] NLM/ PMC2826778
  • [Keywords] NOTNLM ; Metastatic lung cancer / non-small-cell lung cancer / young patients
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62. Zheng S, El-Naggar AK, Kim ES, Kurie JM, Lozano G: A genetic mouse model for metastatic lung cancer with gender differences in survival. Oncogene; 2007 Oct 18;26(48):6896-904
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  • [Title] A genetic mouse model for metastatic lung cancer with gender differences in survival.
  • Lung cancer is a devastating disease with poor prognosis.
  • The design of better therapies for lung cancer patients would be greatly aided by good mouse models that closely resemble the human disease.
  • Unfortunately, current models for lung adenocarcinoma are inadequate due to the absence of metastases.
  • In this study, we incorporated both K-ras and p53 missense mutations into the mouse genome and established a more faithful genetic model for human lung adenocarcinoma, the most common type of lung cancer.
  • Mice with both mutations developed advanced lung adenocarcinomas that were highly aggressive and metastasized to multiple intrathoracic and extrathoracic sites in a pattern similar to that of human lung cancer.
  • These mice also showed a gender difference in cancer-related death.
  • This mouse model recapitulates the metastatic nature of human lung cancer and will be invaluable to further probe the molecular basis of metastatic lung cancer and for translational studies.
  • [MeSH-major] Adenocarcinoma / genetics. Disease Models, Animal. Genes, ras / genetics. Lung Neoplasms / genetics. Mutation, Missense. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 17486075.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Tumor Suppressor Protein p53
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63. Norsa A, Martino V: Somatostatin, retinoids, melatonin, vitamin D, bromocriptine, and cyclophosphamide in chemotherapy-pretreated patients with advanced lung adenocarcinoma and low performance status. Cancer Biother Radiopharm; 2007 Feb;22(1):50-5
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  • [Title] Somatostatin, retinoids, melatonin, vitamin D, bromocriptine, and cyclophosphamide in chemotherapy-pretreated patients with advanced lung adenocarcinoma and low performance status.
  • BACKGROUND: We previously reported on an improvement in survival and quality of life in chemotherapy-naïve patients with advanced non-small-cell lung cancer and low performance status (PS) treated with a combination of biotherapeutical agents and cyclophosphamide.
  • In this study, we assessed the survival, clinical status, and toxicity of this multidrug regimen in chemotherapy-pretreated patients with advanced lung adenocarcinoma and low PS.
  • METHODS: Patients with stage IIIB or IV lung adenocarcinoma, who had progressed after prior standard chemotherapy, and with an Eastern Cooperative Oncology Group PS > or = 2, received a daily combination of somatostatin, retinoids, melatonin, vitamin D, bromocriptine, and cyclophosphamide.
  • CONCLUSIONS: The combined regimen of somatostatin, retinoids, melatonin, vitamin D, bromocriptine, and cyclophosphamide is well tolerated and can improve disease-related symptoms in heavily pretreated patients with late-stage lung adenocarcinoma and poor PS.
  • [MeSH-major] Bromocriptine / therapeutic use. Cyclophosphamide / therapeutic use. Lung Neoplasms / drug therapy. Melatonin / therapeutic use. Retinoids / therapeutic use. Somatostatin / therapeutic use. Vitamin D / therapeutic use
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Adult. Aged. Drug Therapy, Combination. Female. Humans. Male. Middle Aged. Neoplasm Staging. Survival Rate. Treatment Outcome

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  • (PMID = 17627413.001).
  • [ISSN] 1084-9785
  • [Journal-full-title] Cancer biotherapy & radiopharmaceuticals
  • [ISO-abbreviation] Cancer Biother. Radiopharm.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Retinoids; 1406-16-2 / Vitamin D; 3A64E3G5ZO / Bromocriptine; 51110-01-1 / Somatostatin; 8N3DW7272P / Cyclophosphamide; JL5DK93RCL / Melatonin
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64. Shi ZC, Yu Y, Li Y, Fu SB: [The roles of rab5a gene in the mechanism of tumor metastasis]. Yi Chuan; 2005 Sep;27(5):694-8
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  • To study the role of rab5a gene in the mechanism of tumor metastasis, rab5a gene was stable transfected into AGZY83-a cell, a lung adenocarcinoma cell line with low metastatic potential.

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  • (PMID = 16257893.001).
  • [ISSN] 0253-9772
  • [Journal-full-title] Yi chuan = Hereditas
  • [ISO-abbreviation] Yi Chuan
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / CST3 protein, human; 0 / Cystatin C; 0 / NM23 Nucleoside Diphosphate Kinases; 0 / RNA, Neoplasm; 0 / S100 Proteins; 142662-27-9 / S100A4 protein, human; EC 2.7.4.6 / NME1 protein, human; EC 3.6.5.2 / rab5 GTP-Binding Proteins; EC 3.6.5.2 / rac1 GTP-Binding Protein
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65. Thomas KS, Billingsley A, Amarshi N, Nair BA: Elevated international normalized ratio associated with concomitant warfarin and erlotinib. Am J Health Syst Pharm; 2010 Sep 1;67(17):1426-9
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  • SUMMARY: A 47-year-old Caucasian man with a history of atrial fibrillation, anxiety, and a 40-pack-year smoking history was diagnosed with advanced, moderately differentiated adenocarcinoma of the lung.
  • Soon after being diagnosed with non-small-cell lung cancer, warfarin was initiated for the treatment of a venous thromboembolism.
  • CONCLUSION: Concomitant administration of erlotinib and warfarin resulted in an increase in INR values in a 47-year-old man with advanced lung cancer.
  • [MeSH-minor] Adenocarcinoma / drug therapy. Carcinoma, Non-Small-Cell Lung / drug therapy. Drug Interactions. Drug Therapy, Combination. Erlotinib Hydrochloride. Humans. Lung Neoplasms / drug therapy. Male. Middle Aged. Thromboembolism / drug therapy

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  • (PMID = 20720241.001).
  • [ISSN] 1535-2900
  • [Journal-full-title] American journal of health-system pharmacy : AJHP : official journal of the American Society of Health-System Pharmacists
  • [ISO-abbreviation] Am J Health Syst Pharm
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticoagulants; 0 / Quinazolines; 5Q7ZVV76EI / Warfarin; DA87705X9K / Erlotinib Hydrochloride
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66. Chen MW, Yang L, Ni L, Guo X, Tian RZ, Wang XQ: [The effect of 20(R)-ginsenoside Rg3 on the differential expression of cell signaling genes and other related genes in human lung adenocarcinoma cell line A549]. Zhonghua Jie He He Hu Xi Za Zhi; 2005 Jan;28(1):37-40
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  • [Title] [The effect of 20(R)-ginsenoside Rg3 on the differential expression of cell signaling genes and other related genes in human lung adenocarcinoma cell line A549].
  • OBJECTIVE: To study the effect of 20(R)-ginsenoside Rg3 [20(R)-Rg3] on the differential expression of cell signaling genes and other related genes in human lung adenocarcinoma cell line A549.
  • METHODS: The cell line A549 was cultured with 20(R)-Rg3 (10(-6) mol/L) for 72 h, RNA was extracted, and the differential expression of cell signaling genes and other related genes were detected with DNA microarray.
  • Two cell signaling genes & transducin genes were up-regulated.
  • CONCLUSION: 20(R)-Rg3 showed significant effect on the differential expression of cell signaling genes and other related genes in human lung cell line A549.
  • [MeSH-major] Adenocarcinoma / genetics. Antineoplastic Agents, Phytogenic / pharmacology. Gene Expression Regulation, Neoplastic / drug effects. Ginsenosides / pharmacology. Lung Neoplasms / genetics
  • [MeSH-minor] Cell Line, Tumor. Gene Expression Profiling. Humans. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Oligonucleotide Array Sequence Analysis. Panax / chemistry. Signal Transduction

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  • (PMID = 15774190.001).
  • [ISSN] 1001-0939
  • [Journal-full-title] Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases
  • [ISO-abbreviation] Zhonghua Jie He He Hu Xi Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Ginsenosides; 0 / Neoplasm Proteins
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67. Guha U, Chaerkady R, Marimuthu A, Patterson AS, Kashyap MK, Harsha HC, Sato M, Bader JS, Lash AE, Minna JD, Pandey A, Varmus HE: Comparisons of tyrosine phosphorylated proteins in cells expressing lung cancer-specific alleles of EGFR and KRAS. Proc Natl Acad Sci U S A; 2008 Sep 16;105(37):14112-7
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  • [Title] Comparisons of tyrosine phosphorylated proteins in cells expressing lung cancer-specific alleles of EGFR and KRAS.
  • We have used unbiased phosphoproteomic approaches, based on quantitative mass spectrometry using stable isotope labeling with amino acids in cell culture (SILAC), to identify tyrosine phosphorylated proteins in isogenic human bronchial epithelial cells (HBECs) and human lung adenocarcinoma cell lines, expressing either of the two mutant alleles of EGFR (L858R and Del E746-A750), or a mutant KRAS allele, which are common in human lung adenocarcinomas.
  • Phosphorylation of some proteins differed in the two EGFR mutant-expressing cells; for example, some cell junction proteins (beta-catenin, plakoglobin, and E-cadherin) were more phosphorylated in HBECs expressing L858R EGFR than in cells expressing Del EGFR.


68. Amann M, D'Argouges S, Lorenczewski G, Brischwein K, Kischel R, Lutterbuese R, Mangold S, Rau D, Volkland J, Pflanz S, Raum T, Münz M, Kufer P, Schlereth B, Baeuerle PA, Friedrich M: Antitumor activity of an EpCAM/CD3-bispecific BiTE antibody during long-term treatment of mice in the absence of T-cell anergy and sustained cytokine release. J Immunother; 2009 Jun;32(5):452-64
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  • [Title] Antitumor activity of an EpCAM/CD3-bispecific BiTE antibody during long-term treatment of mice in the absence of T-cell anergy and sustained cytokine release.
  • MT110, its human-specific analog, is in a clinical phase 1 trial for treatment of patients with adenocarcinoma of the lung or gastrointestinal tract.
  • Recent studies have shown a therapeutic window for muS110, have explored single-dose toxicity of muS110, and have found that a 1-week low-dose treatment dramatically increased the tolerability of mice to very high doses of muS110 (Cancer Immunol. Immunother. 2009;58:95-109).
  • Here we analyzed the impact of long-term, high-dose treatment of mice with muS110 on antitumor activity and functionality of T cells.
  • Unimpaired T-cell performance was also evident from the effective prevention of orthotopic 4T1 breast tumor outgrowth in mice treated long term with escalating doses of muS110.
  • [MeSH-major] Antibodies, Bispecific / administration & dosage. Antigens, CD3 / immunology. Antigens, Neoplasm / immunology. Cell Adhesion Molecules / immunology. Immunotherapy. Mammary Neoplasms, Experimental / immunology. T-Lymphocytes / immunology
  • [MeSH-minor] Animals. Cell Proliferation / drug effects. Clonal Anergy / drug effects. Cytokines / metabolism. Female. Humans. Immunologic Factors / administration & dosage. Immunologic Factors / adverse effects. Lymphocyte Activation / drug effects. Mice. Mice, Inbred BALB C. Neoplasm Transplantation. Protein Engineering. Time Factors

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  • (PMID = 19609237.001).
  • [ISSN] 1537-4513
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Bispecific; 0 / Antigens, CD3; 0 / Antigens, Neoplasm; 0 / Cell Adhesion Molecules; 0 / Cytokines; 0 / Immunologic Factors; 0 / tumor-associated antigen GA733
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69. Kruewel T, Schenone S, Radi M, Maga G, Rohrbeck A, Botta M, Borlak J: Molecular characterization of c-Abl/c-Src kinase inhibitors targeted against murine tumour progenitor cells that express stem cell markers. PLoS One; 2010;5(11):e14143
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  • [Title] Molecular characterization of c-Abl/c-Src kinase inhibitors targeted against murine tumour progenitor cells that express stem cell markers.
  • BACKGROUND: The non-receptor tyrosine kinases c-Abl and c-Src are overexpressed in various solid human tumours.
  • Here we examined the effects of a new family of pyrazolo [3,4-d] pyrimidines on a panel of 11 different murine lung tumour progenitor cell lines, that express stem cell markers, as well as on the human lung adenocarcinoma cell line A549, the human hepatoma cell line HepG2 and the human colon cancer cell line CaCo2 to obtain insight into the mode of action of these experimental drugs.
  • METHODOLOGY/PRINCIPAL FINDINGS: Treatment with the dual kinase inhibitors blocked c-Abl and c-Src kinase activity efficiently in the nanomolar range, induced apoptosis, reduced cell viability and caused cell cycle arrest predominantly at G0/G1 phase while western blot analysis confirmed repressed protein expression of c-Abl and c-Src as well as the interacting partners p38 mitogen activated protein kinase, heterogenous ribonucleoprotein K, cyclin dependent kinase 1 and further proteins that are crucial for tumour progression.
  • Importantly, a significant repression of the epidermal growth factor receptor was observed while whole genome gene expression analysis evidenced regulation of many cell cycle regulated genes as well integrin and focal adhesion kinase (FAK) signalling to impact cytoskeleton dynamics, migration, invasion and metastasis.
  • CONCLUSIONS/SIGNIFICANCE: Our experiments and recently published in vivo engraftment studies with various tumour cell lines revealed the dual kinase inhibitors to be efficient in their antitumour activity.
  • [MeSH-minor] Animals. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Blotting, Western. Caco-2 Cells. Cell Line, Tumor. Gene Expression Profiling. Gene Expression Regulation, Neoplastic / drug effects. Gene Regulatory Networks / drug effects. Hep G2 Cells. Humans. Mice. Models, Chemical. Molecular Structure. Oligonucleotide Array Sequence Analysis. Signal Transduction / drug effects. src-Family Kinases

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  • (PMID = 21152443.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Protein Kinase Inhibitors; 0 / Pyrazoles; 0 / Pyrimidines; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / CSK tyrosine-protein kinase; EC 2.7.10.2 / Proto-Oncogene Proteins c-abl; EC 2.7.10.2 / src-Family Kinases
  • [Other-IDs] NLM/ PMC2994747
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70. Montgrain PR, Quintana R, Rascon Y, Burton DW, Deftos LJ, Casillas A, Hastings RH: Parathyroid hormone-related protein varies with sex and androgen status in nonsmall cell lung cancer. Cancer; 2007 Sep 15;110(6):1313-20
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  • [Title] Parathyroid hormone-related protein varies with sex and androgen status in nonsmall cell lung cancer.
  • BACKGROUND: In nonsmall cell lung cancer, tumor parathyroid hormone-related protein (PTHrP) expression predicts longer survival in women but not in men.
  • The objectives of this study were to compare lung carcinoma PTHrP expression and carcinoma growth in male and female mice and to determine whether gonadal steroids regulate PTHrP in lung cancer cells.
  • METHODS: Tumor PTHrP content was measured by immunoassay, and tumor burden was assessed with multiple measures in BEN squamous cell orthotopic lung carcinomas in athymic mice.
  • In addition, lung adenocarcinoma PTHrP messenger RNA (mRNA) values determined by microarray analyses were compared between men and women.
  • Cultured lung cancer cells were assayed for PTHrP after treatment with estradiol or R1881, a synthetic androgen.
  • RESULTS: Lung carcinomas contained approximately 3 times more PTHrP in female mice than in male mice.
  • Similarly, levels of PTHrP mRNA were significantly greater in adenocarcinomas from patients who were women than from patients who were men.
  • Androgen treatment reduced PTHrP in 3 lung cancer lines.
  • Testosterone treatment also reduced lung carcinoma PTHrP in female mice.
  • CONCLUSIONS: Lung carcinomas in females expressed more PTHrP than in males possibly because of negative regulation by androgens in males.
  • [MeSH-major] Androgens / metabolism. Carcinoma, Non-Small-Cell Lung / metabolism. Lung Neoplasms / metabolism. Parathyroid Hormone-Related Protein / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Animals. Blotting, Western. Carcinoma, Large Cell / metabolism. Carcinoma, Squamous Cell / metabolism. Female. Gene Expression Regulation, Neoplastic. Gonadal Steroid Hormones / metabolism. Humans. Male. Mice. Mice, Nude. Reverse Transcriptase Polymerase Chain Reaction. Sex Factors. Tumor Burden

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  • [Copyright] (c) 2007 American Cancer Society.
  • (PMID = 17676588.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Gonadal Steroid Hormones; 0 / Parathyroid Hormone-Related Protein
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71. Vlahovic G, Rabbani ZN, Herndon JE 2nd, Dewhirst MW, Vujaskovic Z: Treatment with Imatinib in NSCLC is associated with decrease of phosphorylated PDGFR-beta and VEGF expression, decrease in interstitial fluid pressure and improvement of oxygenation. Br J Cancer; 2006 Oct 23;95(8):1013-9
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  • Elevated intratumoral interstitial fluid pressure (IFP) and tumour hypoxia are independent predictive factors for poor survival and poor treatment response in cancer patients.
  • Interstitial fluid pressure can be reduced by inhibition of phosphorylated platelet-derived growth factor receptor-beta (p-PDGFR-beta), a tyrosine kinase receptor frequently overexpressed in cancer stroma, and/or by inhibition of VEGF, a growth factor commonly overexpressed in tumours overexpressing p-PDGFR-beta.
  • A549 human lung adenocarcinoma xenografts overexpressing PDGFR-beta were grown in nude mice.

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  • (PMID = 17003785.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / K12 RR017630; United States / NCRR NIH HHS / RR / 5K12RR017630-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD31; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / Vascular Endothelial Growth Factor A; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta; S88TT14065 / Oxygen
  • [Other-IDs] NLM/ PMC2360712
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72. Ji Y, He J, Zhou Q, Chen J, Li Q, Zhu J, Liu H: [The inhibiting effect and its molecular mechanism of Tanshinone on human lung cancer cell line in vitro.]. Zhongguo Fei Ai Za Zhi; 2008 Apr 20;11(2):202-5
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  • [Title] [The inhibiting effect and its molecular mechanism of Tanshinone on human lung cancer cell line in vitro.].
  • BACKGROUND: To explore the inhibiting effect and its molecular mechanism of Tanshione on human lung carcinoma cell line.
  • METHODS: Human lung adenocarcinoma cell line (SPC-A-1) was treated IN VITRO with 0.5 mug/mL Tanshinone IIA (Tan IIA) for five days, other equal cells were also treated with all transretinoic acid (RA) and DDP respectively as control.
  • Changes in cell morphology, proliferation dynamics cell cycle distribution and tumor related genes expression were detected, meanwhile the apoptotic cells and apoptosis related genes expression were detected, too.
  • RESULTS: In Tan IIA group, the cell growth and rate of clone formation of SPC-A-1 cells were markedly inhibited, Flow Cytometry demonstrated that S phase cells decreased and G0/G1 phase cells increased observably, many apoptotic cells were observed by light and electron microscope.
  • CONCLUSIONS: Tan IIA can inhibit cell growth in SPC-A-1 cell line and its possible molecular mechanism may be inhibiting DNA synthesis by upregulating gene p53, p21 and down-regulating gene CDKN2.
  • On the other hand, inducing cell apoptosis by up-regulating gene p53, Fas, Bax and down-regulating gene Bcl-2 might be the other molecular mechanism in suppressing the growth of SPC-A-1 cells.

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  • (PMID = 20731902.001).
  • [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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73. Zhu CQ, Popova SN, Brown ER, Barsyte-Lovejoy D, Navab R, Shih W, Li M, Lu M, Jurisica I, Penn LZ, Gullberg D, Tsao MS: Integrin alpha 11 regulates IGF2 expression in fibroblasts to enhance tumorigenicity of human non-small-cell lung cancer cells. Proc Natl Acad Sci U S A; 2007 Jul 10;104(28):11754-9
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  • [Title] Integrin alpha 11 regulates IGF2 expression in fibroblasts to enhance tumorigenicity of human non-small-cell lung cancer cells.
  • Integrin alpha11 (ITGA11/alpha11) is localized to stromal fibroblasts and commonly overexpressed in non-small-cell lung carcinoma (NSCLC).
  • SV40 immortalized mouse embryonic fibroblasts established from wild-type (WT) and Itga11-deficient [knockout (KO)] mice were tested for their tumorigenicity in immune-deficient mice when implanted alone or coimplanted with the A549 human lung adenocarcinoma cells.
  • These findings were validated in two other NSCLC cell lines, NCI-H460 and NCI-H520.
  • The results indicate that alpha11 is an important stromal factor in NSCLC and propose a paradigm for carcinoma-stromal interaction indirectly through interaction between the matrix collagen and stromal fibroblasts to stimulate cancer cell growth.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / metabolism. Fibroblasts / metabolism. Gene Expression Regulation, Neoplastic / physiology. Growth Substances / physiology. Integrin alpha Chains / physiology. Lung Neoplasms / metabolism. Proteins / genetics. Proteins / metabolism
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Animals. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / pathology. Cell Line, Transformed. Cell Line, Tumor. Collagen / metabolism. Extracellular Matrix / genetics. Extracellular Matrix / metabolism. Extracellular Matrix / pathology. Humans. Insulin-Like Growth Factor II. Male. Mice. Mice, Knockout. Mice, SCID. Stromal Cells / metabolism. Stromal Cells / pathology

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  • (PMID = 17600088.001).
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Growth Substances; 0 / IGF2 protein, human; 0 / ITGA11 protein, human; 0 / Integrin alpha Chains; 0 / Proteins; 67763-97-7 / Insulin-Like Growth Factor II; 9007-34-5 / Collagen
  • [Other-IDs] NLM/ PMC1913903
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74. Fenske TS, McMahon C, Edwin D, Jarvis JC, Cheverud JM, Minn M, Mathews V, Bogue MA, Province MA, McLeod HL, Graubert TA: Identification of candidate alkylator-induced cancer susceptibility genes by whole genome scanning in mice. Cancer Res; 2006 May 15;66(10):5029-38
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  • [Title] Identification of candidate alkylator-induced cancer susceptibility genes by whole genome scanning in mice.
  • Cancer susceptibility was a heritable trait for the most common tumor types, lung adenocarcinoma (H(2) = 0.25), T cell lymphoma (H(2) = 0.19), and myeloid malignancies (H(2) = 0.10).
  • Quantitative trait locus mapping identified regions on chromosomes 3, 6, 9, and 15 containing candidate genes associated with lung adenoma, lung carcinoma, and lymphoma susceptibility.
  • This novel mouse model recapitulates many features of human alkylator-associated cancer and supports the hypothesis that susceptibility to this syndrome is influenced by inherited polymorphisms that could be used to make informed clinical treatment decisions.
  • [MeSH-minor] Animals. Ethylnitrosourea / toxicity. Genetic Predisposition to Disease. Hematologic Neoplasms / chemically induced. Hematologic Neoplasms / genetics. Lung Neoplasms / chemically induced. Lung Neoplasms / genetics. Mice. Mutagens / toxicity. Quantitative Trait Loci

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  • (PMID = 16707424.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA101937
  • [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 / Alkylating Agents; 0 / Antineoplastic Agents, Alkylating; 0 / Mutagens; P8M1T4190R / Ethylnitrosourea
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75. Ohtsuki Y, Uomoto M, Hachisuka Y, Kato M, Iguchi M, Lee GH, Furihata M: A rare case of coexistence of pulmonary adenocarcinoma with Langerhans' cell histiocytosis. Med Mol Morphol; 2008 Sep;41(3):175-8
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  • [Title] A rare case of coexistence of pulmonary adenocarcinoma with Langerhans' cell histiocytosis.
  • We report a rare case of coexisting pulmonary adenocarcinoma and Langerhans' cell histiocytosis (LCH) in a 78-year-old woman who did not smoke.
  • Before surgical resection, needle biopsy specimens confirmed the existence of adenocarcinoma.
  • The resected tumor in the left lower lobe was 3.0 x 1.8 x 3.0 cm, and histologically both acinar and bronchioloalveolar cell subtypes of adenocarcinoma were found in cancer foci.
  • In addition to pulmonary adenocarcinoma, Langerhans' cell proliferation associated with marked eosinophil infiltration was incidentally found in a small nodule, approximately 3 x 2 mm in size in the subpleural region.
  • Massive eosinophil infiltration was found around the focus of Langerhans' cell proliferation.
  • The adenocarcinoma and LCH were adjacent, and cancer cells were infiltrated only in the peripheral parts of LCH.
  • The coexistence of adenocarcinoma and LCH appeared to be incidental.
  • The association of adenocarcinoma and LCH is rare, and only several reports of it can be found in the English literature.
  • [MeSH-major] Adenocarcinoma. Histiocytosis, Langerhans-Cell. Lung Neoplasms

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  • [ISSN] 1860-1480
  • [Journal-full-title] Medical molecular morphology
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76. Pan W, Qu J, Chen T, Sun L, Qi J: FLIM and emission spectral analysis of caspase-3 activation inside single living cell during anticancer drug-induced cell death. Eur Biophys J; 2009 Apr;38(4):447-56
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  • [Title] FLIM and emission spectral analysis of caspase-3 activation inside single living cell during anticancer drug-induced cell death.
  • In this study, we use these two techniques to analyze caspase-3 activation inside single living cells during anticancer drug-induced human lung adenocarcinoma (ASTC-a-1) cell death.
  • TPE-ESI of SCAT3, a caspase-3 indicator based on FRET, was performed inside single living cell stably expressing SCAT3.
  • The emission peak at 526 nm disappeared and that of 476 nm increased after STS or bufalin treatment, but taxol treatment did not induce a significant change for the SCAT3 emission spectra, indicating that caspase-3 was activated during STS- or bufalin-induced cell apoptosis, but was not involved in taxol-induced PCD.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Bufanolides / pharmacology. Caspase 3 / metabolism. Cell Death / drug effects. Enzyme Activation. Paclitaxel / pharmacology
  • [MeSH-minor] Cell Line, Tumor. Cell Survival. Fluorescence Resonance Energy Transfer / methods. Green Fluorescent Proteins. Humans. Microscopy, Confocal. Microscopy, Fluorescence. Microscopy, Fluorescence, Multiphoton. Photobleaching. Staurosporine / pharmacology

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  • (PMID = 19132366.001).
  • [ISSN] 1432-1017
  • [Journal-full-title] European biophysics journal : EBJ
  • [ISO-abbreviation] Eur. Biophys. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Bufanolides; 0 / enhanced cyan fluorescent protein; 147336-22-9 / Green Fluorescent Proteins; EC 3.4.22.- / Caspase 3; H88EPA0A3N / Staurosporine; P88XT4IS4D / Paclitaxel; U549S98QLW / bufalin
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77. Lim KH, Huang MJ, Liu HC, Kuo HT, Tzen CY, Hsieh RK: Lack of prognostic value of EGFR mutations in primary resected non-small cell lung cancer. Med Oncol; 2007;24(4):388-93
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  • [Title] Lack of prognostic value of EGFR mutations in primary resected non-small cell lung cancer.
  • PURPOSE: To investigate the prognostic value of epidermal growth factor receptor (EGFR) mutations in a series of Taiwanese patients with primary resected lung adenocarcinomas never treated with epidermal growth factor receptor tyrosine kinase (TK) inhibitor.
  • All 27 patients underwent potentially curative pulmonary resection.
  • CONCLUSION: EGFR mutations do not have significant prognostic value in primary resected non-small cell lung cancer (NSCLC), and further well-designed large prospective studies are warranted to determine the prognostic value of EGFR mutations in NSCLC.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Biomarkers, Tumor / genetics. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Protein Kinase Inhibitors / therapeutic use. Receptor, Epidermal Growth Factor / genetics


78. Wang CC, Tsai MF, Hong TM, Chang GC, Chen CY, Yang WM, Chen JJ, Yang PC: The transcriptional factor YY1 upregulates the novel invasion suppressor HLJ1 expression and inhibits cancer cell invasion. Oncogene; 2005 Jun 9;24(25):4081-93
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  • [Title] The transcriptional factor YY1 upregulates the novel invasion suppressor HLJ1 expression and inhibits cancer cell invasion.
  • By using microarray and an invasion/metastasis lung cell line model, we identified the DnaJ-like heat shock protein 40, HLJ1, and found that the expression of HLJ1 correlates negatively with cancer cell invasion ability.
  • Overexpression of HLJ1 can suppress cancer cell invasion in vitro.
  • A serial deletion of the 1.2 kb at the 5'-flanking region of the human HLJ1 gene was subcloned into a vector containing reporter gene and transfected into human lung adenocarcinoma cell line CL1-0, followed by luciferase activity assay.
  • Furthermore, we also demonstrated that overexpression of YY1 in CL1-0 cells can increase HLJ1 expression and reduce cell invasive capability.
  • The reduction of cancer cell invasive ability is, at least in part, through upregulation of E-cadherin expression.
  • [MeSH-major] DNA-Binding Proteins / metabolism. Heat-Shock Proteins / genetics. Lung Neoplasms / genetics. Transcription Factors / metabolism
  • [MeSH-minor] 5' Untranslated Regions / genetics. Adenocarcinoma. Base Sequence. Cell Line, Tumor. Erythroid-Specific DNA-Binding Factors. Gene Expression Regulation, Neoplastic. HSP40 Heat-Shock Proteins. Humans. Molecular Sequence Data. Neoplasm Invasiveness. Neoplasm Metastasis / prevention & control. Promoter Regions, Genetic. RNA, Small Interfering / genetics. Repressor Proteins / metabolism. Tumor Suppressor Proteins / genetics. YY1 Transcription Factor

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  • (PMID = 15782117.001).
  • [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 / 5' Untranslated Regions; 0 / DNA-Binding Proteins; 0 / DNAJB4 protein, human; 0 / Erythroid-Specific DNA-Binding Factors; 0 / HSP40 Heat-Shock Proteins; 0 / Heat-Shock Proteins; 0 / RNA, Small Interfering; 0 / Repressor Proteins; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / YY1 Transcription Factor; 0 / YY1 protein, human
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79. De Las Heras M, Ortín A, Benito A, Summers C, Ferrer LM, Sharp JM: In-situ demonstration of mitogen-activated protein kinase Erk 1/2 signalling pathway in contagious respiratory tumours of sheep and goats. J Comp Pathol; 2006 Jul;135(1):1-10
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  • Ovine pulmonary adenocarcinoma (OPA) and enzootic nasal adenocarcinoma (ENA) are two contagious neoplastic diseases of secretory epithelial cells in the respiratory system of sheep and goats.
  • However, the cell signalling pathways activated in vivo are not completely understood.
  • This study was based on the use of activation stage antibodies specifically detecting proteins of the extracellular signal regulated kinase Erk 1/2 cell signalling pathway and transcription factors.
  • Tissue sections were collected from four natural cases of OPA, four experimentally induced OPA tumours, four ENA tumours in sheep, four ENA tumours in goats, two normal sheep lungs and two lungs with chronic inflammation.
  • [MeSH-major] Adenocarcinoma / veterinary. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Nose Neoplasms / enzymology. Nose Neoplasms / veterinary. Pulmonary Adenomatosis, Ovine / enzymology. Pulmonary Adenomatosis, Ovine / pathology. Signal Transduction


80. Yang M, Nonaka D: A study of immunohistochemical differential expression in pulmonary and mammary carcinomas. Mod Pathol; 2010 May;23(5):654-61
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  • [Title] A study of immunohistochemical differential expression in pulmonary and mammary carcinomas.
  • The risk of developing a second primary cancer is increased in patients with breast cancer, and the lung is one of the major sites involved.
  • Moreover, the lung is the major metastatic site for breast cancers.
  • A distinction between metastatic breast cancer and primary lung cancer can be histologically difficult, and both show an overlapping CK7+/CK20- immunoprofile in a majority of cases.
  • We investigated differential expressions of TTF-1, Napsin A, surfactant apoprotein A, estrogen receptor, GATA-3, mammaglobin, and GCDFP-15 immunostains in 197 pulmonary carcinomas (158 adenocarcinomas, 39 squamous) and 115 invasive mammary carcinomas (91 ductal, 24 lobular type).
  • All lung squamous cell carcinomas were negative for all markers studied.
  • TTF-1, Napsin A, and surfactant apoprotein A were positive in 80, 77, and 45% of pulmonary adenocarcinomas.
  • GCDFP-15 was focally expressed in 2.5% of pulmonary adenocarcinomas, and estrogen receptor was focally expressed in one case (1.2%) of pulmonary adenocarcinoma.
  • When metastasis from breast cancer is suspected in the lung, a combination of either estrogen receptor/mammaglobin or GATA-3/mammaglobin as breast markers, and a combination of TTF-1 and Napsin A as lung markers may be helpful for differentiating between the two.
  • Caution should be taken in the interpretation of GCDFP-15 due to its occasional expression in pulmonary adenocarcinomas.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor / metabolism. Breast Neoplasms / metabolism. Carcinoma, Squamous Cell / metabolism. Lung Neoplasms / metabolism. Neoplasms, Second Primary / metabolism
  • [MeSH-minor] Aspartic Acid Endopeptidases / metabolism. Diagnosis, Differential. Estrogen Receptor alpha / metabolism. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry

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  • (PMID = 20173733.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Estrogen Receptor alpha; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.- / NAPSA protein, human
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81. Zeng R, Zhou ZW, Wu CF, Zhou YL: [Reversal effect of aloe emodin liposomes on cisplatin resistance line A549/DDP human lung adenocarcinoma cells]. Zhongguo Zhong Yao Za Zhi; 2008 Jun;33(12):1443-5
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  • [Title] [Reversal effect of aloe emodin liposomes on cisplatin resistance line A549/DDP human lung adenocarcinoma cells].
  • OBJECTIVE: To determine the reversal effect of aloe emodin liposomes (AE-L) on cisplatin resistance human lung adenocarcinoma cell line A549/DDP.
  • RESULT: The maximum non-toxic concentration group of AE-L (2.0 mg x L(-1)) increased the sensitivity of cisplatin in A549/DDP, decreased IC50 of cisplatin in A549/DDP from 16.81 mg x L(-1) to 5.86 mg x L(-1), and the hyp-cytotoxic concentration (7.0 mg x L(-1) ) group's IC50 decreased to 4.34 mg x L(-1); AE-L groups significantly increased intracellular concentration of cisplatin in A549/DDP cells.
  • [MeSH-minor] Adenocarcinoma / pathology. Animals. Cell Line, Tumor. Drug Resistance, Multiple / drug effects. Humans. Inhibitory Concentration 50. Lethal Dose 50. Lung Neoplasms / pathology

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  • (PMID = 18837352.001).
  • [ISSN] 1001-5302
  • [Journal-full-title] Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica
  • [ISO-abbreviation] Zhongguo Zhong Yao Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Anthraquinones; 0 / Liposomes; C8IYT9CR7C / aloe emodin; Q20Q21Q62J / Cisplatin
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82. Cao W, Zhang D, Qiao J, Fang C, Hou R: [Expression and its significance of Pin1 and β-catenin in squamous cell carcinoma and adenocarcinoma of the lung]. Zhongguo Fei Ai Za Zhi; 2006 Oct 20;9(5):418-22
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  • [Title] [Expression and its significance of Pin1 and β-catenin in squamous cell carcinoma and adenocarcinoma of the lung].
  • The aim of this study is to explore the relationship between the expression of Pin1 and clinicopathological factors in squamous cell carcinoma and adenocarcinoma of the lung, and to analyze the correlation between Pin1 and β-catenin.
  • METHODS: The expression of Pin1 and β-catenin proteins was detected in 69 lung cancer cases by immunohistochemical SP method, and in 30 fresh lung samples by Western blot.
  • RESULTS: Immunohistochemically, the overexpression of Pin1 and β-catenin in lung cancer was 78.3% (54/69) and 63.8% (44/69), respectively.
  • Western blot results showed that the expression of Pin1 and β-catenin in lung cancer tissues was significantly higher than that of paracancerous lung tissues (P < 0.05).
  • CONCLUSIONS: Pin1 is overexpressed in squamous cell carcinoma and adenocarcinoma of the lung and may play a critical role in oncogenesis of lung cancer.

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  • (PMID = 21176462.001).
  • [ISSN] 1009-3419
  • [Journal-full-title] Zhongguo fei ai za zhi = Chinese journal of lung cancer
  • [ISO-abbreviation] Zhongguo Fei Ai Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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83. Aribi A, Kantarjian HM, Estey EH, Koller CA, Thomas DA, Kornblau SM, Faderl SH, Laddie NM, Garcia-Manero G, Cortes JE: Combination therapy with arsenic trioxide, all-trans retinoic acid, and gemtuzumab ozogamicin in recurrent acute promyelocytic leukemia. Cancer; 2007 Apr 1;109(7):1355-9
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  • Two patients died, 1 secondary to a complication of metastatic lung adenocarcinoma, and the other of sepsis.

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  • [Copyright] (c) 2007 American Cancer Society.
  • (PMID = 17326049.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Arsenicals; 0 / Oxides; 0 / gemtuzumab; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
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84. Nishimura T, Nomura M, Tojo H, Hamasaki H, Fukuda T, Fujii K, Mikami S, Bando Y, Kato H: Proteomic analysis of laser-microdissected paraffin-embedded tissues: (2) MRM assay for stage-related proteins upon non-metastatic lung adenocarcinoma. J Proteomics; 2010 Apr 18;73(6):1100-10
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  • [Title] Proteomic analysis of laser-microdissected paraffin-embedded tissues: (2) MRM assay for stage-related proteins upon non-metastatic lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / diagnosis. Lung Neoplasms / diagnosis. Microdissection. Proteomics / methods

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  • [Copyright] Copyright 2009 Elsevier B.V. All rights reserved.
  • (PMID = 19944198.001).
  • [ISSN] 1876-7737
  • [Journal-full-title] Journal of proteomics
  • [ISO-abbreviation] J Proteomics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Proteome; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.- / NAPSA protein, human
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85. Yamamoto S, Tanaka H, Takeo H, Yasuda K, Mastukuma S: Primary pulmonary choriocarcinoma combined with adenocarcinoma. Pathol Int; 2006 Jul;56(7):402-7
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  • [Title] Primary pulmonary choriocarcinoma combined with adenocarcinoma.
  • An extremely rare autopsy case of primary pulmonary choriocarcinoma combined with adenocarcinomatous components in a 77-year-old Japanese man is described.
  • The patient died of rapidly progressive respiratory dysfunction without ante-mortem diagnosis.
  • Autopsy revealed necro-hemorrhagic areas of the primary lung tumor with a typical biphasic pattern of choriocarcinoma.
  • Topographical analysis suggested that moderately to poorly differentiated adenocarcinoma components partially surrounded the choriocarcinomatous components.
  • The present case suggests that primary lung choriocarcinoma can occur closely related to conventional pulmonary adenocarcinoma, although collision tumor was not completely ruled out.
  • [MeSH-major] Adenocarcinoma / pathology. Choriocarcinoma / pathology. Lung Neoplasms / pathology. Neoplasms, Multiple Primary / pathology

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  • (PMID = 16792550.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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86. Wang H, Huang S, Shou J, Su EW, Onyia JE, Liao B, Li S: Comparative analysis and integrative classification of NCI60 cell lines and primary tumors using gene expression profiling data. BMC Genomics; 2006;7:166
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  • [Title] Comparative analysis and integrative classification of NCI60 cell lines and primary tumors using gene expression profiling data.
  • BACKGROUND: NCI60 cell lines are derived from cancers of 9 tissue origins and have been invaluable in vitro models for cancer research and anti-cancer drug screen.
  • Although extensive studies have been carried out to assess the molecular features of NCI60 cell lines related to cancer and their sensitivities to more than 100,000 chemical compounds, it remains unclear if and how well these cell lines represent or model their tumor tissues of origin.
  • Identification and confirmation of correct origins of NCI60 cell lines are critical to their usage as model systems and to translate in vitro studies into clinical potentials.
  • Here we report a direct comparison between NCI60 cell lines and primary tumors by analyzing global gene expression profiles.
  • RESULTS: Comparative analysis suggested that 51 of 59 cell lines we analyzed represent their presumed tumors of origin.
  • Taking advantage of available clinical information of primary tumor samples used to generate gene expression profiling data, we further classified those cell lines with the correct origins into different subtypes of cancer or different stages in cancer development.
  • For example, 6 of 7 non-small cell lung cancer cell lines were classified as lung adenocarcinomas and all of them were classified into late stages in tumor progression.
  • CONCLUSION: Taken together, we developed and applied a novel approach for systematic comparative analysis and integrative classification of NCI60 cell lines and primary tumors.
  • Our results could provide guidance to the selection of appropriate cell lines for cancer research and pharmaceutical compound screenings.
  • Moreover, this gene expression profile based approach can be generally applied to evaluate experimental model systems such as cell lines and animal models for human diseases.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Cell Line, Tumor. Central Nervous System Neoplasms / genetics. Gene Expression Regulation. Leukemia / genetics. Lung Neoplasms / genetics

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  • (PMID = 16817967.001).
  • [ISSN] 1471-2164
  • [Journal-full-title] BMC genomics
  • [ISO-abbreviation] BMC Genomics
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
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  • [Other-IDs] NLM/ PMC1525183
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87. Jacoby JJ, Erez B, Korshunova MV, Williams RR, Furutani K, Takahashi O, Kirkpatrick L, Lippman SM, Powis G, O'Reilly MS, Herbst RS: Treatment with HIF-1alpha antagonist PX-478 inhibits progression and spread of orthotopic human small cell lung cancer and lung adenocarcinoma in mice. J Thorac Oncol; 2010 Jul;5(7):940-9
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  • [Title] Treatment with HIF-1alpha antagonist PX-478 inhibits progression and spread of orthotopic human small cell lung cancer and lung adenocarcinoma in mice.
  • In prior preclinical studies, it had antitumor activity against various solid tumors in subcutaneous xenografts but had no measurable activity against a non-small cell lung cancer (NSCLC) xenograft.
  • To determine the effectiveness of PX-478 against lung tumors, we investigated HIF-1alpha expression in several lung cancer cell lines, both in vitro and in vivo, and treated orthotopic mouse models of human lung cancer with PX-478.
  • METHODS: Cells from two human lung adenocarcinoma cell models (PC14-PE6 and NCI-H441) or two human small cell lung cancer (SCLC) models (NCI-H187 and NCI-N417) were injected into the left lungs of nude mice and were randomized 16 to 18 days after injection with daily oral treatment with PX-478 or vehicle for 5 days.
  • RESULTS: In the PC14-PE6 NSCLC model, treatment with 20 mg/kg PX-478 significantly reduced the median primary lung tumor volume by 87% (p = 0.005) compared with the vehicle-treated group.
  • In the NCI-H187 model, the median primary lung tumor volume was reduced by 99% (p = 0.0001).
  • In the NCI-N417 model, the median primary lung tumor volume was reduced by 97% (p = 0.008).
  • CONCLUSIONS: We demonstrated that the PX-478, HIF-1alpha inhibitor, had significant antitumor activity against two orthotopic models of lung adenocarcinomas and two models of SCLC.
  • These results suggest the inclusion of lung cancer patients in phase I clinical trials of PX-478.

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  • (PMID = 20512076.001).
  • [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 / CA098920-08; United States / NCI NIH HHS / CA / R01 CA098920; United States / NCI NIH HHS / CA / P01 CA017094; United States / NCI NIH HHS / CA / P01-CA017094; United States / NCI NIH HHS / CA / R01 CA098920-08; United States / NCI NIH HHS / CA / R01-CA098920
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-amino-3-(4'-N,N-bis(2-chloroethyl)amino)phenylpropionic acid N-oxide; 0 / Hif1a protein, mouse; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Mustard Compounds; 0 / Phenylpropionates
  • [Other-IDs] NLM/ NIHMS263343; NLM/ PMC3782111
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88. Ricketts R, Tamboli P, Czerniak B, Guo CC: Tumor-to-tumor metastasis: report of 2 cases of metastatic carcinoma to angiomyolipoma of the kidney. Arch Pathol Lab Med; 2008 Jun;132(6):1016-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Renal cell carcinoma is the most common recipient of tumor-to-tumor metastasis in malignant tumors.
  • In one case, the donor tumor originated from neuroendocrine carcinoma of the pancreas, and in the other case the donor tumor was from adenocarcinoma of the lung.
  • An awareness of this phenomenon is important to avoid an incorrect diagnosis when encountering unusual morphologic features in renal angiomyolipoma.
  • [MeSH-minor] Adenocarcinoma / pathology. Aged. Carcinoma, Neuroendocrine / pathology. Humans. Immunohistochemistry. Lung Neoplasms / pathology. Male. Middle Aged. Pancreatic Neoplasms / pathology

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  • (PMID = 18517262.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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89. 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

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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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90. Sholl LM, Yeap BY, Iafrate AJ, Holmes-Tisch AJ, Chou YP, Wu MT, Goan YG, Su L, Benedettini E, Yu J, Loda M, Jänne PA, Christiani DC, Chirieac LR: Lung adenocarcinoma with EGFR amplification has distinct clinicopathologic and molecular features in never-smokers. Cancer Res; 2009 Nov 1;69(21):8341-8
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  • [Title] Lung adenocarcinoma with EGFR amplification has distinct clinicopathologic and molecular features in never-smokers.
  • In a subset of lung adenocarcinomas, the epidermal growth factor receptor (EGFR) is activated by kinase domain mutations and/or gene amplification, but the interaction between the two types of abnormalities is complex and unclear.
  • For this study, we selected 99 consecutive never-smoking women of East Asian origin with lung adenocarcinomas that were characterized by histologic subtype.
  • Lung adenocarcinomas with EGFR amplification had significantly more EGFR exon 19 deletion mutations than adenocarcinomas with disomy, and low and high polysomy (100% versus 54%, P = 0.009).
  • EGFR amplification was focally distributed in lung cancer specimens, mostly in regions with solid histology.
  • Lung adenocarcinomas with EGFR amplification have a unique association with exon 19 deletion mutations and show distinct clinicopathologic features associated with a significantly worsened prognosis.