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1. Brueckl WM, Schoeberl A, Wirtz RM, Murray S, Hahn EG, Wiest GH: Increased vascular-endothelial growth factor (VEGF) tumor expression and response to epidermal growth factor receptor (EGF-R) inhibitor erlotinib in non-small cell lung cancer (NSCLC). J Thorac Oncol; 2008 Mar;3(3):314-6
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  • [Title] Increased vascular-endothelial growth factor (VEGF) tumor expression and response to epidermal growth factor receptor (EGF-R) inhibitor erlotinib in non-small cell lung cancer (NSCLC).
  • A 37-year-old female never smoker with metastatic large cell carcinoma of the lung had a partial response to a second line palliative therapy with the EGF-R tyrosine kinase inhibitor erlotinib after platinum based first line therapy failed.
  • To our knowledge, this is the first report about a high vascular-endothelial growth factor-A expression in the tumor of a patient responding to an EGF-R inhibitor postulating that there might be a link between both tyrosine kinase pathways.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / metabolism. DNA, Neoplasm / genetics. Gene Expression Regulation, Neoplastic / drug effects. Lung Neoplasms / metabolism. Quinazolines / therapeutic use. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Vascular Endothelial Growth Factor A / genetics
  • [MeSH-minor] Adult. Erlotinib Hydrochloride. Fatal Outcome. Female. Follow-Up Studies. Humans. Liver Neoplasms / diagnosis. Liver Neoplasms / metabolism. Liver Neoplasms / secondary. Mutation. Protein Kinase Inhibitors / therapeutic use. Retrospective Studies

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  • (PMID = 18317076.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; 0 / Vascular Endothelial Growth Factor A; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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2. Tokat AO, Yüksel C, Ozdemir Kumbasar O, Güngör A: [Association of combined small cell and large cell lung cancer with Lambert-Eaton myasthenic syndrome: case report]. Tuberk Toraks; 2005;53(2):177-80
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  • [Title] [Association of combined small cell and large cell lung cancer with Lambert-Eaton myasthenic syndrome: case report].
  • Lambert-Eaton myasthenic syndrome (LEMS) is a rare type of neuromusculer conduction disorder.
  • This disease can be seen with lung cancer and, it is associated with otoimmunity.
  • Among the symptoms of lung cancer LEMS can be seen, but it is very rare.
  • In this case, LEMS symptoms were analyzed before lung cancer symptoms.
  • [MeSH-major] Lambert-Eaton Myasthenic Syndrome / diagnosis
  • [MeSH-minor] Aged. Carcinoma, Large Cell / complications. Carcinoma, Large Cell / diagnosis. Carcinoma, Large Cell / pathology. Carcinoma, Large Cell / radiography. Carcinoma, Small Cell / complications. Carcinoma, Small Cell / diagnosis. Carcinoma, Small Cell / pathology. Carcinoma, Small Cell / radiography. Diagnosis, Differential. Humans. Lung Neoplasms / complications. Lung Neoplasms / diagnosis. Lung Neoplasms / pathology. Lung Neoplasms / radiography. Male. Neoplasms, Multiple Primary / complications. Neoplasms, Multiple Primary / diagnosis. Neoplasms, Multiple Primary / pathology. Neoplasms, Multiple Primary / radiography


3. Ceppi P, Volante M, Ferrero A, Righi L, Rapa I, Rosas R, Berruti A, Dogliotti L, Scagliotti GV, Papotti M: Thymidylate synthase expression in gastroenteropancreatic and pulmonary neuroendocrine tumors. Clin Cancer Res; 2008 Feb 15;14(4):1059-64
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  • EXPERIMENTAL DESIGN: A series of 116 NETs were collected, including 58 gastroenteropancreatic (GEP) and 58 lung NETs.
  • RESULTS: By means of both quantification by real-time PCR and immunohistochemistry, a higher TS expression in pulmonary small cell lung cancer and large cell NEC compared with typical and atypical carcinoids was observed (P < 0.01).
  • [MeSH-major] Digestive System Neoplasms / enzymology. Drug Resistance, Neoplasm / physiology. Lung Neoplasms / enzymology. Neuroendocrine Tumors / enzymology. Thymidylate Synthase / biosynthesis

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  • (PMID = 18281538.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / RNA, Messenger; EC 2.1.1.45 / Thymidylate Synthase; U3P01618RT / Fluorouracil
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4. Califano L, Sanguedolce F, Staibano S, Pannone G, Tortorella S, Serpico R, Lo Muzio L, Bufo P: Large oral soft tissue metastasis from anaplastic carcinoma of the lung mimicking a primitive malignancy: case report and brief review of the literature. Minerva Stomatol; 2008 Sep;57(9):447-51
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  • [Title] Large oral soft tissue metastasis from anaplastic carcinoma of the lung mimicking a primitive malignancy: case report and brief review of the literature.
  • We describe a case of anaplastic carcinoma of the lung in a 60-year-old man, presenting a huge oral metastasis as the first sign of his primitive lung malignancy.
  • Clinically, the oral lesion mimicked a high-grade primitive carcinoma of the oral cavity.
  • The biopsy established the gingival metastasis from lung cancer which was confirmed by a fine-needle aspiration cytology examination.
  • We report an uncommon case of metastatic lung carcinoma to the gingiva emphasizing the differential diagnosis between primary and metastatic tumours; a short discussion on the pathways of metastatization to oral cavity soft tissues, as well as brief review of the literature are also presented.
  • [MeSH-major] Carcinoma / prevention & control. Lung Neoplasms / pathology. Mouth Neoplasms / secondary. Soft Tissue Neoplasms / secondary
  • [MeSH-minor] Diagnosis, Differential. Humans. Male. Middle Aged

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  • (PMID = 18923379.001).
  • [ISSN] 0026-4970
  • [Journal-full-title] Minerva stomatologica
  • [ISO-abbreviation] Minerva Stomatol
  • [Language] eng; ita
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 8
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5. Liu LY, Zhang WZ, Guan J, Tong WC, Cai SX, Shen XB, Hou CC: [Lung cancer in pregnancy: report of two cases and review of literature]. Zhonghua Jie He He Hu Xi Za Zhi; 2010 Nov;33(11):844-8
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  • [Title] [Lung cancer in pregnancy: report of two cases and review of literature].
  • OBJECTIVE: to raise awareness about lung cancer in pregnancy.
  • METHODS: the clinical presentations, diagnosis and treatment of 2 cases of lung cancer in pregnancy were reported, and related literatures were reviewed.
  • Biopsy of the right-supraclavicular lymph node was performed simultaneously, and histopathological examination showed metastatic large cell lung cancer.
  • PET showed right lung cancer with metastases to the pericardium, right pleura, liver and pelvic cavity.
  • Bronchoscopic biopsy showed small-cell lung cancer.
  • CONCLUSIONS: lung cancer in pregnancy is a rare condition with poor prognosis.
  • [MeSH-major] Lung Neoplasms / diagnosis. Pregnancy Complications, Neoplastic / diagnosis

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  • (PMID = 21211373.001).
  • [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] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] China
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6. Hasegawa S, Suda T, Negi K, Hattori Y: Lung large cell carcinoma producing granulocyte-colony-stimulating factor. Ann Thorac Surg; 2007 Jan;83(1):308-10
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  • [Title] Lung large cell carcinoma producing granulocyte-colony-stimulating factor.
  • In recent years, tumors producing granulocyte-colony-stimulating factor have been reported in an increasing number of patients, the majority of which have lung cancer.
  • We experience a case of lung carcinoma producing granulocyte-colony-stimulating factor treated by resection and chemotherapy.
  • He remains well 2 years and 10 months after surgery, with no recurrence of the carcinoma.
  • [MeSH-major] Carcinoma, Large Cell / metabolism. Granulocyte Colony-Stimulating Factor / biosynthesis. Lung Neoplasms / metabolism

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  • (PMID = 17184692.001).
  • [ISSN] 1552-6259
  • [Journal-full-title] The Annals of thoracic surgery
  • [ISO-abbreviation] Ann. Thorac. Surg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor
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7. Lv H, Yan H, Wang M, Li Y, Wan H, Liu H, Wu H, Zhou Q: [Methylation profile difference in human high-metastatic large cell lung cancer cell line L9981 and low-metastatic large cell lung cancer line NL9980]. Zhongguo Fei Ai Za Zhi; 2010 Aug;13(8):763-8
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  • [Title] [Methylation profile difference in human high-metastatic large cell lung cancer cell line L9981 and low-metastatic large cell lung cancer line NL9980].
  • BACKGROUND AND OBJECTIVE: Invasion and metastasis is one of malignant phenotype of lung cancer and the important cause of the death of lung cancer patients.
  • The aim of this study is to explore the methylation profile difference in different metastatic potential cell lines.
  • METHODS: To compare the DNA methylation profile of two large cell lung cancer cell lines with different metastatic potential by MeIP chip hybridization, hypermethylated and hypomethylated genes of L9981 cell lines were analyzed online in NIH-DAVID, KEGG and MILANO webside.
  • RESULTS: Compared with NL9980 cell line, 735 genes are hypermethylated in L9981, including 656 known genes and 79 unknown genes; 809 gene are hypermethylated in L9981, including 698 known genes and 111 unknown genes; the different genes are involved in cell process, signal transduction, cell communication, cell adhesion, cell motility, and angiogenesis.
  • CONCLUSION: Hypermethylation of suppressor genes and negative regulator of signal transduction and hopomethylation of oncogene and cell adhesion molecules (CAMs) in L9981 may promote metastasis of tumor cells.
  • [MeSH-major] Carcinoma, Large Cell / metabolism. DNA Methylation. Lung Neoplasms / metabolism
  • [MeSH-minor] Cell Line, Tumor. Humans. Neoplasm Metastasis

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  • (PMID = 20704814.001).
  • [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] Comparative Study; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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8. Naranjo Gómez JM, Gómez Román JJ: Behaviour and survival of high-grade neuroendocrine carcinomas of the lung. Respir Med; 2010 Dec;104(12):1929-36
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  • [Title] Behaviour and survival of high-grade neuroendocrine carcinomas of the lung.
  • INTRODUCTION: Large-cell neuroendocrine carcinoma is an aggressive variant of large-cell carcinoma of the lung, which has poor survival in most series, resembling that of small-cell lung carcinoma.
  • METHODS: 33 large-cell neuroendocrine carcinomas and 16 peripheral small-cell lung carcinomas were reassessed retrospectively.
  • RESULTS: In large-cell neuroendocrine carcinomas, there were 25 patients with pathologic stage I, 4 with pathologic stage II and 4 with pathologic stage III.
  • In small-cell lung carcinomas, there were 6 patients with pathologic stage I, 3 with pathologic stage II and 7 with pathologic stage III.
  • 12% of large-cell neuroendocrine carcinomas and 62.5% of small-cell lung carcinomas were of advanced disease.
  • CONCLUSION: Large-cell neuroendocrine carcinomas of the lung have poor prognosis even in early stages, with survival rates similar to that of small-cell lung carcinomas.
  • [MeSH-major] Carcinoma, Large Cell / pathology. Carcinoma, Neuroendocrine / pathology. Lung Neoplasms / pathology

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20810262.001).
  • [ISSN] 1532-3064
  • [Journal-full-title] Respiratory medicine
  • [ISO-abbreviation] Respir Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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9. Meyronet D, Massoma P, Thivolet F, Chalabreysse L, Rogemond V, Schlama A, Honnorat J, Thomasset N: Extensive expression of collapsin response mediator protein 5 (CRMP5) is a specific marker of high-grade lung neuroendocrine carcinoma. Am J Surg Pathol; 2008 Nov;32(11):1699-708
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  • [Title] Extensive expression of collapsin response mediator protein 5 (CRMP5) is a specific marker of high-grade lung neuroendocrine carcinoma.
  • The diagnosis of high-grade neuroendocrine tumors has strong clinical relevance because it identifies patients at higher risk of an unfavorable outcome who should receive multimodal treatment.
  • However, these tumors can be mistaken for poorly differentiated nonsmall cell carcinoma or carcinoid lung tumors.
  • In fact, no immunohistochemical marker can currently distinguish between histologic lung subtypes.
  • Because the collapsin response mediator protein (CRMP) family is involved in an autoimmune disease associated with small cell lung carcinoma, we explored the relationship between CRMP5 expression and lung tumor behavior.
  • Using World Health Organization morphologic criteria, 123 lung neuroendocrine tumors and 41 randomly selected non-neuroendocrine tumors were classified.
  • CRMP5 protein expression in tumors, metastases, and healthy lung tissue was assessed using immunostaining method.
  • Strong and extensive CRMP5 expression was seen in 98.6% of high-grade neuroendocrine lung tumors, including small cell lung carcinoma and large cell lung neuroendocrine carcinoma, but not in any of the squamous cell carcinomas or lung adenocarcinomas in our series.
  • In contrast, the majority of low-grade neuroendocrine lung tumors were negative for CRMP5 staining, although weak CRMP5 expression was seen in some, with 2 different staining patterns of either scattered positive cells or small foci of positive cells.
  • Our findings point at CRMP5 as a novel marker for routine pathologic evaluation of lung tumors surgical samples in distinguishing between highly aggressive neuroendocrine carcinoma and the other lung cancers.
  • [MeSH-major] Biomarkers, Tumor / analysis. Carcinoma, Neuroendocrine / metabolism. Carcinoma, Neuroendocrine / pathology. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Nerve Tissue Proteins / biosynthesis

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  • (PMID = 18769332.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DPYSL5 protein, human; 0 / Nerve Tissue Proteins
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10. Nie Q, Zhu W, Liu L, Fu J, Li D, Li Y, Chen J, Wu Z, Zhou Q: [The variation of intracellular distribution and translocation of the protein kinase C alpha among human lung cancer cell line with different metastasis potential.]. Zhongguo Fei Ai Za Zhi; 2008 Jun 20;11(3):363-7
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  • [Title] [The variation of intracellular distribution and translocation of the protein kinase C alpha among human lung cancer cell line with different metastasis potential.].
  • BACKGROUND: Protein Kinase C (PKC) is one of the key kinases in the cell signal transduction passway.
  • There are more reports about it's ability on cell proliferation, but fewer on invasion and metastasis in the past; and it's mechanisms are unclear.
  • The aim of this study is to analyze the variation of intracellular distribution and translocation of the protein kinase C alpha among human high-metastatic large cell lung cancer cell line with different metastasis potential,in order to investigate the correlation between the lung carcinoma invasion and metastasis and the PKC isoforms.
  • The distribution of PKC alpha in cytosol and plasma membrane and translocation were detected among different metastatic potential human pulmonary carcinoma cells L9981, L9981-pLXSN and L9981-nm23-H1 before and after treatment with PKC inhibitor Calphostin C, by Western blot and LSCM.
  • RESULTS: PKC alpha in L9981 and L9981- pLXSN was mainly expressed on membrane, which was remarkably higher than those in L9981-nm23-H1 cell line (P =0.001); while expression of PKC alpha in cytoslol in L9981 and L9981-pLXSN cell lines, was lower than those in L9981-nm23-H1 cell line (P <0.001).
  • The expression of PKC alpha in cytosol in L9981-nm23-H1 cell line was remarkably higher than those in L9981 and L9981-pLXSN cell lines (P <0.001), while expression of PKC alpha in plasma membrane in L9981-nm23-H1 cell line, was significantly lower than those in L9981 and L9981- pLXSN cell lines (P =0.001).
  • PKC alpha is mainly located in nucleus and perinucleus in L9981 and L9981-pLXSN cells, which was in active status, In L9981-nm23-H1 cell line, PKC alpha is mainly located in soluble cytosolic section, which was in inactive status.
  • After treated with PKC inhibitor Calphostin C, the expression of PKC alpha in membrane in L9981, L9981-pLXSN and L9981-nm23-H1 was downregulated, and PKC alpha were observed mainly located in cytosolic site in all the three cell lines, which was mainly in inactive status.
  • CONCLUSIONS: The study suggests that PKC isoforms is closely correlated with human lung cancer invasion and metastasis.

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  • (PMID = 20731935.001).
  • [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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11. Meng Q, Lux A, Holloschi A, Li J, Hughes JM, Foerg T, McCarthy JE, Heagerty AM, Kioschis P, Hafner M, Garland JM: Identification of Tctex2beta, a novel dynein light chain family member that interacts with different transforming growth factor-beta receptors. J Biol Chem; 2006 Dec 01;281(48):37069-80
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  • Endoglin is a membrane-inserted protein that is preferentially synthesized in angiogenic vascular endothelial and smooth muscle cells.
  • Although endoglin is known to affect cell responses to TGF-beta, its mode of action is largely unknown.
  • We performed yeast two-hybrid screening of a human placental cDNA library and isolated a new endoglin-binding partner, a novel 221-amino acid member of the Tctex1/2 family of cytoplasmic dynein light chains named Tctex2beta, as the founder of a new Tctex1/2 subfamily.
  • Reverse transcription-PCR showed expression of Tctex2beta in a wide range of tissues, including vascular endothelial and smooth muscle cells, placenta, and testis, as well as in several tumor cell lines.
  • High expression levels were found in human umbilical vein endothelial cells and the large cell lung cancer cell line.
  • [MeSH-minor] Amino Acid Sequence. Animals. Base Sequence. Bone Morphogenetic Protein Receptors, Type II / metabolism. COS Cells. Cercopithecus aethiops. Dyneins. Humans. Mice. Mink. Molecular Sequence Data. NIH 3T3 Cells. Phylogeny. Protein Binding. Sequence Homology, Amino Acid. t-Complex Genome Region

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  • (PMID = 16982625.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ DQ132441
  • [Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / / BBS/B/02436; United Kingdom / Medical Research Council / / G0900414
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Drosophila Proteins; 0 / Dynlt1b protein, mouse; 0 / Microtubule-Associated Proteins; 0 / Nuclear Proteins; 0 / Receptors, Transforming Growth Factor beta; EC 2.7.11.30 / Bone Morphogenetic Protein Receptors, Type II; EC 3.6.4.2 / Dyneins
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12. Molina JR, Yang P, Cassivi SD, Schild SE, Adjei AA: Non-small cell lung cancer: epidemiology, risk factors, treatment, and survivorship. Mayo Clin Proc; 2008 May;83(5):584-94
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  • [Title] Non-small cell lung cancer: epidemiology, risk factors, treatment, and survivorship.
  • Lung cancer is the leading cause of cancer-related mortality not only in the United States but also around the world.
  • In North America, lung cancer has become more predominant among former than current smokers.
  • Yet in some countries, such as China, which has experienced a dramatic increase in the cigarette smoking rate during the past 2 decades, a peak in lung cancer incidence is still expected.
  • Non-small cell lung cancer accounts for 85% of all lung cancer cases in the United States.
  • After the initial diagnosis, accurate staging of non-small cell lung cancer using computed tomography or positron emission tomography is crucial for determining appropriate therapy.
  • However, close to 70% of patients with lung cancer present with locally advanced or metastatic disease at the time of diagnosis.
  • Chemotherapy is beneficial for patients with metastatic disease, and the administration of concurrent chemotherapy and radiation is indicated for stage III lung cancer.
  • The introduction of angiogenesis, epidermal growth factor receptor inhibitors, and other new anti-cancer agents is changing the present and future of this disease and will certainly increase the number of lung cancer survivors.
  • Key terms used for this search included non-small cell lung cancer, adenocarcinoma, squamous cell carcinoma, bronchioalveolar cell carcinoma, large cell carcinoma, lung cancer epidemiology, genetics, survivorship, surgery, radiation therapy, chemotherapy, targeted therapy, bevacizumab, erlotinib, and epidermal growth factor receptor.

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  • (PMID = 18452692.001).
  • [ISSN] 1942-5546
  • [Journal-full-title] Mayo Clinic proceedings
  • [ISO-abbreviation] Mayo Clin. Proc.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA090628-08; United States / NCI NIH HHS / CA / K12 CA090628; United States / NCI NIH HHS / CA / K12 CA090628-08
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Quinazolines; 0 / Tobacco Smoke Pollution; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
  • [Number-of-references] 115
  • [Other-IDs] NLM/ NIHMS121782; NLM/ PMC2718421
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13. Katano H, Sato Y, Hoshino S, Tachikawa N, Oka S, Morishita Y, Ishida T, Watanabe T, Rom WN, Mori S, Sata T, Weiden MD, Hoshino Y: Integration of HIV-1 caused STAT3-associated B cell lymphoma in an AIDS patient. Microbes Infect; 2007 Nov-Dec;9(14-15):1581-9
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  • [Title] Integration of HIV-1 caused STAT3-associated B cell lymphoma in an AIDS patient.
  • High expression of STAT3 has also been implicated in cancer and lymphoma.
  • Here, we show a case of B cell lymphoma in which a defective human immunodeficiency virus 1 (HIV-1) integrated upstream of the first STAT3 coding exon.
  • The lymphoma cells with anaplastic large cell morphology formed multiple nodular lesions in the lung of an acquired immunodeficiency syndrome (AIDS) patient with Kaposi's sarcoma.
  • Immunohistochemistry showed increased expression of STAT3 in the nuclei of lymphoma cells.
  • Transfection of STAT3 resulted in transient cell proliferation in primary B cells in vitro.
  • Although this is a very rare case of HIV-1-integrated lymphoma, these data suggest that up-regulation of STAT3 caused by HIV-1 integration resulted in the development of B cell lymphoma in this special case.

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  • (PMID = 18024124.001).
  • [ISSN] 1286-4579
  • [Journal-full-title] Microbes and infection
  • [ISO-abbreviation] Microbes Infect.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / M01 RR000096; United States / NIDA NIH HHS / DA / R21 DA022162-02; United States / NCRR NIH HHS / RR / MO1 RR00096; United States / NIDA NIH HHS / DA / R21 DA022162-01; United States / NIDA NIH HHS / DA / DA022162; United States / NIDA NIH HHS / DA / DA022162-01; United States / NHLBI NIH HHS / HL / HL 59832; United States / NHLBI NIH HHS / HL / R01 HL059832; United States / NIDA NIH HHS / DA / DA022162-02; United States / NIDA NIH HHS / DA / R21 DA022162; United States / NHLBI NIH HHS / HL / HL57879; United States / NHLBI NIH HHS / HL / R01 HL057879
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / DNA, Viral; 0 / STAT3 Transcription Factor
  • [Other-IDs] NLM/ NIHMS36353; NLM/ PMC2200298
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14. Nie Q, Zhu W, Liu L, Fu J, Li D, Li Y, Chen J, Liu H, Zhou Q: [The mechanism and influence on the biological behavior of human high-metastatic large cell lung cancer cell lines with transfection of nm23-H1 gene.]. Zhongguo Fei Ai Za Zhi; 2008 Jun 20;11(3):349-53
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  • [Title] [The mechanism and influence on the biological behavior of human high-metastatic large cell lung cancer cell lines with transfection of nm23-H1 gene.].
  • The aim of this study is to compare the biological behavior changes among three human high-metastatic large cell lung cancer cell lines which transfected and untransfected nm23-H1 gene, and to study the mechanism of nm23-H1 gene supressing the metastasis.
  • METHODS: Boyden Chamber and MTT method were used to detect the rates of invasion and proliferation among different human pulmonary carcinoma cells of transfected and untransfected nm23-H1 gene; meanwhile The three lung cancer cell lines were treated with PKC inhibitor Calphostin C, and the above measurements were also performed.
  • RESULTS: The ability of invasion and proliferation of L9981 and L9981-PLXSN human high-metastatic large cell lung cancer cells,which lack of nm23-H1gene, was higher than that of L9981-nm23-H1 human high-metastatic large cell line, which transfected with nm23-H1gene (P <0.001).
  • There was no difference beteween L9981 and L9981-PLXSN cell lines (P >0.05).
  • After treated with PKC inhibitor Calphstin C,the invasion and proliferation ability of three lung cancer cell lines were obviously go down (P <0.001), however, the invasion and proliferation ability of L9981-nm23-H1 lung cancer cell line was still lower than those of L9981 and L9981-PLXSN lung cancer cell lines (P <0.001), and there was also no significant difference between two later cell lines (P >0.05).
  • CONCLUSIONS: Our data suggest that nm23-H1 gene can significantly inhibit the cell proliferation and invasion in L9981 lung cancer line.
  • The effect of nm23-H1 might be correlated with downregulation of PKC signal transduction in human high-metastatic large cell lung cancer cell line.

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  • (PMID = 20731932.001).
  • [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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15. Liao HT, Chien CH, Chen CH, Wang HP, Huang DF: Recurrent autoimmune inner ear disease (AIED) and polyarteritis nodosa in a patient with large cell lung carcinoma. Clin Rheumatol; 2007 Jun;26(6):1008-10
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  • [Title] Recurrent autoimmune inner ear disease (AIED) and polyarteritis nodosa in a patient with large cell lung carcinoma.
  • Autoimmune inner ear disease (AIED) is a very rare disorder with distinct clinical features and can occur in patients with malignancy or autoimmune diseases.
  • During the period of treatment, three episodes of AIED occurred, and eventually, lung cancer developed.
  • From the time relationship and clinical manifestations of neuropathy and livedo reticularis, the first episode of hearing loss was more likely to be related to vasculitis itself, while the third episode may well have been associated with the development of lung cancer given the dramatic improvement in the clinical condition following treatment of the tumor by excision and cancer chemotherapy.
  • [MeSH-major] Autoimmune Diseases / complications. Carcinoma, Large Cell / complications. Carcinoma, Non-Small-Cell Lung / complications. Labyrinth Diseases / immunology. Lung Neoplasms / complications. Polyarteritis Nodosa / complications


16. Fukazawa T, Maeda Y, Durbin ML, Nakai T, Matsuoka J, Tanaka H, Naomoto Y, Tanaka N: Pulmonary adenocarcinoma-targeted gene therapy by a cancer- and tissue-specific promoter system. Mol Cancer Ther; 2007 Jan;6(1):244-52
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  • [Title] Pulmonary adenocarcinoma-targeted gene therapy by a cancer- and tissue-specific promoter system.
  • Gene therapy is one of the approaches used to treat lung cancer.
  • The benefit of cancer gene therapy is that different types of tumors can be selectively targeted by tumor-specific expression of therapeutic genes that include an apoptosis gene to destroy the tumor.
  • Previously, we described a promoter (TTS promoter) that we designed that is specifically targeted to lung cancer cells but not to other types of cancer or normal cells including stem cells.
  • In this pursuit, we further characterize the specificity of the TTS promoter in four types of lung cancer cells (squamous cell lung carcinoma, pulmonary adenocarcinoma, small-cell lung carcinoma, large-cell lung carcinoma).
  • The TTS promoter is highly active only in pulmonary adenocarcinoma cells but not in the other three types of lung cancer cells.
  • The TTS/Bax selectively causes BAX expression and cell death in pulmonary adenocarcinoma but not in other cells.
  • Cell death caused by the BAX expression was also observed in pulmonary adenocarcinoma that is resistant to the anticancer drug gefitinib (epidermal growth factor receptor tyrosine kinase inhibitor).
  • BAX expression and cell death can be suppressed by dexamethasone (a glucocorticoid) treatment through negative glucocorticoid elements in the TTS promoter.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / therapy. Genetic Therapy / methods. Lung Neoplasms / genetics. Lung Neoplasms / therapy. Promoter Regions, Genetic / genetics
  • [MeSH-minor] Adenoviridae. Animals. Cell Death / drug effects. Cell Line, Tumor. DNA-Binding Proteins / genetics. Dexamethasone / pharmacology. Gene Expression Regulation, Neoplastic / drug effects. Glucocorticoids / pharmacology. Humans. Mice. Organ Specificity. Pulmonary Surfactant-Associated Protein A / genetics. RNA, Messenger / genetics. RNA, Messenger / metabolism. Stem Cells / drug effects. Transcription, Genetic / drug effects. bcl-2-Associated X Protein / metabolism

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  • (PMID = 17237283.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Glucocorticoids; 0 / Pulmonary Surfactant-Associated Protein A; 0 / RNA, Messenger; 0 / SFTPA1 protein, human; 0 / TTF1 protein, human; 0 / bcl-2-Associated X Protein; 7S5I7G3JQL / Dexamethasone
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17. Shindo G, Endo T, Onda M, Shimada T, Inou T, Hiruta H: [Pulmonary large cell carcinoma contiguous to bullae with massive bullous hematoma and hemoptysis; with special reference to 20 cases of Japanese reports]. Kyobu Geka; 2005 Aug;58(9):787-93
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  • [Title] [Pulmonary large cell carcinoma contiguous to bullae with massive bullous hematoma and hemoptysis; with special reference to 20 cases of Japanese reports].
  • A 50-year-old man with continuous hemosputa and large hematoma of left upper lobe contiguous to bilateral emphysematous bullous disease was admitted for surgery to stop hemorrhage and to resect left lung hematoma and multiple bullae.
  • Pathological examination, however, revealed anaplastic carcinoma inside bulla of S(1+2)c with minimal invasion into adhered parietal pleura (p 3).
  • The final pathological diagnosis was large cell carcinoma of left S(1+2)c with the staging pT3N0M0 and stage II.
  • Clinical analysis of Japanese 20 cases of lung carcinoma with initial signs of hemosputa and/or hemoptysis contiguous to emphysematous bullae elucidate following important facts.
  • Hemosputa and hemoptysis play important role for early finding and diagnosis of lung cancer contiguous to bullous disease, especially in patients of early clinical stage with or without computed tomography (CT) exams and promise to better surgical prognosis and survivals as compared with non hemosputa ones.
  • [MeSH-major] Blister / surgery. Carcinoma, Large Cell / diagnosis. Hematoma / surgery. Lung Diseases / surgery. Lung Neoplasms / diagnosis. Pneumonectomy

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  • (PMID = 16104563.001).
  • [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; Review
  • [Publication-country] Japan
  • [Number-of-references] 25
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18. Che G, Chen J, Liu L, Wang Y, Li L, Qin Y, Zhou Q: Transfection of nm23-H1 increased expression of beta-Catenin, E-Cadherin and TIMP-1 and decreased the expression of MMP-2, CD44v6 and VEGF and inhibited the metastatic potential of human non-small cell lung cancer cell line L9981. Neoplasma; 2006;53(6):530-7
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  • [Title] Transfection of nm23-H1 increased expression of beta-Catenin, E-Cadherin and TIMP-1 and decreased the expression of MMP-2, CD44v6 and VEGF and inhibited the metastatic potential of human non-small cell lung cancer cell line L9981.
  • In this report, we transfected nm23-H1 cDNA into L9981, a human large cell lung cancer cell line with nm23 negative expression, and made a stable transfectant.
  • L9981-nm23-H1 cells exhibited lower cells proliferation rate, more G0/G1 phase growth and an increase in apoptosis with a dramatic decreased in the tumor cells ability to metastasize.
  • L9981-nm23-H1 cells also demonstrated a significantly reduced lymph node and pulmonary metastatic capacity in vivo when injected into the nude mice.
  • Furthermore, we used DNA microarray analysis to explore the change in expression of the metastasis-related genes in L9981-nm23-H1 cells.
  • These results demonstrated that nm23-H1 can suppress the mobility and metastatic capacity of cancer cells and the molecular mechanism by which nm23-H1 suppresses tumor metastasis may be via increasing the expression of metastasis-related genes such as beta-Catenin, E-Cadherin and TIMP-1 and decreasing the expression of MMP-2, CD44V6 and VEGF.
  • [MeSH-major] Adenocarcinoma / secondary. Antigens, CD44 / metabolism. Cadherins / metabolism. Carcinoma, Non-Small-Cell Lung / therapy. Glycoproteins / metabolism. Matrix Metalloproteinase 2 / metabolism. Nucleoside-Diphosphate Kinase / genetics. Tissue Inhibitor of Metalloproteinase-1 / metabolism. Vascular Endothelial Growth Factor A / metabolism. beta Catenin / metabolism
  • [MeSH-minor] Animals. Biomarkers, Tumor. Blotting, Western. Cell Proliferation. Gene Expression Profiling. Humans. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Lung Neoplasms / therapy. Male. Mice. Mice, Inbred BALB C. Mice, Nude. NM23 Nucleoside Diphosphate Kinases. Neoplasm Invasiveness. Oligonucleotide Array Sequence Analysis. Transfection. Tumor Cells, Cultured

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  • (PMID = 17167724.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Antigens, CD44; 0 / Biomarkers, Tumor; 0 / CD44v6 antigen; 0 / Cadherins; 0 / Glycoproteins; 0 / NM23 Nucleoside Diphosphate Kinases; 0 / Tissue Inhibitor of Metalloproteinase-1; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 0 / beta Catenin; EC 2.7.4.6 / NME1 protein, human; EC 2.7.4.6 / Nme1 protein, mouse; EC 2.7.4.6 / Nucleoside-Diphosphate Kinase; EC 3.4.24.24 / Matrix Metalloproteinase 2
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19. Tambo Y, Kasahara K, Fujimura M, Tamori S, Araya T, Sone T, Nakao S: [A case of advanced large cell lung carcinoma for whom fourth-line chemotherapy of cisplatin and gemcitabine proved effective for the first time]. Gan To Kagaku Ryoho; 2007 Feb;34(2):217-9
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  • [Title] [A case of advanced large cell lung carcinoma for whom fourth-line chemotherapy of cisplatin and gemcitabine proved effective for the first time].
  • Chest X-ray revealed a lung mass shadow in the lower left lung field.
  • We diagnosed it as an advanced large cell carcinoma after conducting transbronchial lung biopsy and neck lymphnode biopsy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Large Cell / drug therapy. Lung Neoplasms / drug therapy. Lymph Nodes / pathology

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  • (PMID = 17301530.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Taxoids; 0W860991D6 / Deoxycytidine; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 15H5577CQD / docetaxel; 5V9KLZ54CY / Vinblastine; 5VT6420TIG / Oxonic Acid; B76N6SBZ8R / gemcitabine; BG3F62OND5 / Carboplatin; Q20Q21Q62J / Cisplatin; Q6C979R91Y / vinorelbine
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20. Liu Y, Zhang L, Han X, Zhou T: [A case report and literature review of small intestinal metastasis of large cell lung cancer]. Zhongguo Fei Ai Za Zhi; 2010 Jun;13(6):655-8
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  • [Title] [A case report and literature review of small intestinal metastasis of large cell lung cancer].
  • [MeSH-major] Carcinoma, Large Cell / secondary. Intestinal Neoplasms / secondary. Intestine, Small / pathology. Lung Neoplasms / pathology

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  • (PMID = 20681458.001).
  • [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] Case Reports; Journal Article; Review
  • [Publication-country] China
  • [Number-of-references] 20
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21. Le Deley MC, Rosolen A, Williams DM, Horibe K, Wrobel G, Attarbaschi A, Zsiros J, Uyttebroeck A, Marky IM, Lamant L, Woessmann W, Pillon M, Hobson R, Mauguen A, Reiter A, Brugières L: Vinblastine in children and adolescents with high-risk anaplastic large-cell lymphoma: results of the randomized ALCL99-vinblastine trial. J Clin Oncol; 2010 Sep 1;28(25):3987-93
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  • [Title] Vinblastine in children and adolescents with high-risk anaplastic large-cell lymphoma: results of the randomized ALCL99-vinblastine trial.
  • PURPOSE: The impact of adding vinblastine to a 4-month chemotherapy regimen, based on the Non-Hodgkin's Lymphoma Berlin-Frankfurt-Münster 90 protocol, in childhood high-risk anaplastic large-cell lymphoma (ALCL) was assessed.
  • PATIENTS AND METHODS: Children and adolescents with high-risk ALCL, defined by mediastinal, lung, liver, spleen, or skin involvement, were eligible for the trial.
  • [MeSH-minor] Adolescent. Child. Disease-Free Survival. Humans. Lymphoma, Large-Cell, Anaplastic / drug therapy

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  • [CommentIn] J Clin Oncol. 2011 Feb 1;29(4):e90-1; author reply e92-3 [21172896.001]
  • (PMID = 20679620.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 5V9KLZ54CY / Vinblastine
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22. Kruczynski A, Mayer P, Marchand A, Vispé S, Fournier E, Annereau JP, Brel V, Barret JM, Delsol G, Imbert T, Fahy J, Bailly C: Antitumor activity of pyridoisoquinoline derivatives F91873 and F91874, novel multikinase inhibitors with activity against the anaplastic lymphoma kinase. Anticancer Drugs; 2009 Jun;20(5):364-72
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  • [Title] Antitumor activity of pyridoisoquinoline derivatives F91873 and F91874, novel multikinase inhibitors with activity against the anaplastic lymphoma kinase.
  • The anaplastic lymphoma kinase (ALK) is a validated target for the therapy of different malignancies.
  • Aberrant expression of constitutively active ALK chimeric proteins has been implicated in the pathogenesis of anaplastic large-cell lymphoma (ALCL) and has been detected in other cancers such as inflammatory myofibroblastic tumors, diffuse large B-cell lymphomas, certain non-small-cell lung cancers, rhabdomyosarcomas, neuroblastomas and glioblastomas.
  • In the course of a screening program aimed at identifying kinase inhibitors with novel scaffolds, the two pyridoisoquinoline derivatives F91873 and F91874, were identified as multikinase inhibitors with activity against ALK in a biochemical screen.
  • F91873 and F91874 also inhibited nucleophosmin-ALK and signal transducer and activator of transcription 3 phosphorylation in the ALCL cell line COST with the same potency.
  • Both F91873 and F91874 behaved as ATP noncompetitive inhibitors and inhibited cell proliferation of the ALK(+) ALCL cell lines COST, PIO, and Karpas299 ALCL.
  • This growth inhibition effect was associated with a G1-phase cell cycle arrest.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Lymphoma, Large-Cell, Anaplastic / drug therapy. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Quinolizines / therapeutic use. Thiazoles / therapeutic use
  • [MeSH-minor] Animals. Carcinoma, Non-Small-Cell Lung / enzymology. Carcinoma, Non-Small-Cell Lung / pathology. Cell Line, Tumor / drug effects. Cell Line, Tumor / enzymology. Female. G1 Phase / drug effects. Lung Neoplasms / enzymology. Lung Neoplasms / pathology. Mice. Mice, Inbred ICR. Mice, SCID. Ovarian Neoplasms / enzymology. Ovarian Neoplasms / pathology. Protein Structure, Tertiary. Receptor Protein-Tyrosine Kinases. Recombinant Fusion Proteins / antagonists & inhibitors. Xenograft Model Antitumor Assays

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  • (PMID = 19322071.001).
  • [ISSN] 1473-5741
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / F 91873; 0 / F 91874; 0 / Protein Kinase Inhibitors; 0 / Quinolizines; 0 / Recombinant Fusion Proteins; 0 / Thiazoles; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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23. Su CC, Yang JS, Lu CC, Chiang JH, Wu CL, Lin JJ, Lai KC, Hsia TC, Lu HF, Fan MJ, Chung JG: Curcumin inhibits human lung large cell carcinoma cancer tumour growth in a murine xenograft model. Phytother Res; 2010 Feb;24(2):189-92
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  • [Title] Curcumin inhibits human lung large cell carcinoma cancer tumour growth in a murine xenograft model.
  • Curcumin can decrease viable cells through the induction of apoptosis in human lung cancer NCI-H460 cells in vitro.
  • However, there are no reports that curcumin can inhibit cancer cells in vivo.
  • In this study, NCI-H460 lung tumour cells were implanted directly into nude mice and divided randomly into four groups to be treated with vehicle, curcumin (30 mg/kg of body weight), curcumin (45 mg/kg of body weight) and doxorubicin (8 mg/kg of body weight).
  • ), with treatment starting 4 weeks after inoculation with the NCI-H460 cells.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Carcinoma, Large Cell / drug therapy. Curcumin / pharmacology
  • [MeSH-minor] Animals. Cell Line, Tumor. Doxorubicin / pharmacology. Female. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. Xenograft Model Antitumor Assays

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  • [Copyright] (c) 2010 John Wiley & Sons, Ltd.
  • (PMID = 20077433.001).
  • [ISSN] 1099-1573
  • [Journal-full-title] Phytotherapy research : PTR
  • [ISO-abbreviation] Phytother Res
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 80168379AG / Doxorubicin; IT942ZTH98 / Curcumin
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24. Otera H, Ikeda F, Nakagawa S, Kono Y, Sakurai T, Tada K, Hashimoto K, Ikeda A: Intussusception of small intestine due to metastasis of large cell carcinoma of the lung with a rhabdoid phenotype. Eur Respir Rev; 2010 Sep;19(117):248-52
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  • [Title] Intussusception of small intestine due to metastasis of large cell carcinoma of the lung with a rhabdoid phenotype.
  • Large cell carcinoma of the lung with a rhabdoid phenotype is a rare type of lung cancer, and does not commonly metastasize to the small intestine.
  • Herein we describe a 63-yr-old Japanese male with ileus resulting from small intestinal metastasis from lung cancer.
  • [MeSH-major] Carcinoma, Large Cell / complications. Carcinoma, Large Cell / secondary. Intussusception / etiology. Intussusception / pathology. Lung Neoplasms / complications. Lung Neoplasms / pathology

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  • (PMID = 20956201.001).
  • [ISSN] 1600-0617
  • [Journal-full-title] European respiratory review : an official journal of the European Respiratory Society
  • [ISO-abbreviation] Eur Respir Rev
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
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25. den Bakker MA, Willemsen S, Grünberg K, Noorduijn LA, van Oosterhout MF, van Suylen RJ, Timens W, Vrugt B, Wiersma-van Tilburg A, Thunnissen FB: Small cell carcinoma of the lung and large cell neuroendocrine carcinoma interobserver variability. Histopathology; 2010 Feb;56(3):356-63
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  • [Title] Small cell carcinoma of the lung and large cell neuroendocrine carcinoma interobserver variability.
  • AIMS: To test the hypothesis that the published morphological criteria permit reliable segregation of small cell carcinoma of the lung (SCLC) and large cell neuroendocrine carcinoma (LCNEC) cases by determining the interobserver variation.
  • METHODS AND RESULTS: One hundred and seventy cases of SCLC, LCNEC and cases diagnosed as neuroendocrine lung carcinoma before LCNEC had been established as a diagnostic category were retrieved from the archives of the assessor's institutes.
  • Unanimity of diagnosis was achieved for only 20 cases; a majority diagnosis was reached for 115 cases.
  • In 35 cases no consensus diagnosis could be reached.
  • [MeSH-major] Carcinoma, Large Cell / epidemiology. Carcinoma, Neuroendocrine / epidemiology. Lung Neoplasms / epidemiology. Small Cell Lung Carcinoma / epidemiology

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  • (PMID = 20459535.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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26. Brahmbhatt R, Dorsogna L, Cooke P: Primary lung cancer involving mediastinum and mimicking left atrial myxoma: a case report and review of literature. Heart Lung Circ; 2005 Mar;14(1):48-50
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  • [Title] Primary lung cancer involving mediastinum and mimicking left atrial myxoma: a case report and review of literature.
  • We report a case of primary large cell carcinoma of the lung invading the heart and mimicking a left atrial myxoma.
  • This case highlights the problems we face in diagnosis and management of a very unusual presentation of poorly differentiated primary large ('non-small') cell lung cancer with extension into the left atrium.
  • It is important to have a high index of suspicion for a primary lung malignancy in chronic heavy smokers with none to minimal respiratory symptoms for early diagnosis and full staging procedures, as some of these tumours may be suitable for lung resection.
  • [MeSH-major] Carcinoma, Large Cell / diagnosis. Heart Atria. Heart Neoplasms / diagnosis. Lung Neoplasms / diagnosis. Myxoma / diagnosis

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  • (PMID = 16352252.001).
  • [ISSN] 1443-9506
  • [Journal-full-title] Heart, lung & circulation
  • [ISO-abbreviation] Heart Lung Circ
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
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27. Yasuda M, Mizukami M, Hanagiri T, Shigematsu Y, Fukuyama T, Nagata Y, So T, Ichiki Y, Sugaya M, Takenoyama M, Sugio K, Yasumoto K: Antigens recognized by IgG derived from tumor-infiltrating B lymphocytes in human lung cancer. Anticancer Res; 2006 Sep-Oct;26(5A):3607-11
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antigens recognized by IgG derived from tumor-infiltrating B lymphocytes in human lung cancer.
  • BACKGROUND: Lung cancer tissues are often infiltrated by B lymphocytes, but it is not clear whether these infiltrations represent tumor-specific immune response or a nonspecific reaction.
  • MATERIALS AND METHODS: The serological analysis of recombinant cDNA expression libraries (SEREX) were previously modified using a severe combined immunodeficient (SCID) mice model engrafted with fresh human lung cancer.
  • Here, a panel of antigens recognized by tumor-infiltrating B lymphocytes (TIB) in human lung cancer were characterized.
  • RESULTS: The modified SEREX analysis identified 22 distinct antigens in a large cell carcinoma of the lung.
  • CONCLUSION: The results of this study indicate that the humoral immune response of TIB in lung cancer patients can be detected in the xenotransplanted SCID mouse model and our modification shows high sensitivity and specificity for identification of tumor antigens.
  • [MeSH-major] Antigens, Neoplasm / immunology. B-Lymphocytes / immunology. Lung Neoplasms / immunology. Lymphocytes, Tumor-Infiltrating / immunology
  • [MeSH-minor] Animals. Antibodies, Neoplasm / immunology. Antibodies, Neoplasm / metabolism. Carcinoma, Large Cell / immunology. Carcinoma, Large Cell / metabolism. Female. Flow Cytometry / methods. Humans. Immunoglobulin G / biosynthesis. Immunoglobulin G / metabolism. Mice. Mice, SCID. Transplantation, Heterologous

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  • (PMID = 17094490.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antibodies, Neoplasm; 0 / Antigens, Neoplasm; 0 / Immunoglobulin G
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28. Sabbatini P, Korenchuk S, Rowand JL, Groy A, Liu Q, Leperi D, Atkins C, Dumble M, Yang J, Anderson K, Kruger RG, Gontarek RR, Maksimchuk KR, Suravajjala S, Lapierre RR, Shotwell JB, Wilson JW, Chamberlain SD, Rabindran SK, Kumar R: GSK1838705A inhibits the insulin-like growth factor-1 receptor and anaplastic lymphoma kinase and shows antitumor activity in experimental models of human cancers. Mol Cancer Ther; 2009 Oct;8(10):2811-20
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  • [Title] GSK1838705A inhibits the insulin-like growth factor-1 receptor and anaplastic lymphoma kinase and shows antitumor activity in experimental models of human cancers.
  • GSK1838705A blocks the in vitro proliferation of cell lines derived from solid and hematologic malignancies, including multiple myeloma and Ewing's sarcoma, and retards the growth of human tumor xenografts in vivo.
  • GSK1838705A also inhibits the anaplastic lymphoma kinase (ALK), which drives the aberrant growth of anaplastic large-cell lymphomas, some neuroblastomas, and a subset of non-small cell lung cancers.
  • [MeSH-minor] Animals. Blood Glucose / metabolism. Cell Proliferation / drug effects. Enzyme Activation / drug effects. Humans. Mice. Phosphorylation / drug effects. Receptor Protein-Tyrosine Kinases. Receptor, Insulin / metabolism. Signal Transduction / drug effects


29. Takahashi T, Sonobe M, Kobayashi M, Yoshizawa A, Menju T, Nakayama E, Mino N, Iwakiri S, Sato K, Miyahara R, Okubo K, Manabe T, Date H: Clinicopathologic features of non-small-cell lung cancer with EML4-ALK fusion gene. Ann Surg Oncol; 2010 Mar;17(3):889-97
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  • [Title] Clinicopathologic features of non-small-cell lung cancer with EML4-ALK fusion gene.
  • BACKGROUND: A fusion gene between echinoderm microtubule-associated protein-like 4 (EML4) and the anaplastic lymphoma kinase (ALK) has recently been identified in nonsmall-cell lung cancers (NSCLCs).
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / pathology. Lung Neoplasms / genetics. Lung Neoplasms / pathology. Mutation / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Aged. Carcinoma, Large Cell / genetics. Carcinoma, Large Cell / pathology. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / pathology. Female. Humans. Male. Middle Aged. Neoplasm Staging. Prognosis. Proto-Oncogene Proteins / genetics. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptor, Epidermal Growth Factor / genetics. Receptor, ErbB-2 / genetics. Reverse Transcriptase Polymerase Chain Reaction. ras Proteins / genetics


30. Oshita H, Itai J, Omori K, Okamoto N, Awaya Y: [Pulmonary embolism in a patient with large cell lung carcinoma during chemotherapy-case report]. Gan To Kagaku Ryoho; 2009 Jan;36(1):105-7
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  • [Title] [Pulmonary embolism in a patient with large cell lung carcinoma during chemotherapy-case report].
  • The patient, a 64-year-old woman, was diagnosed as having large cell carcinoma(stageIV)eighteen months ago.
  • Insertion of a vena cava filter and continuation of anticoagulant therapy were performed to prevent recurrence of PE.
  • Thrombosis is a frequent complication in cancer patients and represents an important cause of morbidity and mortality.
  • Great care should be taken for complications of thrombosis in cancer treatment.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Large Cell / complications. Carcinoma, Large Cell / drug therapy. Lung Neoplasms / complications. Lung Neoplasms / drug therapy. Pulmonary Embolism / complications

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  • (PMID = 19151573.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Anticoagulants; 0 / Antineoplastic Agents
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31. Tanaka T, Sekimura A, Tanaka H, Tonegawa K, Ogawa K, Haneda H: [Gallbladder metastasis of large cell lung cancer]. Kyobu Geka; 2009 Nov;62(12):1069-72
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  • [Title] [Gallbladder metastasis of large cell lung cancer].
  • A man, who received right upper lobectomy of the lung due to stage IIB large cell carcinoma 7 and half years ago, visited our hospital complaining of right upper abdominal pain.
  • Pathological diagnosis was adenosquamous cell carcinoma After 1 year and 4 months later, left adrenal gland tumor was found by CT scan, and the surgery was conducted.
  • Pathologically, it was diagnosed as metastasis from lung cancer.
  • By reevaluation of pathology of the gallbladder, the tumor was found to have similar component of resected lung cancer, suggesting the possibility of the tumor to be metastatic.
  • [MeSH-major] Carcinoma, Large Cell / pathology. Gallbladder Neoplasms / secondary. Lung Neoplasms / pathology

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  • (PMID = 19894573.001).
  • [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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32. Webb TR, Slavish J, George RE, Look AT, Xue L, Jiang Q, Cui X, Rentrop WB, Morris SW: Anaplastic lymphoma kinase: role in cancer pathogenesis and small-molecule inhibitor development for therapy. Expert Rev Anticancer Ther; 2009 Mar;9(3):331-56
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  • [Title] Anaplastic lymphoma kinase: role in cancer pathogenesis and small-molecule inhibitor development for therapy.
  • Anaplastic lymphoma kinase (ALK), a receptor tyrosine kinase in the insulin receptor superfamily, was initially identified in constitutively activated oncogenic fusion forms - the most common being nucleophosmin-ALK - in anaplastic large-cell lymphomas, and subsequent studies have identified ALK fusions in diffuse large B-cell lymphomas, systemic histiocytosis, inflammatory myofibroblastic tumors, esophageal squamous cell carcinomas and non-small-cell lung carcinomas.
  • In addition to those cancers for which a causative role for aberrant ALK activity is well validated, more circumstantial links implicate the full-length, normal ALK receptor in the genesis of other malignancies - including glioblastoma and breast cancer - via a mechanism of receptor activation involving autocrine and/or paracrine growth loops with the reported ALK ligands, pleiotrophin and midkine.

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  • (PMID = 19275511.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA069129-10; United States / NCI NIH HHS / CA / R01 CA69129; United States / NCI NIH HHS / CA / R01 CA069129; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / R01 CA069129-10
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carrier Proteins; 0 / Cytokines; 0 / Enzyme Inhibitors; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; 134034-50-7 / pleiotrophin; 137497-38-2 / midkine; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Number-of-references] 304
  • [Other-IDs] NLM/ NIHMS105118; NLM/ PMC2780428
  •  go-up   go-down


33. Gao LW, Zhu W, Feng ZH, An N: [Comparative proteomic analysis of human large cell lung cancer cell line with high and low metastasis potentials]. Sichuan Da Xue Xue Bao Yi Xue Ban; 2008 Sep;39(5):706-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Comparative proteomic analysis of human large cell lung cancer cell line with high and low metastasis potentials].
  • OBJECTIVE: A comparative proteomic analysis on two human large cell lung cancer strains with high metastasis potential (L9981) and low metastasis potential (NL9980) were conducted.
  • METHODS: The total proteins of the two cell lines were separated by immobilized pH gradient (IPG )-based two-dimensional gel electrophoresis.
  • The differential expression proteins of the two cell lines were analyzed using image analysis software.
  • MS and biological informatics study found that the expressions of heat shock 70 kD protein 9B precursor, MTHSP75 and glutathione synthetas incerased in L9981 cells.
  • However, a variant of P47 protein, immunoglobulin heavy chain variable region, enolasel, heat shock protein and eukaryotic translation initiation fact 3 were down-regulated in L9981 cells.
  • Pyruvate kinase (PK) was only expressed in L9981 cells while WD-40 repeat protein was only expressed in NL9980 cells.
  • CONCLUSIONS: The metastatic lung cancer cell lines display different protein profiles compared to the non metastatic lung cancer cell lines.
  • The identified proteins are likely to be associated with tumor metastasis, 4hich could serve as a basis for searching potential prognosis markers of lung cancer and elucidating the mechanisms of the metastasis of lung cancer.
  • [MeSH-major] Carcinoma, Large Cell / pathology. Lung Neoplasms / pathology. Neoplasm Metastasis / pathology. Proteomics / methods
  • [MeSH-minor] Humans. Tumor Cells, Cultured

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  • (PMID = 19024295.001).
  • [ISSN] 1672-173X
  • [Journal-full-title] Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition
  • [ISO-abbreviation] Sichuan Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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34. Fernandez FG, Denlinger CE, Crabtree TD: Primary non-Hodgkin's lymphoma of the trachea. J Thorac Oncol; 2010 Mar;5(3):403-4
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  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / pathology. Tracheal Neoplasms / pathology

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  • (PMID = 20186028.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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36. Pratz KW, Ma C, Aubry MC, Vrtiska TJ, Erlichman C: Large cell carcinoma with calcitonin and vasoactive intestinal polypeptide-associated Verner-Morrison syndrome. Mayo Clin Proc; 2005 Jan;80(1):116-20
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  • [Title] Large cell carcinoma with calcitonin and vasoactive intestinal polypeptide-associated Verner-Morrison syndrome.
  • Verner-Morrison syndrome, characterized by diarrhea, hypokalemia, and hypochlorhydria, is caused most commonly by vasoactive intestinal polypeptide-secreting islet cell tumors of the pancreas.
  • Verner-Morrison syndrome has not been described as a paraneoplastic syndrome in non-small cell lung cancer.
  • We describe a 38-year-old man with metastatic non-small cell lung cancer of large cell carcinoma with neuroendocrine differentiation who presented with bone metastasis and intractable secretory diarrhea that was unresponsive to pharmacological treatment, including octreotide.
  • To our knowledge, this is the first published case of large cell carcinoma with neuroendocrine differentiation associated with treatment-responsive paraneoplastic Verner-Morrison syndrome.
  • [MeSH-major] Calcitonin / secretion. Carcinoma, Large Cell / secretion. Lung Neoplasms / secretion. Pancreatic Neoplasms / etiology. Paraneoplastic Endocrine Syndromes / etiology. Vasoactive Intestinal Peptide / metabolism. Vipoma / etiology

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  • (PMID = 15667039.001).
  • [ISSN] 0025-6196
  • [Journal-full-title] Mayo Clinic proceedings
  • [ISO-abbreviation] Mayo Clin. Proc.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 37221-79-7 / Vasoactive Intestinal Peptide; 9007-12-9 / Calcitonin; RWM8CCW8GP / Octreotide
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37. Zhang L, Wu G: Complete atelectasis of the left lung from anaplastic large-cell lymphoma. ScientificWorldJournal; 2010;10:1332-3
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  • [Title] Complete atelectasis of the left lung from anaplastic large-cell lymphoma.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / complications. Pulmonary Atelectasis / etiology


38. Ardini E, Magnaghi P, Orsini P, Galvani A, Menichincheri M: Anaplastic Lymphoma Kinase: role in specific tumours, and development of small molecule inhibitors for cancer therapy. Cancer Lett; 2010 Dec 28;299(2):81-94
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  • [Title] Anaplastic Lymphoma Kinase: role in specific tumours, and development of small molecule inhibitors for cancer therapy.
  • The Anaplastic Lymphoma Kinase (ALK) is a receptor tyrosine kinase first identified as the product of a gene rearrangement in Anaplastic Large Cell Lymphoma.
  • ALK has subsequently been found to be rearranged, mutated, or amplified in a further series of tumours including neuroblastoma, and Non-Small Cell Lung Cancer.
  • These observations have sparked the development of small molecule kinase inhibitors, the most advanced of which is currently in clinical testing and which has shown promising preliminary activity in the subset of lung cancer patients whose tumours harbour activated ALK.

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  • [Copyright] Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20934803.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / GSK 1838705A; 0 / NVP-TAE684; 0 / PF-2341066; 0 / Piperidines; 0 / Pyridines; 0 / Pyrimidines; 0 / Pyrroles; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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39. Sampson JB, Smith SM, Smith AG, Singleton JR, Chin S, Pestronk A, Flanigan KM: Paraneoplastic myopathy: response to intravenous immunoglobulin. Neuromuscul Disord; 2007 May;17(5):404-8
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  • A third case represents the first association of anti-signal recognition particle (anti-SRP) syndrome with large-cell lung cancer.
  • These cases highlight the role of histopathologic diagnosis in directing the treatment of paraneoplastic myopathy, and the role for IVIG in treatment of the syndrome.

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  • (PMID = 17336069.001).
  • [ISSN] 0960-8966
  • [Journal-full-title] Neuromuscular disorders : NMD
  • [ISO-abbreviation] Neuromuscul. Disord.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Complement Membrane Attack Complex; 0 / Immunoglobulins, Intravenous
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40. Schmid I, Fliegner M: [Digital ischemia of a patient with undifferentiated large cell lung cancer]. Internist (Berl); 2008 Mar;49(3):346-8
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  • [Title] [Digital ischemia of a patient with undifferentiated large cell lung cancer].
  • [Transliterated title] Digitale Ischämien bei einer Patientin mit grosszelligem Lungenkarzinom.
  • A Raynaud's phenomenon with acral ischemia till necrosis is a rare form of a paraneoplasia.
  • We report about a woman with a metastatic lung cancer, who was admitted because of pain in her left hand with necrosis of the fingertips and of the fifth right toe.
  • The course of a paraneoplastic syndrome is often determined by the underlying malignoma and if the antineoplastic treatment is ineffective, the chances to treat the paraneoplasia may be limited.
  • [MeSH-major] Carcinoma, Large Cell / complications. Carcinoma, Large Cell / diagnosis. Lung Neoplasms / diagnosis. Paraneoplastic Syndromes / diagnosis. Raynaud Disease / diagnosis. Raynaud Disease / etiology
  • [MeSH-minor] Diagnosis, Differential. Female. Humans. Middle Aged

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  • (PMID = 18214409.001).
  • [ISSN] 1432-1289
  • [Journal-full-title] Der Internist
  • [ISO-abbreviation] Internist (Berl)
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
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41. Zhong D, Guo L, de Aguirre I, Liu X, Lamb N, Sun SY, Gal AA, Vertino PM, Zhou W: LKB1 mutation in large cell carcinoma of the lung. Lung Cancer; 2006 Sep;53(3):285-94
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  • [Title] LKB1 mutation in large cell carcinoma of the lung.
  • Germline inactivation of LKB1 is responsible for Peutz-Jeghers syndrome, an autosomal dominant disorder characterized by benign hamartomas of the GI tract and an increased predisposition to certain cancers, including lung.
  • Acquired mutations in LKB1 are rarely observed in most sporadic tumor types except for adenocarcinomas of the lung where up to 50% harbor inactivating mutations.
  • In this study, we focused on LKB1 mutations in lung cancer cell lines originating from large cell carcinomas.
  • We identified a novel 1.5kb interstitial deletion within LKB1 gene in H157 cancer cells.
  • The truncated transcript was expressed at relatively low levels, and the truncated LKB1 protein was virtually undetectable in this cell line.
  • Phosphorylation of AMPK-alpha was attenuated in H157 cells treated with 2-deoxyglucose, and could be rescued by expression of an exogenous GFP-LKB1 fusion protein.
  • Of the four cell lines and six primary tumors of large cell lung carcinoma origin that have been evaluated in this and other studies, LKB1 mutations have been found in three cases.
  • These results suggest that, in addition to adenocarcinomas, acquired loss of function mutations in LKB1 may also be frequently involved in the pathogenesis of large cell lung carcinomas.
  • [MeSH-major] Carcinoma, Large Cell / metabolism. Gene Expression Regulation, Neoplastic. Lung Neoplasms / genetics. Protein-Serine-Threonine Kinases / genetics. Protein-Serine-Threonine Kinases / physiology
  • [MeSH-minor] AMP-Activated Protein Kinases. Alleles. Cell Line, Tumor. DNA, Complementary / metabolism. Gene Deletion. Green Fluorescent Proteins / metabolism. Homozygote. Humans. Loss of Heterozygosity. Multienzyme Complexes / metabolism. Mutation. Phosphorylation. Protein Structure, Tertiary

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  • (PMID = 16822578.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA077337
  • [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] Ireland
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / Multienzyme Complexes; 147336-22-9 / Green Fluorescent Proteins; EC 2.7.1.- / STK11 protein, human; EC 2.7.11.1 / AMP-Activated Protein Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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42. Malki AM, Gentry J, Evans SC: Differential effect of selected methylxanthine derivatives on radiosensitization of lung carcinoma cells. Exp Oncol; 2006 Mar;28(1):16-24
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  • [Title] Differential effect of selected methylxanthine derivatives on radiosensitization of lung carcinoma cells.
  • AIM: Using caffeine as a reference derivative, this study was performed to investigate how other methylxanthine derivatives, theophylline, 3-isobutyl-methylxanthine and 1,3-dipropyl-7-methylxanthine, sensitize cells to radiation by modifying cell cycle checkpoints and inducing the apoptotic response.
  • The effect of the methylxanthine derivatives was studied in response to gamma and ultraviolet radiation in a human large cell lung carcinoma cell line, null for p53, a normal lung epithelial cell line and the large cell lung carcinoma cell line stably transfected with p53.
  • METHODS: Effects of theophylline, 3-isobutyl-methylxanthine and 1,3-dipropyl 7-methylxanthine on cell-radiosensitization in comparison to caffeine tested by clonogenic survival assay, MTT assay, ELISA based apoptotic assay, flow cytometry, caspase-3 activity, TUNEL assay, and western blot analysis.
  • RESULTS: All the derivatives, except 3-isobutyl-methylxanthine, increased tumor cell sensitization to radiation by inducing apoptosis in the p53-null lung cancer cell line.
  • The pattern of cell cycle progression revealed that these derivatives increased the number of cells in G1 phase by abrogating the G2/M checkpoint, directing the cells to apoptose through a p53-independent mechanism.
  • In contrast, 3-isobutyl-methylxanthine was more potent than the other derivatives in radiosensitization of normal lung epithelial cells and the lung carcinoma cells stably transfected with wild-type p53.
  • IBMX increased p53 protein level more than caffeine in lung carcinoma cells stably transfected with wild-type p53.
  • [MeSH-major] Cell Survival / drug effects. Cell Survival / radiation effects. Lung Neoplasms. Radiation-Sensitizing Agents / pharmacology. Xanthines / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Apoptosis / radiation effects. Caffeine / pharmacology. Carcinoma, Large Cell. Cell Line, Tumor. Flow Cytometry. Gamma Rays. Humans. Theophylline / pharmacology

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  • (PMID = 16614702.001).
  • [ISSN] 1812-9269
  • [Journal-full-title] Experimental oncology
  • [ISO-abbreviation] Exp. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Radiation-Sensitizing Agents; 0 / Xanthines; 28109-92-4 / methylxanthine; 3G6A5W338E / Caffeine; C137DTR5RG / Theophylline
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43. Hillion J, Wood LJ, Mukherjee M, Bhattacharya R, Di Cello F, Kowalski J, Elbahloul O, Segal J, Poirier J, Rudin CM, Dhara S, Belton A, Joseph B, Zucker S, Resar LM: Upregulation of MMP-2 by HMGA1 promotes transformation in undifferentiated, large-cell lung cancer. Mol Cancer Res; 2009 Nov;7(11):1803-12
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  • [Title] Upregulation of MMP-2 by HMGA1 promotes transformation in undifferentiated, large-cell lung cancer.
  • Although lung cancer is the leading cause of cancer death worldwide, the precise molecular mechanisms that give rise to lung cancer are incompletely understood.
  • Here, we show that HMGA1 is an important oncogene that drives transformation in undifferentiated, large-cell carcinoma.
  • First, we show that the HMGA1 gene is overexpressed in lung cancer cell lines and primary human lung tumors.
  • Forced overexpression of HMGA1 induces a transformed phenotype with anchorage-independent cell growth in cultured lung cells derived from normal tissue.
  • Conversely, inhibiting HMGA1 expression blocks anchorage-independent cell growth in the H1299 metastatic, undifferentiated, large-cell human lung carcinoma cells.
  • We also show that the matrix metalloproteinase-2 (MMP-2) gene is a downstream target upregulated by HMGA1 in large-cell carcinoma cells.
  • In chromatin immunoprecipitation experiments, HMGA1 binds directly to the MMP-2 promoter in vivo in large-cell lung cancer cells, but not in squamous cell carcinoma cells.
  • In large-cell carcinoma cell lines, there is a significant, positive correlation between HMGA1 and MMP-2 mRNA.
  • Moreover, interfering with MMP-2 expression blocks anchorage-independent cell growth in H1299 large-cell carcinoma cells, indicating that the HMGA1-MMP-2 pathway is required for this transformation phenotype in these cells.
  • Blocking MMP-2 expression also inhibits migration and invasion in the H1299 large-cell carcinoma cells.
  • Our findings suggest an important role for MMP-2 in transformation mediated by HMGA1 in large-cell, undifferentiated lung carcinoma and support the development of strategies to target this pathway in selected tumors.

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  • (PMID = 19903768.001).
  • [ISSN] 1557-3125
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA092339-01A1; United States / NCI NIH HHS / CA / R01 CA092339; United States / NCI NIH HHS / CA / P50 CA058184; United States / NCI NIH HHS / CA / CA076130-04; United States / NCI NIH HHS / CA / R29 CA076130; United States / NCI NIH HHS / CA / 1R01CA092339; United States / NCI NIH HHS / CA / R29 CA076130-04
  • [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 / RNA, Messenger; 124544-67-8 / HMGA1a Protein; EC 3.4.24.24 / Matrix Metalloproteinase 2
  • [Other-IDs] NLM/ NIHMS149386; NLM/ PMC3069640
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44. Cluzeau T, Pécuchet N, Mounier N, Vignot S: [Implications of ALK (anaplastic lymphoma kinase) in oncohematology]. Bull Cancer; 2010 Aug;97(8):991-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Implications of ALK (anaplastic lymphoma kinase) in oncohematology].
  • [Transliterated title] Implications d'ALK (anaplastic lymphoma kinase) en oncohématologie.
  • The anaplastic lymphoma kinase gene (ALK) code for a receptor tyrosine-kinase.
  • The fusion proteins from the ALK gene have been identified in oncohaematology malignancies including ALK positive anaplastic lymphoma large cell and non small cells lung cancer with EML4-ALK fusion gene.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / enzymology. Lung Neoplasms / enzymology. Lymphoma, Large-Cell, Anaplastic / enzymology. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics

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  • (PMID = 20483705.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / EML4-ALK fusion protein, human; 0 / Neoplasm Proteins; 0 / Nucleoplasmins; 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 27
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45. Liu H, Li L, Li XQ, Liu XJ, Zhen YS: Enediyne lidamycin enhances the effect of epidermal growth factor receptor tyrosine kinase inhibitor, gefitinib, in epidermoid carcinoma A431 cells and lung carcinoma H460 cells. Anticancer Drugs; 2009 Jan;20(1):41-9
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  • [Title] Enediyne lidamycin enhances the effect of epidermal growth factor receptor tyrosine kinase inhibitor, gefitinib, in epidermoid carcinoma A431 cells and lung carcinoma H460 cells.
  • In this report, the cytotoxic and biochemical activity of LDM and gefitinib on human epidermoid carcinoma A431 cells and human large cell lung cancer H460 cells as a single agent or in combination has been evaluated.
  • In the MTT assay, LDM showed much more potent cytotoxicity than gefitinib to both cell lines.
  • A431 cells with a highly EGFR-expressing level were more sensitive to gefitinib than H460 cells, which expressed EGFR at an intermediate level.
  • LDM plus gefitinib showed potentiation of antiproliferative activity and apoptosis induction, which were associated with downregulation of EGFR signaling pathway and nuclear factor-kappa B expression, and the increase of cleaved poly (adenosine diphosphate-ribose) polymerase in the two cell lines, although to a lesser degree in H460 cells.
  • Combined treatment induced G1 phase arrest similar to that of gefitinib alone in A431 cells and intensified G2/M phase accumulation in H460 cells.
  • The above results indicate that LDM potentiates the effects of gefitinib in both gefitinib sensitive and less sensitive cells in association with enhanced inhibition of EGFR-dependent signaling.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Carcinoma / enzymology. Carcinoma, Squamous Cell / enzymology. Lung Neoplasms / enzymology. Receptor, Epidermal Growth Factor / antagonists & inhibitors
  • [MeSH-minor] Aminoglycosides / pharmacology. Antibiotics, Antineoplastic / pharmacology. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Dose-Response Relationship, Drug. Drug Synergism. Enediynes / pharmacology. Humans. Phosphorylation. Protein Kinase Inhibitors / pharmacology. Quinazolines / pharmacology. Signal Transduction / drug effects

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  • (PMID = 19342999.001).
  • [ISSN] 1473-5741
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents; 0 / Enediynes; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; 120177-69-7 / C 1027; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
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46. Ma W, Chen J, Xue X, Wang Z, Liu H, Wang T, Bai Y, Tang SC, Zhou Q: Alteration in gene expression profile and biological behavior in human lung cancer cell line NL9980 by nm23-H1 gene silencing. Biochem Biophys Res Commun; 2008 Jul 4;371(3):425-30
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  • [Title] Alteration in gene expression profile and biological behavior in human lung cancer cell line NL9980 by nm23-H1 gene silencing.
  • Lung cancer is the leading cause of cancer death in both men and women.
  • Tumor metastasis is an essential aspect of lung cancer progression. nm23-H1 is a metastasis suppressor gene.
  • Here, we compared the gene expression profile of human large cell lung cancer cell line NL9980 by nm23-H1 gene silencing with that of negative control cells to comprehensively investigate nm23-H1-mediated changes in gene expression of NL9980 cells.
  • Furthermore, we confirmed by Western blot that the expression of MMP-1 and -2 were significantly increased while that of cystatin B was dramatically decreased in NL9980-nm23-H1 silencing cells.
  • The NL9980-nm23-H1 silencing cells exhibited significantly more S phase growth and invasive ability.
  • Thus, silencing of nm23-H1 gene caused metastasis-related gene expression changes in lung cancer cells.
  • The knockdown of nm23-H1 expression may change the lung cancer cells to a more invasive phenotype through alteration in the expression of a set of genes.
  • [MeSH-major] Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Lung Neoplasms / genetics. Lung Neoplasms / pathology. NM23 Nucleoside Diphosphate Kinases / genetics. NM23 Nucleoside Diphosphate Kinases / physiology
  • [MeSH-minor] Cell Line, Tumor. Humans. Neoplasm Invasiveness. Neoplasm Metastasis. RNA Interference. RNA, Small Interfering / genetics


47. Bestvater F, Dallner C, Spiess E: The C-terminal subunit of artificially truncated human cathepsin B mediates its nuclear targeting and contributes to cell viability. BMC Cell Biol; 2005;6(1):16
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  • [Title] The C-terminal subunit of artificially truncated human cathepsin B mediates its nuclear targeting and contributes to cell viability.
  • Although Delta51CB is supposed to be devoid of the typical CB enzymatic activity, it might play a role in malignancies and trigger cell death/apoptosis independent from the function of the regular enzyme.
  • RESULTS: We investigated such "aberrant" proteins by artificial CB-GFP chimeras covering various sequence parts in respect to their enzymatic activity, their localization in different cell types, and the effects on the cell viability.
  • Unlike the entire full length CB form, the artificial single chain form was not processed and did not reveal typical enzymatic CB activity during transient overexpression in large cell lung carcinoma cells.
  • In contrast, the shorter artificial CB constructs localized in the cytoplasm, inside the cell nucleus, and in the midbodies of dividing cells.
  • Nuclear accumulation of artificially truncated CB variants led to disintegration of nuclei, followed by cell death.
  • CONCLUSION: We propose that cell death associated with CB is not necessarily triggered by its regular enzymatic activity but alternatively by a yet unknown activity profile of truncated CB.
  • Cytoplasmic CB might be able to enter the cell nucleus.
  • The results suggest that besides the N-terminal signal peptide also other CB domains contain patterns which are responsible for a differentiated targeting of the molecule, e.g. to the mitochondria, to the nucleus, or to vesicles.
  • [MeSH-major] Active Transport, Cell Nucleus. Cathepsin B / genetics. Cathepsin B / metabolism
  • [MeSH-minor] Carcinoma, Large Cell / pathology. Cell Line, Tumor. Cell Survival. Cytoplasm / chemistry. Humans. Lung Neoplasms / pathology. Mitochondria / chemistry. Mutagenesis, Site-Directed. Protein Sorting Signals. Protein Subunits. Protein Transport. Signal Transduction. Transfection

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  • (PMID = 15807897.001).
  • [ISSN] 1471-2121
  • [Journal-full-title] BMC cell biology
  • [ISO-abbreviation] BMC Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protein Sorting Signals; 0 / Protein Subunits; EC 3.4.22.1 / Cathepsin B
  • [Other-IDs] NLM/ PMC1087480
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48. Liu J, Zhong X, Zhou Q, Gao AC, Wang Y, Zhu W, Ma L, Zhang Z: [Primary experimental results of methylseleninic acid on the proliferation inhibition and apoptotic induction in human high-metastatic large cell lung cancer cell line L9981]. Zhongguo Fei Ai Za Zhi; 2006 Apr 20;9(2):103-8
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  • [Title] [Primary experimental results of methylseleninic acid on the proliferation inhibition and apoptotic induction in human high-metastatic large cell lung cancer cell line L9981].
  • BACKGROUND: It has been proved that selenium has remarkable effects in the prevention of cancer and proliferation inhibition for breast cancer and prostate cancer.
  • Up to now, little is known, however, if methylseleninic acid (MSA) has the anticancer effect on lung cancer or not.
  • The objective of this study is to detect the effect of MSA on proliferation inhibition and apoptotic induction for human high-metastatic large cell lung cancer cell line L9981, and to explore the molecular mechanisms.
  • METHODS: The changes of proliferation, clone formation, apoptotic level and cell cycles were detected in L9981 by trypan blue staining, clone formation suppression test, and flow cytometry before and after treating with different concentration of MSA.
  • RESULTS: (1)The proliferation ability of L9981 was remarkably inhibited at the concentration of 0.5μmol/L of MSA (P < 0.05), and the cells were arrested at G0/G1 phase after treating with the same concentration. (2)Apoptosis of L9981 was remarkably induced by MSA at the concentration of 2.5μmol/L (P < 0.05). (3)The clone formation ability of L9981 was significantly suppressed by MSA at the concentration of 5.0μmol/L (P < 0.05). (4)The expression levels of P53, P21, Fas, FasL and Bax were remarkably up-regulated after treatment with MSA.
  • CONCLUSIONS: (1)MSA can significantly suppress the proliferation and clone formation ability of human high-metastatic large cell lung cancer cell line L9981, and also induce apoptosis of L9981. (2)The anticancer effects of MSA might be related to regulate the expression of cell cycle-related genes and apoptotic-related genes in the human high-metastatic large cell lung cancer line L9981.

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  • (PMID = 21144291.001).
  • [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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49. Attili VS, Reddy CO: An interesting case of lung mass. J Lab Physicians; 2009 Jan;1(1):25-6
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  • [Title] An interesting case of lung mass.
  • Anaplastic large cell lymphoma of lung.
  • Although lung involvement in cases of lymphoma is observed in as high as 40% of cases, in autopsy series, the exact clinical incidence is not known.
  • However, primary pulmonary lymphomas have been extremely rare (0.4%), and whenever present they are of (Mucosa Associate Lymphoid tissue) MALT type, with occasional diffuse large cell lymphomas.
  • The anaplastic variant is extremely uncommon.
  • Here we report the case of anaplastic primary nonHodgkin's lymphoma of lung and review the literature.

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  • (PMID = 21938246.001).
  • [ISSN] 0974-2727
  • [Journal-full-title] Journal of laboratory physicians
  • [ISO-abbreviation] J Lab Physicians
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC3167963
  • [Keywords] NOTNLM ; Primary pulmonary lymphoma / immuno histo chemistry / treatment
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50. Huang EH, Liao Z, Cox JD, Guerrero TM, Chang JY, Jeter M, Borghero Y, Wei X, Fossella F, Herbst RS, Blumenschein GR Jr, Moran C, Allen PK, Komaki R: Comparison of outcomes for patients with unresectable, locally advanced non-small-cell lung cancer treated with induction chemotherapy followed by concurrent chemoradiation vs. concurrent chemoradiation alone. Int J Radiat Oncol Biol Phys; 2007 Jul 1;68(3):779-85
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  • [Title] Comparison of outcomes for patients with unresectable, locally advanced non-small-cell lung cancer treated with induction chemotherapy followed by concurrent chemoradiation vs. concurrent chemoradiation alone.
  • PURPOSE: To retrospectively compare outcomes for patients with unresectable locally advanced non-small-cell lung cancer (NSCLC) treated at our institution with concurrent chemoradiation with or without induction chemotherapy.
  • A planned subgroup analysis showed that induction chemotherapy was associated with a significant overall survival benefit for patients with adenocarcinoma or large-cell carcinoma (5-year rate, 24% vs. 8%; p = 0.003) but not for those with squamous cell carcinoma.
  • A multivariate analysis of patients with adenocarcinoma or large-cell carcinoma confirmed that induction chemotherapy was the most significant factor associated with better overall survival, with a hazard ratio of 0.47 (95% confidence interval, 0.28-0.78; p = 0.003).
  • CONCLUSION: Our retrospective analysis suggests that in combination with concurrent chemoradiation, induction chemotherapy may provide a small but significant survival benefit for patients with unresectable locally advanced adenocarcinoma or large-cell carcinoma of the lung.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / mortality. Carcinoma, Non-Small-Cell Lung / therapy. Drug Therapy / mortality. Lung Neoplasms / mortality. Lung Neoplasms / therapy. Radiotherapy, Adjuvant / mortality. Risk Assessment / methods

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  • (PMID = 17418967.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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51. Rodig SJ, Shapiro GI: Crizotinib, a small-molecule dual inhibitor of the c-Met and ALK receptor tyrosine kinases. Curr Opin Investig Drugs; 2010 Dec;11(12):1477-90
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  • Crizotinib (PF-02341066), under development by Pfizer, is an orally bioavailable, ATP-competitive, small-molecule inhibitor of the receptor tyrosine kinases (RTKs) c-Met (also known as hepatocyte growth factor receptor) and anaplastic lymphoma kinase (ALK), for the potential treatment of cancers dependent on these oncogenic kinases for growth and survival.
  • Since the first published characterizations of crizotinib only a few years ago, the drug has been extensively validated as a highly specific inhibitor of c-Met and ALK among > 120 different RTKs surveyed.
  • In preclinical tumor xenograft studies, crizotinib inhibited the growth and survival of cell lines dependent upon c-Met or ALK enzymatic activity.
  • Crizotinib has been particularly effective against anaplastic large cell lymphoma and non-small cell lung cancer (NSCLC) cell lines that harbor ALK translocations resulting in expression of oncogenic ALK fusion proteins.
  • At the time of publication, an ongoing phase III clinical trial is comparing crizotinib with standard second-line chemotherapy in previously treated patients with NSCLC harboring ALK rearrangement, and a phase III trial comparing crizotinib with standard chemotherapy in the first-line setting in non-squamous lung cancer is planned.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Protein Kinase Inhibitors / therapeutic use. Proto-Oncogene Proteins c-met / antagonists & inhibitors. Pyrazoles / therapeutic use. Pyridines / therapeutic use. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors
  • [MeSH-minor] Animals. Cell Line, Tumor. Clinical Trials as Topic. Drug Approval. Drug Evaluation, Preclinical. Humans

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  • (PMID = 21154129.001).
  • [ISSN] 2040-3429
  • [Journal-full-title] Current opinion in investigational drugs (London, England : 2000)
  • [ISO-abbreviation] Curr Opin Investig Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; 0 / Pyrazoles; 0 / Pyridines; 53AH36668S / crizotinib; EC 2.7.10.1 / Proto-Oncogene Proteins c-met; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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52. Hu B, Chen J, Liu H, Wu H, Wu Z, Wang Y, Bai Y, Li Y, Zhou Q: [Genome-wide detection of loss of heterozygosity and copy number variation in a human lung large cell carcinoma cell line by affymetrix single-nucleotide polymorphism array 500K.]. Zhongguo Fei Ai Za Zhi; 2008 Jun 20;11(3):327-32
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  • [Title] [Genome-wide detection of loss of heterozygosity and copy number variation in a human lung large cell carcinoma cell line by affymetrix single-nucleotide polymorphism array 500K.].
  • BACKGROUND: Loss of heterozygosity (LOH) and Copy number copy number variation (CNV) of DNA sequences is a common feature of cancer genomes, which is thought to be linked to tumorigenesis and progression.
  • High-density singlenucleotide polymorphism (SNP) genotyping array are able to provided a genotype and copy number information with genome-wide coverage, which is suitable for the analysis of complex genetic alterations present in cancer.
  • Thus a human lung large cell carcinoma cell line NL9980 was assayed for the global profile of LOH and CNV.
  • METHODS: Genomic DNA from the cell line was screened for LOH and CNV using Affymetrix GeneChip(R) Human Mapping array 500K Set.
  • The hybridization intensity data of 500 000 SNP loci was analyzed using Affymetrix proprietary software for genotyping and copy number of each locus, and a genome-wide map of LOH and CNV of the cell line was constructed.
  • And it is possible to achieve high performance outcomes using Affymetrix SNP array 500K to interrogate LOH and CNV in lung cancer genome.
  • This advance of highresolution with allelic information should substantially improve the ability to further understanding of the genetic basis of lung cancers.

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  • (PMID = 20731928.001).
  • [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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53. Oyama T, Rombel IT, Samli KN, Zhou X, Brown KC: Isolation of multiple cell-binding ligands from different phage displayed-peptide libraries. Biosens Bioelectron; 2006 Apr 15;21(10):1867-75
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  • [Title] Isolation of multiple cell-binding ligands from different phage displayed-peptide libraries.
  • A technical challenge in the development of biosensor devices for cancer detection and diagnosis is the identification of ligands that recognize cancer cells with high affinity and specificity.
  • Furthermore, it is unlikely that one cell-binding ligand will provide sufficient biological information, thus, multiple ligands for a given cancer type will be needed for confident clinical diagnosis.
  • Biopanning of phage displayed peptide libraries is a route to isolation of specific cell-binding reagents.
  • A potential approach towards isolation of multiple ligands for a single cell type is to pan against the same cell type using different peptide libraries.
  • Here we report the synthesis of a new 20-mer peptide-phage library and its use to select a peptide that binds to the large cell lung carcinoma cell line, H1299.
  • The isolated phage clone binds H1299 cells 80 times better than a control phage and can distinguish between H1299 and normal control cells.
  • The phage clone also binds to the lung pleura epidermoid cell line, Calu-1 but not to all lung carcinoma cell lines.
  • The tetrameric peptide can be used to deliver a fluorescent quantum dot to H1299 cells.
  • Our results imply that cell-based biopanning can isolate cell-binding ligands that may be of utility for cancer diagnosis, and isolation of cell-targeting peptides from different peptide libraries can expand the repertoire of cell-binding reagents.

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  • (PMID = 16386888.001).
  • [ISSN] 0956-5663
  • [Journal-full-title] Biosensors & bioelectronics
  • [ISO-abbreviation] Biosens Bioelectron
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA106646; United States / NCI NIH HHS / CA / 1 R01 CA 106646-01
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Ligands; 0 / Peptide Library
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54. Tomas D, Ledinsky M, Belicza M, Kruslin B: Multiple metastases to the small bowel from large cell bronchial carcinomas. World J Gastroenterol; 2005 Mar 7;11(9):1399-402
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  • [Title] Multiple metastases to the small bowel from large cell bronchial carcinomas.
  • AIM: Metastases from lung cancer to gastrointestinal tract are not rare at postmortem studies but the development of clinically significant symptoms from the gastrointestinal metastases is very unusual.
  • RESULTS: We observed three patients who presented with multiple metastases from large cell bronchial carcinoma to small intestine.
  • Microscopically, all tumors showed a same histological pattern and consisted almost exclusively of strands and sheets of poorly cohesive, polymorphic giant cells with scanty, delicate stromas.
  • Few smaller polygonal anaplastic cells dispersed between polymorphic giant cells, were also observed.
  • Immunohistochemistry showed positive staining of the tumor cells with cytokeratin and vimentin.
  • Microscopically and immunohistochemically all metastases had a similar pattern to primary anaplastic carcinoma of the small intestine.
  • CONCLUSION: In patients with small intestine tumors showing anaplastic features, especially with multiple tumors, metastases from large cell bronchial carcinoma should be first excluded, because it seems that they are more common than expected.
  • [MeSH-major] Bronchial Neoplasms / pathology. Carcinoma, Large Cell / secondary. Intestinal Neoplasms / secondary. Intestine, Small / pathology
  • [MeSH-minor] Anaplasia / pathology. Female. Giant Cells / pathology. Humans. Male. Middle Aged

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  • (PMID = 15761985.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  • [Other-IDs] NLM/ PMC4250694
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55. Wang T, Xu J, Zhong NS: [Relationship between the acquired multi-drug resistance of human large cell lung cancer cell line NCI-H460 by cisplatin selection and p53 mutation]. Zhonghua Jie He He Hu Xi Za Zhi; 2005 Feb;28(2):102-7
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  • [Title] [Relationship between the acquired multi-drug resistance of human large cell lung cancer cell line NCI-H460 by cisplatin selection and p53 mutation].
  • OBJECTIVE: To explore the role of p53 mutation in the development of acquired multi-drug resistance during lung cancer chemotherapy.
  • METHODS: A resistance large cell lung carcinoma cell line (H460/DDP) was established by high dose (50 micromol/L) cisplatin intermittent selection from its parental cell NCI-H460 that had wild type p53 (wtp53).
  • Several multi-drug resistant proteins (MRP) including lung relative protein (LRP), P-gp, MRP, glutathione transferase-pi, topoisomerase II and P53 were checked by immunocytochemistry.
  • The H460/DDP cells were transected with plasmid pShuttle-CMV-wtp53 cDNA and measurement of drug sensitivity was performed after transfection.
  • RESULTS: The resistance index to cisplatin and carboplatin in H460/DDP cell line was 10.21 and 9.98 respectively, and the cell line also exhibited cross-resistance to 5-fluorouracil, etoposide, methotrexate, adriamycin, epirubicin, bleomycin and novantrone, except for taxol.
  • H460/DDP cells transfected with plasmid pShuttle-CMV-wtp53 cDNA reversed partly (53.2%) the resistance to cisplatin/carboplatin, compared to the H460/DDP cells transfected with blank vector.
  • CONCLUSIONS: p53 mutation induced by cisplatin/carboplatin might play an important role in the development of acquired multi-drug resistance of lung cancer chemotherapy. wtp53 substitute therapy during chemotherapy may be an effective method to overcome the acquired drug resistance.
  • [MeSH-major] Carcinoma, Large Cell / pathology. Drug Resistance, Neoplasm / genetics. Lung Neoplasms / pathology. Multidrug Resistance-Associated Proteins / biosynthesis. Mutation. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Cell Line, Tumor. Cisplatin. Drug Resistance, Multiple / genetics. Humans. P-Glycoprotein / biosynthesis. Transfection


56. Jokoji R, Yamasaki T, Minami S, Komuta K, Sakamaki Y, Takeuchi K, Tsujimoto M: Combination of morphological feature analysis and immunohistochemistry is useful for screening of EML4-ALK-positive lung adenocarcinoma. J Clin Pathol; 2010 Dec;63(12):1066-70
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  • [Title] Combination of morphological feature analysis and immunohistochemistry is useful for screening of EML4-ALK-positive lung adenocarcinoma.
  • BACKGROUND: A subset of lung cancers harbours the fusion gene echinoderm microtubule-associated protein-like-4-anaplastic lymphoma kinase (EML4-ALK).
  • Recently, immunohistochemistry for ALK has shown sensitivity for the detection of EML4-ALK-positive lung adenocarcinoma almost equal to that of the fluorescence in situ hybridisation (FISH) assay.
  • AIMS: To study the clinicopathological features of EML4-ALK-positive lung adenocarcinoma in a large number of surgically resected samples using immunohistochemistry, in order to establish a useful screening method for EML4-ALK-positive lung adenocarcinoma.
  • METHODS: Immunohistochemistry for ALK was used to screen for EML4-ALK-positive lung adenocarcinomas in 254 cases of surgically resected samples.
  • RESULTS: EML4-ALK-positive cases were detected in 3.1% of lung adenocarcinomas (8/254).
  • EML4-ALK-positive lung adenocarcinomas showed significant associations with intra- and/or extra-cytoplasmic mucin (p=0.0001), and cribriform pattern with excessive extracytoplasmic mucin (p<0.0001).
  • Signet-ring cell appearance alone lacked significance (p=0.149).
  • CONCLUSION: EML4-ALK-positive lung adenocarcinoma has a tendency to express a characteristic morphological pattern.
  • The combined use of morphological feature analysis and immunohistochemistry may be a useful and cost effective screening method for EML4-ALK lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Biomarkers, Tumor / metabolism. Early Detection of Cancer / methods. Lung Neoplasms / pathology. Oncogene Proteins, Fusion / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Differentiation. Cytoplasm / enzymology. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Neoplasm Proteins / metabolism

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  • (PMID = 20935334.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / EML4-ALK fusion protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion
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57. Martin AC, Friedlander M, Kiernan MC: Paraneoplastic mononeuritis multiplex in non-small-cell lung carcinoma. J Clin Neurosci; 2006 Jun;13(5):595-8
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  • [Title] Paraneoplastic mononeuritis multiplex in non-small-cell lung carcinoma.
  • A 60-year-old man developed two selective peripheral mononeuropathies of the peroneal and later the radial nerve, shortly after a diagnosis of large-cell lung carcinoma.
  • Subsequent magnetic resonance imaging of the lower limb excluded focal compression or malignant infiltration along the course of the peroneal nerve, and there was no signal change within the nerve, prompting a diagnosis of paraneoplastic mononeuritis multiplex.
  • Neither the patient's large-cell lung carcinoma nor mononeuritis multiplex responded to chemotherapy, and he died within 6 months of the initial diagnosis.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / radiography. Paraneoplastic Polyneuropathy / radiography. Peroneal Neuropathies / radiography. Radial Neuropathy / radiography

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  • (PMID = 16564174.001).
  • [ISSN] 0967-5868
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Scotland
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58. Willemsen MA, Breedveld GJ, Wouda S, Otten BJ, Yntema JL, Lammens M, de Vries BB: Brain-Thyroid-Lung syndrome: a patient with a severe multi-system disorder due to a de novo mutation in the thyroid transcription factor 1 gene. Eur J Pediatr; 2005 Jan;164(1):28-30
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  • [Title] Brain-Thyroid-Lung syndrome: a patient with a severe multi-system disorder due to a de novo mutation in the thyroid transcription factor 1 gene.
  • He died from large cell lung carcinoma at the age of 23 years.
  • A de novo heterozygous insertion mutation 859-860insC in the TITF-1 gene was demonstrated.
  • CONCLUSION: TITF-1 gene mutations should be considered in paediatric and adult patients with unexplained (combinations of) chorea, mental retardation, primary hypothyroidism, and chronic lung disease.
  • Introduction of a name for the disorder, e.g.
  • Brain-Thyroid-Lung syndrome, would probably facilitate further recognition.
  • Whether the TITF-1 gene mutation in this patient predisposed to the development of lung cancer remains speculative.

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  • [ISSN] 0340-6199
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  • [ISO-abbreviation] Eur. J. Pediatr.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
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59. Petrović M, Tomić I, Ilić S: [Neuroendocrine differentiation as a survival prognostic factor in advanced non-small cell lung cancer]. Vojnosanit Pregl; 2007 Aug;64(8):525-9
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  • [Title] [Neuroendocrine differentiation as a survival prognostic factor in advanced non-small cell lung cancer].
  • BACKGROUND/AIM: Neuroendrocine lung tumors are histologically heterogenous group of cancers with different clinical progression.
  • In non-small cell lung cancer (NSCLC) neuroendocrine differentiation exists in 10-30% of patients.
  • The aim of this study was to determine the frequency and influence of neuroendocrine differentiation on survival of treated patients with advanced non-small cell lung cancer (NSCLC).
  • METHODS: A clinical trial included 158 patients (74% males and 26% females), with the diagnosis of NSCLC, determined by histological verification.
  • RESULTS: A total of 53 patients (34%) had NSCLC with neuroendocrine differentiation, confirmed rather in large cell lung cancer and lung adenocarcinoma (66.7% and 40%, respectively).
  • One year follow-up survival time was longer in the patients with neuron specific enolase and chromogranin A expression lung cancer (p < 0.001).
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / mortality. Chromogranin A / analysis. Lung Neoplasms / mortality. Phosphopyruvate Hydratase / analysis. Synaptophysin / analysis


60. Settleman J: Cell culture modeling of genotype-directed sensitivity to selective kinase inhibitors: targeting the anaplastic lymphoma kinase (ALK). Semin Oncol; 2009 Apr;36(2 Suppl 1):S36-41
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  • [Title] Cell culture modeling of genotype-directed sensitivity to selective kinase inhibitors: targeting the anaplastic lymphoma kinase (ALK).
  • Selective kinase inhibitors have emerged as an important class of cancer therapeutics.
  • The clinical success of drugs such as imatinib, erlotinib, and lapatinib, together with findings demonstrating the important relationship between specific tumor genotypes and clinical response to these agents, also has brought to the forefront the concept of "personalized cancer medicine."
  • The potential broader significance of this relationship has been further highlighted in preclinical studies using tumor-derived cell lines as a model system that can faithfully recapitulate the association of specific genotypes with drug sensitivity, suggesting the utility of cancer cell lines to identify novel candidate biomarkers for predicting clinically responsive patient subsets for newly developed anticancer agents.
  • The case of the anaplastic lymphoma kinase (ALK) nicely exemplifies this, and cell line profiling has revealed that ALK mutations present in a subset of anaplastic large cell lymphomas (ALCLs), non-small cell lung cancers (NSCLCs), and neuroblastomas appear to sensitize cancer cells to treatment with selective ALK kinase inhibitors.
  • Such findings suggest that genotype-based stratification of cancer patients for treatment with selective kinase inhibitors, even across multiple diseases of distinct tissue origin, may be essential for maximizing their clinical benefit.
  • [MeSH-minor] Cells, Cultured. Drug Design. Humans. Receptor Protein-Tyrosine Kinases

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  • (PMID = 19393834.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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61. Uchida N, Fukino S, Kodama W, Tamai N, Hiroe T, Fukata T: Large-cell carcinoma of the lung with a remarkable preoperative elevation of serum carcinoembryonic antigen level. Gen Thorac Cardiovasc Surg; 2007 May;55(5):217-21
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  • [Title] Large-cell carcinoma of the lung with a remarkable preoperative elevation of serum carcinoembryonic antigen level.
  • Carcinoembryonic antigen, a serum tumor marker, is useful for diagnosing cancer and for following the response to therapy in cancer cases.
  • Chest computed tomography revealed a tumor in the posterior segment of the right lung and a swollen right interlobar lymph node.
  • Right lung pneumonectomy and node dissection were performed.
  • A histological diagnosis determined that the tumor was a large-cell carcinoma at clinical stage IIA.
  • Immunohistochemical analysis detected the production of carcinoembryonic antigen by the tumor cells.
  • This is a rare case of lung cancer with no evidence of recurrence and metastasis for 8 years despite markedly elevated preoperative carcinoembryonic antigen levels.
  • [MeSH-major] Carcinoembryonic Antigen / blood. Carcinoma, Large Cell / immunology. Lung Neoplasms / immunology

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62. Cheng M, Ott GR: Anaplastic lymphoma kinase as a therapeutic target in anaplastic large cell lymphoma, non-small cell lung cancer and neuroblastoma. Anticancer Agents Med Chem; 2010 Mar;10(3):236-49
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  • [Title] Anaplastic lymphoma kinase as a therapeutic target in anaplastic large cell lymphoma, non-small cell lung cancer and neuroblastoma.
  • Anaplastic lymphoma kinase (ALK), a receptor tyrosine kinase in the insulin receptor superfamily, was originally identified as the oncogenic NPM (nucleophosmin)-ALK fusion protein due to a t (2;5) chromosomal translocation in anaplastic large cell lymphomas.
  • Many other chromosomal rearrangements or gene mutations/amplification leading to enhanced ALK activity have subsequently been identified and characterized in a number of human cancer types.
  • The recent reports of EML4 (echinoderm microtubule-associated protein-like 4)-ALK oncogenic proteins in non-small cell lung cancer (NSCLC) and the identification of ALK activating point mutations and gene amplification in neuroblastoma have indicated ALK as a potential major therapeutic target for human cancers.
  • In this review, the role of oncogenic ALK in development of various human cancers is summarized and the efforts and progress of developing small molecule ALK inhibitors as potential cancer therapeutics are updated.
  • The challenges and future directions of developing small molecule ALK inhibitors as cancer therapeutics are discussed.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Lymphoma, Large-Cell, Anaplastic / drug therapy. Neuroblastoma / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors


63. Palmer RH, Vernersson E, Grabbe C, Hallberg B: Anaplastic lymphoma kinase: signalling in development and disease. Biochem J; 2009 Jun 15;420(3):345-61
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  • [Title] Anaplastic lymphoma kinase: signalling in development and disease.
  • The ALK (anaplastic lymphoma kinase) RTK was originally identified as a member of the insulin receptor subfamily of RTKs that acquires transforming capability when truncated and fused to NPM (nucleophosmin) in the t(2;5) chromosomal rearrangement associated with ALCL (anaplastic large cell lymphoma).
  • To date, many chromosomal rearrangements leading to enhanced ALK activity have been described and are implicated in a number of cancer types.
  • Recent reports of the EML4 (echinoderm microtubule-associated protein like 4)-ALK oncoprotein in NSCLC (non-small cell lung cancer), together with the identification of activating point mutations in neuroblastoma, have highlighted ALK as a significant player and target for drug development in cancer.
  • [MeSH-minor] Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / metabolism. Carcinoma, Non-Small-Cell Lung / pathology. Humans. Lung Neoplasms / genetics. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / genetics. Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology. Models, Biological. Neuroblastoma / genetics. Neuroblastoma / metabolism. Neuroblastoma / pathology. Nuclear Proteins / genetics. Nuclear Proteins / metabolism. Oncogene Proteins, Fusion / genetics. Oncogene Proteins, Fusion / metabolism. Receptor Protein-Tyrosine Kinases

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  • (PMID = 19459784.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / EML4-ALK fusion protein, human; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Number-of-references] 237
  • [Other-IDs] NLM/ PMC2708929
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64. Nakazato Y, Imai K, Abe T, Tamura N, Shimazu K: Unpleasant sweet taste: a symptom of SIADH caused by lung cancer. J Neurol Neurosurg Psychiatry; 2006 Mar;77(3):405-6
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  • [Title] Unpleasant sweet taste: a symptom of SIADH caused by lung cancer.
  • A 56 year old woman with large cell lung carcinoma complained of an unpleasant sweet taste (dysgeusia).
  • [MeSH-major] Carcinoma, Large Cell / diagnosis. Dysgeusia / etiology. Hyponatremia / complications. Inappropriate ADH Syndrome / etiology. Lung Neoplasms / diagnosis. Taste
  • [MeSH-minor] Diagnosis, Differential. Female. Humans. Middle Aged. Reference Values. Sodium / blood

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  • (PMID = 16484655.001).
  • [ISSN] 0022-3050
  • [Journal-full-title] Journal of neurology, neurosurgery, and psychiatry
  • [ISO-abbreviation] J. Neurol. Neurosurg. Psychiatry
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 9NEZ333N27 / Sodium
  • [Other-IDs] NLM/ PMC2077685
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65. Swarts JC, Vosloo TG, Cronje SJ, Du Plessis WC, Van Rensburg CE, Kreft E, Van Lier JE: Cytotoxicity of a series of ferrocene-containing beta-diketones. Anticancer Res; 2008 Sep-Oct;28(5A):2781-4
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  • [Title] Cytotoxicity of a series of ferrocene-containing beta-diketones.
  • In contrast, reduced ferrocene derivatives frequently only show activity if cell components can oxidise them inside cells to the ferrocenium species.
  • MATERIALS AND METHODS: Ferrocene-containing beta-diketones of the type FcCOCH2COR with Fc=ferrocenyl and R=CF3, CCl3, CH3, Ph(=C6H5, phenyl) and Fc, were tested for cytotoxicity against HeLa (human cervix epitheloid), COR L23 (human large cell lung carcinoma) and platinum resistant CoLo320DM (human colorectal) and COR L23/CPR cancer cell lines.
  • Cell survival was measured by means of the colorometric 3-(4,5-dimethylthiazol-2-yl)-diphenyltetrazolium bromide (MTT) assay.
  • RESULTS: The mean drug concentration from 3 experiments causing 50% cell growth inhibition, (IC50) values, varied between 4.5 and 85.0 micromol dm(-3'), with the CF3(-) containing beta-diketone being the most active.
  • Drug activity was inversely proportional to the formal reduction potential, Eo', of the ferrocenyl group, and dependent on the R group in the general beta-diketone structure.
  • The CF3 complex was more cytotocic than cisplatin inter alia against platinum-resistant cell lines, and at least eight times more reactive against cancer cell lines than against PHA (phytohaemagglutinin)-stimulated lymphocyte cultures.

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  • (PMID = 19035310.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ferrous Compounds; 0 / Ketones; 0 / Phytohemagglutinins; 12125-80-3 / ferrocenium; U96PKG90JQ / ferrocene
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66. Bai XY, Shen H: [Quantitative study of thyroid transcription factor-1 protein expression in lung carcinoma cell nucleus by tissue microarray]. Nan Fang Yi Ke Da Xue Xue Bao; 2006 Oct;26(10):1423-6
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  • [Title] [Quantitative study of thyroid transcription factor-1 protein expression in lung carcinoma cell nucleus by tissue microarray].
  • OBJECTIVE: To investigate thyroid transcription factor-1 (TTF-1) expression in normal human adult type II alveolar epithelial cells, embryonic pneumocytes, lung carcinoma cells and lymph node metastases of lung cancer.
  • METHODS: Lung carcinoma tissue microarray was constructed containing 765 cores of 20 normal adult lung tissues, 15 embryonic lung tissues, 100 lung carcinomas and 55 corresponding lymph node metastases.
  • RESULTS: The number TTF-1 positive units (PU) was smaller in the nuclei of embryonic pneumocytes than in those of normal adult type II alveolar epithelial cells (P<0.001).
  • The nuclei of lung carcinoma cells had smaller TTF-1 PU than normal adult type II alveolar epithelial cells and embryonic pneumocyte nuclei (P<0.001).
  • The lung adenocarcinoma and small cell lung carcinoma cell nuclei had greater TTF-1 PU than squamous cell carcinoma and large cell lung carcinoma cell nuclei (P<0.001).
  • TTF-1 PU was greater in squamous cell carcinoma cell nuclei than in large cell lung carcinoma cell nuclei (P<0.001).
  • In lung adenocarcinoma, squamous cell lung carcinoma and large cell lung carcinoma, TTF-1 PU was greater in the cancerous cell nuclei of lymph node metastases than in the corresponding primary carcinoma cell nuclei (P<0.001, P<0.001, and P<0.05, respectively).
  • In small cell lung carcinoma, TTF-1 PU of the cancerous cell nuclei of lymph node metastases was similar to that of primary carcinomas (P>0.05).
  • TTF-1 PU was greater in lung carcinoma with lymph node metastases than in those without metastalsis (P<0.001).
  • TTF-1 PU of the cell nuclei was not associated with the tumor growth pattern, differentiation and patients' gender (P>0.05), but was greater in TNM stage II-IV than in stage I (P<0.001).
  • CONCLUSIONS: The amount of TTF-1 in the cell nuclei decreases in the order of normal adult type II alveolar epithelial cells, embryonic pneumocytes and lung carcinoma cells.
  • TTF-1 expression is higher in adenocarcinoma and small cell carcinoma and lower in squamous carcinoma and large cell carcinoma.
  • Stronger TTF-1 expression is associated with greater likeliness of lung carcinoma metastatie, and can be an important hallmark for metastasis potential of lung adenocarcinoma, squamous cell carcinoma and large cell carcinoma.
  • [MeSH-major] Cell Nucleus / metabolism. Lung Neoplasms / metabolism. Nuclear Proteins / biosynthesis. Tissue Array Analysis / methods. Transcription Factors / biosynthesis
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Biomarkers, Tumor / metabolism. Carcinoma, Small Cell / metabolism. Carcinoma, Small Cell / pathology. Humans. Immunohistochemistry. Lymphatic Metastasis

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  • (PMID = 17062341.001).
  • [ISSN] 1673-4254
  • [Journal-full-title] Nan fang yi ke da xue xue bao = Journal of Southern Medical University
  • [ISO-abbreviation] Nan Fang Yi Ke Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / thyroid nuclear factor 1
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67. Kasuganti D, Cimbaluk D, Gattuso P: Lymph node metastasis of large-cell carcinoma of the lung in a seventeen-year-old patient: diagnosis by fine-needle aspiration. Diagn Cytopathol; 2006 Dec;34(12):852-3
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  • [Title] Lymph node metastasis of large-cell carcinoma of the lung in a seventeen-year-old patient: diagnosis by fine-needle aspiration.
  • [MeSH-major] Carcinoma, Large Cell / pathology. Lung Neoplasms / pathology

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  • (PMID = 17115438.001).
  • [ISSN] 8755-1039
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
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68. Voltolini L, Rapicetta C, Luzzi L, Ghiribelli C, Ligabue T, Paladini P, Gotti G: Lung cancer with chest wall involvement: predictive factors of long-term survival after surgical resection. Lung Cancer; 2006 Jun;52(3):359-64
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  • [Title] Lung cancer with chest wall involvement: predictive factors of long-term survival after surgical resection.
  • Multimodal management of lung cancer extending to chest wall and type of surgical procedure to be performed are still debated.
  • The aim of this retrospective analysis was to analyze the predictive factors of long-term survival after surgery, focusing on depth of infiltration, type of surgical intervention and possible role of preoperative therapies, comparing survival of these patients with that of a group of patients affected by a Pancoast tumour and surgical treated in the same period.
  • Histology revealed adenocarcinoma in 23 cases, squamous cell carcinoma in 34, large cells anaplastic carcinoma in 8, adenosquamous carcinoma in 3.
  • Histological type was adenocarcinoma in 10 cases, squamous cell carcinoma in 4 and adenosquamous carcinoma in 1.
  • A univariate analysis performed in the CW group showed that survival was significantly affected by nodal status, stage, extension of chest wall invasion, type of lung resection and residual disease.
  • [MeSH-major] Carcinoma / mortality. Lung Neoplasms / mortality. Thoracic Wall

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  • (PMID = 16644062.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Ireland
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69. Monica V, Ceppi P, Righi L, Tavaglione V, Volante M, Pelosi G, Scagliotti GV, Papotti M: Desmocollin-3: a new marker of squamous differentiation in undifferentiated large-cell carcinoma of the lung. Mod Pathol; 2009 May;22(5):709-17
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  • [Title] Desmocollin-3: a new marker of squamous differentiation in undifferentiated large-cell carcinoma of the lung.
  • Lung cancer classification in small-cell and non-small-cell types was recently challenged by data on the differential efficacy of new cytotoxic agents in specific histotypes.
  • An accurate histotype definition has therefore gained interest in both preoperative and surgical materials, but is a hard task especially in undifferentiated large-cell tumors lacking morphological signs of squamous or glandular differentiation.
  • On the basis of gene expression profiling data, reporting a remarkable differential expression of desmocollin-3 (a protein localized in desmosomal junctions of stratified epithelial) between adeno- and squamous cancers, we immunostained 62 cases of resected undifferentiated large-cell lung carcinomas for desmocollin-3 (and for TTF-1, p63 and mucin stain), to test its ability to identify a (residual) squamous phenotype, if present.
  • Desmocollin-3 was expressed in almost half of the undifferentiated large-cell cancers and was mutually exclusive with TTF-1 (positive in 39%; the remaining 18 % of cases was double negative).
  • Special large-cell carcinoma variants expressed desmocollin-3 in 6 of 6 basaloid, 7 of 12 clear-cell types, again mutually exclusive with TTF-1 expression.
  • In 31 cytological samples diagnosed as 'non-small-cell lung carcinoma', desmocollin-3 was again mutually exclusive with TTF-1 and stained all squamous carcinomas, 1 of 19 adenocarcinoma only, and 50% of large-cell carcinoma (all histologically confirmed).
  • This combined morphophenotypic approach may represent a valid adjunct (for both surgical and cytological samples) in the selection of patients with lung cancer to medical treatments tailored according to different efficacy in different lung carcinomas of the squamous, adeno- and large-cell types.
  • [MeSH-major] Biomarkers, Tumor / analysis. Carcinoma, Large Cell / pathology. Carcinoma, Squamous Cell / pathology. Desmocollins / biosynthesis. Lung Neoplasms / pathology

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  • (PMID = 19287461.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / DSC3 protein, human; 0 / Desmocollins; 0 / TTF1 protein, human
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70. Liao L, Zhou Q, Chen J, Zhu D, Ma L, Yan H, Zhu W, Liu H: [Construction and screening of the subtracted cDNA library of human large cell lung cancer lines with different metastatic potentials]. Zhongguo Fei Ai Za Zhi; 2007 Jun 20;10(3):163-7
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  • [Title] [Construction and screening of the subtracted cDNA library of human large cell lung cancer lines with different metastatic potentials].
  • BACKGROUND: Screening metastatic-related genes of lung cancer is helpful to understand the molecular mechanisms of lung cancer invasion and metastasis.
  • In order to screen the differential expression genes related to metastasis of lung cancer, we constructed and preliminarily screened the subtracted cDNA libraries of human large cell lung cancer cell lines with different metastatic potentials in this study.
  • METHODS: Subtracted cDNA library was constructed in the different metastastic potential cell lines NL9980 and L9981 by suppression subtractive hybridization (SSH) method.
  • RESULTS: The subtracted cDNA libraries were successfully constructed in the different metastastic potential cell lines NL9980 and L9981.
  • The forward and reverse subtracted cDNA libraries of different metastastic potential cell lines are constructed by this method.
  • The differential expression genes related to tumor metastasis might exist in the human large cell lung cancer cell lines with different metastasis potential.

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  • (PMID = 21118638.001).
  • [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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71. Bergner A, Kellner J, Tufman A, Huber RM: Endoplasmic reticulum Ca2+-homeostasis is altered in Small and non-small Cell Lung Cancer cell lines. J Exp Clin Cancer Res; 2009;28:25
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  • [Title] Endoplasmic reticulum Ca2+-homeostasis is altered in Small and non-small Cell Lung Cancer cell lines.
  • BACKGROUND: Knowledge of differences in the cellular physiology of malignant and non-malignant cells is a prerequisite for the development of cancer treatments that effectively kill cancer without damaging normal cells.
  • We aimed to investigate if the endoplasmic reticulum (ER) Ca2+-homeostasis is different in lung cancer and normal human bronchial epithelial (NHBE) cells.
  • RESULTS: In a Small Cell Lung Cancer (H1339) and an Adeno Carcinoma Lung Cancer (HCC) cell line but not in a Squamous Cell Lung Cancer (EPLC) and a Large Cell Lung Cancer (LCLC) cell line the ER Ca2+-content was reduced compared to NHBE.
  • Lowering the ER Ca2+-content with CPA led to increased proliferation NHBE and lung cancer cells.
  • CONCLUSION: The significant differences in Ca2+-homeostasis between lung cancer and NHBE cells could represent a new target for cancer treatments.
  • [MeSH-major] Calcium / metabolism. Carcinoma, Non-Small-Cell Lung / metabolism. Endoplasmic Reticulum / metabolism. Lung Neoplasms / metabolism. Small Cell Lung Carcinoma / metabolism
  • [MeSH-minor] Calcium-Binding Proteins / metabolism. Cell Line, Tumor. Homeostasis. Humans. Immunohistochemistry. Microscopy, Fluorescence. Sarcoplasmic Reticulum Calcium-Transporting ATPases / metabolism


72. Petersen I, Kotb WF, Friedrich KH, Schlüns K, Böcking A, Dietel M: Core classification of lung cancer: correlating nuclear size and mitoses with ploidy and clinicopathological parameters. Lung Cancer; 2009 Sep;65(3):312-8
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  • [Title] Core classification of lung cancer: correlating nuclear size and mitoses with ploidy and clinicopathological parameters.
  • We attempted to establish a microscopy based tumour characterization providing insight into the genetics of cancer cells and in particular their DNA ploidy.
  • This classification was applied to 155 lung cancer samples from all major histologic types and the results were correlated with the analysis by DNA image cytometry and patient survival.
  • The morphological assessments correlated highly significantly with the DNA ploidy parameters, e.g. small cell lung carcinomas showed the smallest values for nuclear size (mean core score of 1.18) and DNA content (DNA index mean of 2.08c) being highly significantly different from adenocarcinomas (1.95/3.10c), large cell lung carcinoma (2.00/3.26c) and squamous cell carcinoma (2.20/3.42c).
  • In non-small cell lung carcinoma (NSCLC) in general and adenocarcinoma in particular, the core size variability correlated significantly with grading and survival.
  • As a complement to histologic tumour diagnosis the core classification should help to better stratify cancer subtypes.
  • [MeSH-major] Cell Nucleus / ultrastructure. DNA, Neoplasm / analysis. Lung Neoplasms / classification. Lung Neoplasms / genetics

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  • (PMID = 19168259.001).
  • [ISSN] 1872-8332
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / DNA, Neoplasm
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73. Yang CJ, Huang YJ, Wang CY, Wang PH, Hsu HK, Tsai MJ, Chen YC, Bharath Kumar V, Huang MS, Weng CF: Antiproliferative effect of Toona sinensis leaf extract on non-small-cell lung cancer. Transl Res; 2010 Jun;155(6):305-14
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  • [Title] Antiproliferative effect of Toona sinensis leaf extract on non-small-cell lung cancer.
  • However, their effect against cancer cells is not well explored.
  • In this study, to understand the cytotoxic effect and molecular mechanism stimulated by TSL-1 (TS leaf extract fraction) we employed three different non-small-cell lung cancer (NSCLC) cell lines: H441 cells (lung adenocarcinoma), H661 cells (lung large cell carcinoma) and H520 cells (lung squamous cell carcinoma).
  • IC50 value was varied between these three cell lines, the least IC(50) value was observed in TSL-1-treated H661cells.
  • Exposure of NSCLC cells to TSL-1 caused cell-cycle arrest in subG1 phase and caused apoptosis.
  • Moreover, TSL-1 treatment decreased the cell-cycle regulators; cyclin D1 and CDK4 proteins by up regulating p27 expression in a dose-dependent manner.
  • Thus, the TSL-1-induced apoptosis was further confirmed by cell morphology, subG1 peak accumulation, poly(adenosine diphosphate [ADP]-ribose) polymerase (PARP) cleavage, propidium iodide (PI)-Annexin-V double staining, and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay.
  • The decreased Bcl2 protein level was concurrent with an increased Bax protein level in all 3 cell lines.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / pathology. Lung Neoplasms / pathology. Plant Extracts / therapeutic use. Plant Leaves / chemistry
  • [MeSH-minor] Animals. Apoptosis / drug effects. Carcinoma, Squamous Cell / pathology. Cell Cycle / drug effects. Cell Division / drug effects. Cell Line, Tumor. Female. G1 Phase / drug effects. Humans. Male. Mice. Mice, Nude


74. Ye S, Feng Z, Zhu W, Cai C, Li L, Sun L, Wan H, Ma L, Zhou Q: [Construction of the suppression subtractive cDNA libraries of human large cell lung cancer line L9981 before and after transfection with nm23-H1 gene.]. Zhongguo Fei Ai Za Zhi; 2008 Aug 20;11(4):482-8
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  • [Title] [Construction of the suppression subtractive cDNA libraries of human large cell lung cancer line L9981 before and after transfection with nm23-H1 gene.].
  • BACKGROUND: It has been proven that nm23-H1 gene is an important metastaticsuppressed gene of lung cancer.
  • In order to screen the differential expression genes related to nm23-H1 , we constructed the suppression subtractive cDNA libraries of human large cell lung cancer line L9981 transfected and untransfected with nm23-H1 gene by suppression subtractive hybridization (SSH) in this study, which lay a solid foundation for further screening and cloning metastatic-related genes of nm23-H1.
  • METHODS: The forward and reverse suppression subtractive cDNA libraries were constructed in the human large cell lung cancer line L9981 before and after transfection with nm23-H1 gene (L9981 and L9981-nm23-H1) by SSH method.
  • RESULTS: The suppression subtractive cDNA libraries were successfully constructed in the human large cell lung cancer line L9981 transfected and untransfected with nm23-H1 gene (L9981-nm23-H1 and L9981).
  • The forward and reverse suppression subtractive cDNA libraries of human large cell lung cancer line L9981 transfected and untransfected with nm23-H1 gene (L9981-nm23-H1 and L9981) are successfully constructed by SSH and T/A cloning technology.
  • The expression of nm23-H1 gene in the human large cell lung cancer cell lines may affect the differential expression of some metastatic-related genes.

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  • (PMID = 20735954.001).
  • [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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75. Pardo J, Martinez-Peñuela AM, Sola JJ, Panizo A, Gúrpide A, Martinez-Peñuela JM, Lozano MD: Large cell carcinoma of the lung: an endangered species? Appl Immunohistochem Mol Morphol; 2009 Oct;17(5):383-92
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  • [Title] Large cell carcinoma of the lung: an endangered species?
  • This study aims to evaluate large cell carcinomas (LCC) of the lung with a panel of immunohistochemical markers in an attempt to identify tumors belonging to other categories.
  • The tumors were 82 (81.3%) classic LCC, 7 (6.9%) neuroendocrine LCC, 6 (5.9%) lymphoepithelioma-like LCC, 3 (2.9%) basaloid LCC, 2 (2%) clear cell LCC, and 1 (1%) LCC with rhabdoid phenotype.
  • Characteristic classic LCC immunophenotype was loss of staining with CK5/6, CK14 positive in most squamous cell carcinoma (SCC), lack of MOC 31 positive in most adenocarcinomas, and positive immunoreactivity to EGFR, PDGFR-alpha and c-kit.
  • 16 (19.5%) of 82 classic LCC correspond to undifferentiated adenosquamous carcinomas, since they displayed conflicting immunostaining for markers of both SCC and adenocarcinomas.
  • The use of 7 immunohistochemical markers, consisting of TTF-1, CK7, CK19, p63, 34betaE12, thrombomodulin, and CD44v6, markedly reduces dramatically to less than 10%, the number of classic LCC by readily identifying cases of poorly differentiated SCCs, adenosquamous carcinoma and adenocarcinomas.

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  • (PMID = 19444077.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal
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76. Zhang Z, Fan Y, Zhou Q, Wang Y, Ma L, Chen X, Zhu W, Yang X, Zhao Y: [Effects of polysaccharid on expression of angiogenic-related genes in human high-metastatic large cell lung cancer cell line L9981]. Zhongguo Fei Ai Za Zhi; 2006 Apr 20;9(2):137-42
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  • [Title] [Effects of polysaccharid on expression of angiogenic-related genes in human high-metastatic large cell lung cancer cell line L9981].
  • BACKGROUND: Lung cancer is one of the most malignant cancers which is hazarding the people's health and life in the world.
  • The aim of this study is to observe the effects of polysaccharid (PS-T) on expression of angiogenic-related gene mRNA in human high-metastatic large cell lung cancer cell line L9981, and to explore its possible molecular mechanism.
  • CONCLUSIONS: (1)PT-S could inhibit the growth of human high-metastatic large cell lung cancer cell line L9981 in vitro, the effect is dose-dependent. (2)PS-T can down- or up-regulate the mRNA transcript expression of some angiogenic-related gene mRNA. (3)PS-T has remarkably coordinating effects with cisplatin in the L9981 lung cancer cell line.

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  • (PMID = 21144298.001).
  • [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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77. Zou LJ, Li GQ, Gong LL, Wang Y, Jin W, Zhao JY, Ma HY, Yang PM, Shao SJ: [Expression of aurora-A kinase in human lung cancer cell lines PG, A549, and NCI-H460]. Ai Zheng; 2005 Jul;24(7):792-5
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  • [Title] [Expression of aurora-A kinase in human lung cancer cell lines PG, A549, and NCI-H460].
  • This study was to detect the expression of Aurora-A in lung cancer cell lines PG (highly-metastatic giant cell lung cancer), A549 (lung adenocarcinoma), and NCI-H460 (large cell lung cancer) and explore its correlation to DNA content, provide a theoretical basis for screening tumor marker and molecular therapeutic target of lung cancer.
  • METHODS: mRNA and protein levels of Aurora-A in PG, A549, and NCI-H460 cells were detected by reverse transcription-polymerase chain reaction(RT-PCR) and Western blot.
  • Flow cytometry was used to analyze DNA contents in cell cycles of PG, A549, and NCI-H460 cells.
  • RESULTS: mRNA level of Aurora-A was 1.14 in PG cells, 1.16 in A549 cells, and 0.84 in NCI-H460 cells, respectively; protein level of Aurora-A was 8.96 in PG cells, 21.13 in A549 cells, and 6.43 in NCI-H460 cells, respectively.
  • The proportion of cells with tetraploid DNA was 19.88% in PG cells, 14.97% in A549 cells, and 10.6% in NCI-H460 cells, respectively (P<0.01); the proportion of cells with polyploid DNA was 2.66% in PG cells, 3.59% in A549 cells, and 2.30% in NCI-H460 cells, respectively.
  • CONCLUSION: Aurora-A is overexpressed in the 3 lung cancer cell lines, but the mRNA levels are different.
  • [MeSH-major] Adenocarcinoma / metabolism. Carcinoma, Giant Cell / metabolism. Carcinoma, Large Cell / metabolism. Lung Neoplasms / metabolism. Protein-Serine-Threonine Kinases / biosynthesis
  • [MeSH-minor] Aurora Kinases. Cell Line, Tumor. DNA, Neoplasm / genetics. Humans. Polyploidy. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16004802.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / RNA, Messenger; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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78. Pavićević R, Bubanović G, Franjević A, Stancić-Rokotov D, Samarzija M: CYFRA 21-1 in non-small cell lung cancer--standardisation and application during diagnosis. Coll Antropol; 2008 Jun;32(2):485-98
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  • [Title] CYFRA 21-1 in non-small cell lung cancer--standardisation and application during diagnosis.
  • Standardisation is achieved by determining the reference range in asymptomatic population, benign and malignant lung diseases, and benign and malignant diseases of other organs.
  • The cut-off level of CYFRA 21-1 for non-small cell lung cancer (NSCLC) is 1.72 ng/mL in the Croatian population.
  • It is based on the clinically applicable sensitivity of 78% and specificity of 95% in benign lung diseases.
  • For clinicians the level of CYFRA 21-1 is an early sign of NSCLC in relation to all the benign lung diseases and all the benign diseases of other organs, of which it was confirmed that they can influence the above level, provided that NSCLC is verified using standard diagnostic methods.
  • The sensitivity of CYFRA 21-1 in NSCLC is 78%, in squamous cell lung cancer (SQC) 84.6%, in adenocarcinomas (AD) 74.3% and in large cell lung cancer (LCC) 75.3%.
  • The level of CYFRA 21-1 prompts clinicians to repeat the clinical procedure during diagnosis, and helps to detect the disease earlier and implement treatment in NSCLC.
  • [MeSH-major] Antigens, Neoplasm / blood. Biomarkers, Tumor / blood. Carcinoma, Non-Small-Cell Lung / diagnosis. Keratins / blood. Lung Neoplasms / diagnosis

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  • (PMID = 18756899.001).
  • [ISSN] 0350-6134
  • [Journal-full-title] Collegium antropologicum
  • [ISO-abbreviation] Coll Antropol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Croatia
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Keratin-19; 0 / antigen CYFRA21.1; 68238-35-7 / Keratins
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79. Mossé YP, Wood A, Maris JM: Inhibition of ALK signaling for cancer therapy. Clin Cancer Res; 2009 Sep 15;15(18):5609-14
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  • [Title] Inhibition of ALK signaling for cancer therapy.
  • Paradigm shifting advances in cancer can occur after discovering the key oncogenic drivers of the malignant process, understanding their detailed molecular mechanisms, and exploiting this transdisciplinary knowledge therapeutically.
  • A variety of human malignancies have anaplastic lymphoma kinase (ALK) translocations, amplifications, or oncogenic mutations, including anaplastic large cell lymphoma, inflammatory myofibroblastic tumors, non-small cell lung cancer, and neuroblastoma.
  • The identification of the downstream effector pathways controlled by ALK should pave the way for the rational design of ALK-inhibition therapies for the treatment of a subset of human cancers that harbor ALK aberrations.

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  • (PMID = 19737948.001).
  • [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 / PHS HHS / / K08-111733; United States / NCI NIH HHS / CA / R01-CA124709; United States / NCI NIH HHS / CA / R01-CA78454
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Number-of-references] 57
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80. Roy PP, Basu N: Bilateral adrenal metastases from large cell carcinoma of lung in a female non-smoker patient. J Assoc Physicians India; 2006 Jun;54:504-6
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  • [Title] Bilateral adrenal metastases from large cell carcinoma of lung in a female non-smoker patient.
  • [MeSH-major] Adrenal Gland Neoplasms / secondary. Carcinoma, Large Cell / pathology. Lung Neoplasms / pathology

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  • (PMID = 16912999.001).
  • [ISSN] 0004-5772
  • [Journal-full-title] The Journal of the Association of Physicians of India
  • [ISO-abbreviation] J Assoc Physicians India
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] India
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81. Armstrong F, Lamant L, Hieblot C, Delsol G, Touriol C: TPM3-ALK expression induces changes in cytoskeleton organisation and confers higher metastatic capacities than other ALK fusion proteins. Eur J Cancer; 2007 Mar;43(4):640-6
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  • Translocations of the anaplastic lymphoma kinase (ALK) gene result in the production of a number of oncogenic ALK fusion proteins implicated in tumour development.
  • We have previously shown that X-ALK fusion proteins have differential effects on the proliferation, transformation, and invasion properties of NIH3T3 cells in vitro.
  • In the present study, we have investigated the metastatic potential of various X-ALK expressing cell lines using an experimental lung metastasis assay.
  • We have shown that TPM3-ALK expression bestows higher metastatic capacities than other X-ALK fusion proteins and in addition, that TPM3-ALK fusion protein expression specifically induces changes in cell morphology and cytoskeleton organisation.
  • Together the specific actions of TPM3-ALK on the cytoskeleton organisation offer an interesting hypothesis with respect to the higher cell motility and metastatic potential of this fusion protein.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / genetics. Protein-Tyrosine Kinases / genetics. Tropomyosin / genetics
  • [MeSH-minor] Animals. Blotting, Western. Cytoskeleton / metabolism. Humans. Immunohistochemistry. Lung Neoplasms / metabolism. Lung Neoplasms / secondary. Mice. Mice, Nude. NIH 3T3 Cells. Receptor Protein-Tyrosine Kinases. Transfection

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  • (PMID = 17276053.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / TPM3 protein, human; 0 / Tropomyosin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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82. Ashidi JS, Houghton PJ, Hylands PJ, Efferth T: Ethnobotanical survey and cytotoxicity testing of plants of South-western Nigeria used to treat cancer, with isolation of cytotoxic constituents from Cajanus cajan Millsp. leaves. J Ethnopharmacol; 2010 Mar 24;128(2):501-12
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  • [Title] Ethnobotanical survey and cytotoxicity testing of plants of South-western Nigeria used to treat cancer, with isolation of cytotoxic constituents from Cajanus cajan Millsp. leaves.
  • AIM OF STUDY: To document plants commonly used to treat cancer in South-western Nigeria and to test the scientific basis of the claims using in vitro cytotoxicity tests.
  • Three cancer cell lines (human breast adenocarcinoma cell line MCF-7, human large cell lung carcinoma cell line COR-L23 and human amelanotic melanoma C32) and one normal cell line (normal human keratinocytes SVK-14) were used for the screening of the extracts and the fractions obtained.
  • Pinostrobin and longistylins A and C were tested for cytotoxicity on the cancer cell lines.
  • In addition, an adriamycin-sensitive acute T-lymphoblastic leukaemia cell line (CCRF-CEM) and its multidrug-resistant sub-line (CEM/ADR5000) were used in an XTT assay to evaluate the activity of the pure compounds obtained.
  • The dichloromethane fraction of Cajanus cajan had IC(50) value 5-10 microg/mL, with the two constituent stilbenes, longistylins A and C, being primarily responsible, with IC(50) values of 0.7-14.7 microM against the range of cancer cell lines.
  • CONCLUSIONS: Most of the species tested had some cytotoxic effect on the cancer cell lines, which to some extent supports their traditional inclusion in herbal preparations for treatment of cancer.
  • However, little selectivity for cancer cells was observed, which raises concerns over their safety and efficacy in traditional treatment.
  • [MeSH-minor] Cell Line, Tumor. Data Collection. Ethnopharmacology. Flavanones / isolation & purification. Flavanones / toxicity. Humans. Male. Nigeria. Oleanolic Acid / analogs & derivatives. Oleanolic Acid / isolation & purification. Oleanolic Acid / toxicity. Plant Leaves / chemistry. Sitosterols / isolation & purification. Sitosterols / toxicity

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  • [Copyright] Copyright (c) 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20064598.001).
  • [ISSN] 1872-7573
  • [Journal-full-title] Journal of ethnopharmacology
  • [ISO-abbreviation] J Ethnopharmacol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Flavanones; 0 / Sitosterols; 0 / pinostrobin; 5LI01C78DD / gamma-sitosterol; 6SMK8R7TGJ / Oleanolic Acid; KM8353IPSO / amyrin
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83. Singh N, Srinivas R, Bal A, Aggarwal AN: Lung carcinoma mimicking hydatid cyst: a case report and review of the literature. Med Oncol; 2009 Dec;26(4):424-8
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  • [Title] Lung carcinoma mimicking hydatid cyst: a case report and review of the literature.
  • It is unusual for a malignant lung tumor to present clinically as a cystic lesion.
  • A case of large cell carcinoma of the lung mimicking pulmonary hydatid cyst is reported herein.
  • The patient was found to have positive serological test for Echinococcus granulosus and therefore the preoperative diagnosis was that of complicated pulmonary hydatid cyst.
  • Intra-operative findings included presence of a large cavity filled with necrotic material and "daughter cysts".
  • Histopathological evaluation of the excised specimen showed large cell carcinoma.
  • The case highlights the fact that a lung carcinoma may rarely have clinical, radiological, and serological features similar to those of a pulmonary hydatid cyst.
  • [MeSH-major] Carcinoma, Large Cell / diagnosis. Echinococcosis, Pulmonary / diagnosis. Lung Neoplasms / diagnosis
  • [MeSH-minor] Aged. Animals. Diagnosis, Differential. Echinococcosis / diagnostic imaging. Echinococcosis / pathology. Echinococcosis / surgery. Echinococcus granulosus. Humans. Male. Prognosis. Tomography, X-Ray Computed

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  • (PMID = 19067256.001).
  • [ISSN] 1559-131X
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 14
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84. Khan N, Golzar J, Smith NL, Movahed A: Intracardiac extension of a large cell undifferentiated carcinoma of lung. Heart; 2005 Apr;91(4):512
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  • [Title] Intracardiac extension of a large cell undifferentiated carcinoma of lung.
  • [MeSH-major] Carcinoma, Large Cell / pathology. Lung Neoplasms / pathology. Myocardium / pathology

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  • (PMID = 15772215.001).
  • [ISSN] 1468-201X
  • [Journal-full-title] Heart (British Cardiac Society)
  • [ISO-abbreviation] Heart
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1768849
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85. Zhao J, Wang MZ, Li LY, Zhang L, Zhong W: [Clinical features of pulmonary malignancies in patients younger than 30 years of age]. Zhongguo Yi Xue Ke Xue Yuan Xue Bao; 2010 Apr;32(2):174-8
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  • The mean time from the onset of disease to confirmed diagnosis was (5.98+/-8.95) months.
  • The proportions of advanced-stage patients (stage III B and IV) and moderate to poor-differentiated tumor accounted for 59.26% (16/27) and 77.8% (14/18), respectively in 27 patients with non-small cell lung cancer.
  • The proportion of tumors in limited stage was 72.73% in 11 patients with small cell lung cancer, and most patients (54.55) were not sensitive to conventional chemotherapy.
  • Immunohistochemical staining showed that the tumor cells were positive for CD99.
  • Multiple nodules in bilateral lungs were presented in 2 patients with anaplastic large cell lymphomas, in which CD30 was positive in tumor cells; chemotherapy was the main therapy for these two patients.
  • [MeSH-major] Lung Neoplasms

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  • (PMID = 20450548.001).
  • [ISSN] 1000-503X
  • [Journal-full-title] Zhongguo yi xue ke xue yuan xue bao. Acta Academiae Medicinae Sinicae
  • [ISO-abbreviation] Zhongguo Yi Xue Ke Xue Yuan Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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86. Li S, Han L, Sun L, Zheng D, Liu J, Fu Y, Huang X, Wang Z: Synthesis and antitumor activities of phenanthrene-based alkaloids. Molecules; 2009;14(12):5042-53
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  • A series of phenanthrene-based tylophorine derivatives (PBTs) were synthesized and their cytotoxic activities against the H460 human large-cell lung carcinoma cell line were evaluated.

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  • (PMID = 20032876.001).
  • [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 / Alkaloids; 0 / Antineoplastic Agents; 0 / Phenanthrenes; 448J8E5BST / phenanthrene
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87. Zhu W, Deng Y, Zhou Q, Chen X, Wang Y, Liu L, Che G: [Analysis of two-dimension gel electrophoresis of human large cell lung cancer cell lines with different metastasis potentials]. Zhongguo Fei Ai Za Zhi; 2005 Feb 20;8(1):1-7
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  • [Title] [Analysis of two-dimension gel electrophoresis of human large cell lung cancer cell lines with different metastasis potentials].
  • BACKGROUND: Metastasis is not only the malignant characteristics of lung can- cer, but also the chief cause of failure to cure and high mortality of lung cancer.
  • To better explore and understand the mechanism of lung cancer metastasis and to search for potential markers for early diagnosing and reversing lung cancer metastasis, differential proteomic analysis is conducted in two human large cell lung cancer cell lines with high metastasis potentials (L9981) and low metastasis potentials (NL9980) by two-dimension gel electrophoresis (2-DE).
  • METHODS: The total proteins of the two cell lines were separated by immobilized pH gradient (IPG)-based 2-DE.
  • The differentially expressed proteins of the two cell lines were analyzed using image analysis software.
  • RESULTS: A high resolution and reproducible 2-DE image was successfully obtained.
  • The average total number of protein spots was 902±169 in L9981 cells and 941±173 in NL9980 cells in three repeated experiments.
  • Image analysis of siliver-stained 2-DE image revealed that 4 protein spots had significant differential expressions in L9981 and NL9980 (student's t-test, P < 0.05).
  • CONCLUSIONS: The results in this study suggest that an obviously differential proteomic expression exists between the human high- and low-metastatic large cell lung cancer cell lines.
  • It will be helpful to further understand the molecular mechanisms of lung cancer invasion and metastasis, and provide new experimental evidence for searching metastatic-related molecule of lung cancer.

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  • (PMID = 21187015.001).
  • [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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88. Xiao D, Zeng Y, Hahm ER, Kim YA, Ramalingam S, Singh SV: Diallyl trisulfide selectively causes Bax- and Bak-mediated apoptosis in human lung cancer cells. Environ Mol Mutagen; 2009 Apr;50(3):201-12
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  • [Title] Diallyl trisulfide selectively causes Bax- and Bak-mediated apoptosis in human lung cancer cells.
  • We now demonstrate that garlic constituent diallyl trisulfide (DATS) suppresses viability of cultured human lung cancer cell lines H358 (anon-small cell lung cancer cell line) and H460 (a large cell lung cancer cell line) by causing G2-M phase cell cycle arrest and apoptotic cell death.
  • On the other hand, a normal human bronchial epithelial cell line BEAS-2B was significantly more resistant to growth inhibition and apoptosis induction by DATS compared with lung cancer cells.
  • For example, DATS was significantly more effective than either diallyl sulfide or diallyl disulfide against proliferation of lung cancer cells.
  • The DATS-mediated G2-M phase cell cycle arrest was explained by down-regulation of cyclin-dependent kinase 1 (Cdk1) and cell division cycle 25C protein expression leading to accumulation of Tyr15 phosphorylated (inactive) Cdk1.
  • The DATS-induced apoptosis correlated with induction of pro-apoptotic proteins Bax, Bak and BID, and a decrease in the expression of anti-apoptotic proteins Bcl-2 and Bcl-xL in lung cancer cells but not in BEAS-2B.
  • In conclusion, the present study indicates that Bax and Bak proteins are critical targets of DATS-induced apoptosis in human lung cancer cells.

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  • (PMID = 18800351.001).
  • [ISSN] 1098-2280
  • [Journal-full-title] Environmental and molecular mutagenesis
  • [ISO-abbreviation] Environ. Mol. Mutagen.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA113363-04; United States / NCI NIH HHS / CA / R01 CA113363; United States / NCI NIH HHS / CA / CA113363; United States / NCI NIH HHS / CA / R01 CA113363-04
  • [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 / Allyl Compounds; 0 / BAK1 protein, human; 0 / BAX protein, human; 0 / BH3 Interacting Domain Death Agonist Protein; 0 / Bid protein, mouse; 0 / Sulfides; 0 / bcl-2 Homologous Antagonist-Killer Protein; 0 / bcl-2-Associated X Protein; 0ZO1U5A3XX / diallyl trisulfide
  • [Other-IDs] NLM/ NIHMS65467; NLM/ PMC2656596
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89. Inamura K, Takeuchi K, Togashi Y, Nomura K, Ninomiya H, Okui M, Satoh Y, Okumura S, Nakagawa K, Soda M, Choi YL, Niki T, Mano H, Ishikawa Y: EML4-ALK fusion is linked to histological characteristics in a subset of lung cancers. J Thorac Oncol; 2008 Jan;3(1):13-7
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  • [Title] EML4-ALK fusion is linked to histological characteristics in a subset of lung cancers.
  • INTRODUCTION: Very recently, we have found a novel fusion product between the echinoderm microtubule-associated protein-like4 (EML4) and the anaplastic lymphoma kinase (ALK) in non-small cell lung cancers (NSCLCs).
  • Herein, we present results of a first large scale study of EML4-ALK fusion in lung cancers.
  • METHODS: Using reverse transcription-polymerase chain reaction for EML4-ALK fusion mRNA, we investigated 149 lung adenocarcinomas, 48 squamous cell carcinomas, 3 large-cell neuroendocrine carcinomas, and 21 small-cell carcinomas.
  • CONCLUSIONS: In the present first investigation of EML4-ALK fusion in a large study of lung cancers (5/221), we found an interesting histotype-genotype relationship.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / pathology. Lung Neoplasms / genetics. Lung Neoplasms / pathology. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Adenocarcinoma / pathology. Carcinoma, Neuroendocrine / pathology. Carcinoma, Squamous Cell / pathology. Cell Cycle Proteins / genetics. Chromosome Inversion. Chromosomes, Human, Pair 2. DNA Mutational Analysis. Female. Humans. Immunohistochemistry. Male. Microtubule-Associated Proteins / genetics. Protein-Tyrosine Kinases / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / metabolism. Receptor Protein-Tyrosine Kinases. Reverse Transcriptase Polymerase Chain Reaction. Serine Endopeptidases / genetics. Survival Analysis

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  • (PMID = 18166835.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / EML4-ALK fusion protein, human; 0 / Microtubule-Associated Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 3.4.21.- / EML4 protein, human; EC 3.4.21.- / Serine Endopeptidases
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90. Li BZ, Zhou XY, Ye HT, Yang WT, Fan YZ, Lu HF, Shi DR: [Abnormal expression of bcl-10 protein in extranodal marginal zone B cell lymphoma of mucosa-associated lymphoid tissue lymphoma type]. Zhonghua Bing Li Xue Za Zhi; 2007 Dec;36(12):819-24
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  • [Title] [Abnormal expression of bcl-10 protein in extranodal marginal zone B cell lymphoma of mucosa-associated lymphoid tissue lymphoma type].
  • OBJECTIVE: To evaluate the diagnostic role of nuclear expression of bcl-10 protein in extranodal marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue (MALT) type.
  • METHODS: One hundred and forty cases of MALT lymphoma were collected from Cancer Hospital of Fudan University (including 38 cases from stomach, 35 cases from ocular adnexa, 16 cases from intestine, 15 cases from skin, 15 cases from salivary gland, 14 cases from lung, 3 cases from thyroid and 4 cases from other sites).
  • Ten cases of reactive follicular hyperplasia of tonsil, 5 cases of reactive lymphoid hyperplasia of orbit and 143 cases of non-Hodgkin's lymphoma other than MALT lymphoma (including 20 cases of NK/T cell lymphoma, 20 cases of follicular lymphomas, 20 cases of anaplastic large cell lymphomas, 20 cases of nodal diffuse large cell B-cell lymphoma (DLBCL), 10 cases of gastric diffuse large B-cell lymphoma, 13 cases of nodal marginal zone B-cell lymphoma, 12 cases of mantle cell lymphoma, 11 cases of splenic marginal zone B-cell lymphoma, 6 cases of angioimmunoblastic T-cell lymphoma, 6 cases of peripheral T-cell lymphoma, not otherwise specified, 3 cases of small lymphocytic lymphoma, 1 case of lymphoplasmacytic lymphoma and 1 case of plasmacytoma were used as controls.
  • RESULTS: In reactive follicular hyperplasia of tonsil, bcl-10 was moderately or strongly expressed in the cytoplasm of germinal center B cells, while the mantle cells were negative and the marginal zone cells and paracortical T cells showed weak staining.
  • In the 5 cases of reactive lymphoid hyperplasia of orbit, 2 were bcl-10-negative and the remaining 3 expressed bcl-10 in the cytoplasm of germinal center B cells.
  • In some cases of lymphoma, bcl-10 was expressed in tumor cells but not in reactive lymphoid cells.
  • Dual staining with CD20 showed that the bcl-10-positive cells were also CD20-positive, though the number of bcl-10-positive cells were less than that of CD20-positive cells.
  • In some cases of lymphoma, bcl-10 is expressed in tumor cells but not in reactive lymphoid cells, suggesting a possible role of abnormal bcl-10 expression in tumorgenesis.
  • Nuclear expression of bcl-10 is seen mainly in MALT lymphoma, especially when occurring in ocular adnexa and lung.
  • This is in contrast to loss of bcl-10 expression in residual germinal center cells.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / genetics. Gene Expression Regulation, Neoplastic. Lymphoma, B-Cell, Marginal Zone / genetics. Lymphoma, B-Cell, Marginal Zone / pathology
  • [MeSH-minor] Antigens, CD20 / immunology. Cell Nucleus / genetics. Cytoplasm / genetics. Humans. Lymphocytes / pathology. Palatine Tonsil / pathology. Pseudolymphoma / genetics

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  • (PMID = 18346354.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Antigens, CD20; 0 / BCL10 protein, human
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91. El Hage F, Vergnon I, Grunenwald D, Soria JC, Chouaib S, Mami-Chouaib F: Generation of diverse mutated tumor antigen-specific cytotoxic T lymphocytes in a lung cancer patient with long survival. Oncol Rep; 2005 Sep;14(3):763-9
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  • [Title] Generation of diverse mutated tumor antigen-specific cytotoxic T lymphocytes in a lung cancer patient with long survival.
  • We have identified an antigen recognized on a large cell carcinoma of the lung by tumor-specific cytotoxic T lymphocytes (CTL).
  • Using HLA-A2-peptide tetramers, we have derived from patient peripheral blood lymphocytes (PBL) and autologous tumor infiltrating lymphocytes (TIL) several mutated alpha-actinin-4-specific T cell clones.
  • These clones displayed similar tetramer staining but distinct T cell receptor (TCR) usage and antitumor reactivity.
  • Indeed, TIL clones lysed more efficiently the autologous tumor cells and released higher cytokine levels than PBL clones.
  • Importantly, treatment of cancer cells with interferon-gamma enhanced their susceptibility to PBL clone-mediated lysis correlated with increase in HLA-class I expression.
  • The present findings provide evidence that an immune T cell response took place in a lung cancer patient with favorable clinical evolution and suggest that CTL, recognizing a truly tumor-specific antigen, may contribute to controlling the tumor.
  • [MeSH-major] Actinin / genetics. Carcinoma, Large Cell / pathology. Lung Neoplasms / pathology. Microfilament Proteins / genetics. T-Lymphocytes, Cytotoxic / immunology

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  • (PMID = 16077989.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Cytokines; 0 / HLA-A2 Antigen; 0 / Microfilament Proteins; 11003-00-2 / Actinin
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92. Varamini P, Soltani M, Ghaderi A: Cell cycle analysis and cytotoxic potential of Ruta graveolens against human tumor cell lines. Neoplasma; 2009;56(6):490-3
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  • [Title] Cell cycle analysis and cytotoxic potential of Ruta graveolens against human tumor cell lines.
  • The aim of the present study was to evaluate in vitro cytotoxicity of the total extract of R. graveolens against tumor cell lines of different origin.
  • Aerial parts of the plant was extracted with 70% ethanol by sonication method and cytotoxic activity was examined on RAJI, RAMOS, RPMI8866, U937, Jurkat, MDA-MB-453, MCF-7, LNCap-FGC-10, 5637, HeLa, SK-OV-3, A549, Mehr-80 and also peripheral blood mononuclear cells (PBMC) by the use of WST-1 assay.
  • Results were expressed as IC(50) values. R. graveolens extract showed high cytotoxic activity against RAJI and RAMOS, two Burkitt's lymphoma cell lines, with an IC(50) equal to 24.3 microg/ml and 35.2 microg/ml respectively and LNCap-FGC-10, a prostate adenocarcinoma cell line with an IC(50) equal to 27.6 microg/ml as well as Mehr-80, a newly established Large Cell Lung Carcinoma (IC(50)=46.2 microg/ml).
  • No significant anti-proliferative activity was observed on other cell lines including MCF-7, MDA-MB-453, SK-OV-3, HeLa, 5637, JURKAT and RPMI8866.
  • Adverse cytotoxic effect of R. graveolens was investigated against PBMCs and a significantly lower effect of this extract (IC(50)=104 microg/ml) was seen on normal cells compared with RAJI and RAMOS, two haematopoietic cell lines.
  • [MeSH-major] Cell Proliferation / drug effects. G1 Phase / drug effects. Neoplasms / drug therapy. Phytotherapy. Plant Extracts / pharmacology. Ruta / chemistry
  • [MeSH-minor] Cell Line, Tumor. Female. Humans. Male

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  • (PMID = 19728756.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Plant Extracts
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93. Kasprzak A, Zabel M, Biczysko W: Selected markers (chromogranin A, neuron-specific enolase, synaptophysin, protein gene product 9.5) in diagnosis and prognosis of neuroendocrine pulmonary tumours. Pol J Pathol; 2007;58(1):23-33
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  • [Title] Selected markers (chromogranin A, neuron-specific enolase, synaptophysin, protein gene product 9.5) in diagnosis and prognosis of neuroendocrine pulmonary tumours.
  • Neuroendocrine tumours of lungs represent a subgroup of pulmonary tumours with typical morphofunctional traits.
  • In light microscopy, the four principal types of the tumours (typical and atypical carcinoids, small cell lung cancer, large cell neuroendocrine carcinoma) demonstrate typical arrangement of cells (organoid nesting, palisading, a trabecular pattern, and rosette-like structures), variable number of mitoses, presence or absence of necrosis.
  • In ultrastructure, neuroendocrine tumours manifest groups of cells with cytoplasmic granules (and the so called dense-core neurosecretory granules in particular).
  • Neuroendocrine cells release hormones to circulation or in a paracrine manner.
  • Until now, the most sensitive and specific marker or marker combination for early detection of neuroendocrine subtypes of lung tumours has not been identified.
  • Both in endocrine and non-endocrine tumours, neuron-specific enolase (NSE) is thought to represent mainly a prognostic index, and only quantitation of serum concentrations of the protein or of the fraction of immunopositive cells may permit to differentiate between subtypes of the tumours.
  • With increasing frequency, PGP 9.5 is regarded to provide a prognostic marker in diagnosis of non-small cell lung carcinomas rather than of typical neuroendocrine tumours.
  • [MeSH-major] Chromogranin A / metabolism. Lung Neoplasms / diagnosis. Neuroendocrine Tumors / diagnosis. Phosphopyruvate Hydratase / metabolism. Synaptophysin / metabolism. Ubiquitin Thiolesterase / metabolism

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  • (PMID = 17585539.001).
  • [ISSN] 1233-9687
  • [Journal-full-title] Polish journal of pathology : official journal of the Polish Society of Pathologists
  • [ISO-abbreviation] Pol J Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Chromogranin A; 0 / Synaptophysin; EC 3.1.2.15 / UCHL1 protein, human; EC 3.1.2.15 / Ubiquitin Thiolesterase; EC 4.2.1.11 / Phosphopyruvate Hydratase
  • [Number-of-references] 114
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94. Shen DQ, Wu ZP, Wu XW, An ZY, Bu XZ, Gu LQ, Huang ZS, An LK: Synthesis and antiproliferative activity of indolizinophthalazine-5,12-dione derivatives, DNA topoisomerase IB inhibitors. Eur J Med Chem; 2010 Sep;45(9):3938-42
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  • Some of synthesized compounds exhibited significant in vitro antiproliferative activity at micromolar level toward four human tumor cell lines, including lung adenocarcinoma cell, large-cell lung carcinoma cell, breast carcinoma cell and ardriamycin-resistance breast carcinoma cell.
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation / drug effects. Drug Design. Humans. Inhibitory Concentration 50. Nitrogen / chemistry

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  • [Copyright] 2010. Published by Elsevier Masson SAS.
  • (PMID = 20638158.001).
  • [ISSN] 1768-3254
  • [Journal-full-title] European journal of medicinal chemistry
  • [ISO-abbreviation] Eur J Med Chem
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Indolizines; 0 / Phthalazines; 0 / Topoisomerase I Inhibitors; EC 5.99.1.2 / DNA Topoisomerases, Type I; N762921K75 / Nitrogen
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95. Palumbo G, Grana CM, Cocca F, De Santis R, Del Principe D, Baio SM, Mei R, Paganelli G: Pretargeted antibody-guided radioimmunotherapy in a child affected by resistant anaplastic large cell lymphoma. Eur J Haematol; 2007 Sep;79(3):258-62
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  • [Title] Pretargeted antibody-guided radioimmunotherapy in a child affected by resistant anaplastic large cell lymphoma.
  • Anaplastic large cell lymphoma (ALCL) is characterized by preferential paracortical and intrasinusoidal lymph node involvement by large anaplastic tumor cells expressing the CD30 antigen.
  • In these cases, the highly aggressive clinical course of ALCL, associated with systemic symptoms and extranodal involvement, has been treated with different approaches in various cooperative trials, including conventional chemotherapy and human stem cell transplantation (HSCT).
  • More recently, radioimmunotherapy has been studied with encouraging results in cancer patients, including non-Hodgkin's lymphoma.
  • Here we describe the case of a pediatric ALCL, relapsing after HSCT, treated with pretargeted antibody-guided radioimmunotherapy, obtaining a complete remission, with excellent quality of life over the past 10 months.
  • [MeSH-major] Antibodies, Neoplasm / therapeutic use. Lymphoma, Large-Cell, Anaplastic / radionuclide imaging. Radioimmunotherapy / methods
  • [MeSH-minor] Child. Female. Hematopoietic Stem Cell Transplantation. Humans. Lung Neoplasms / secondary. Salvage Therapy / methods


96.