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1. 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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2. 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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  • [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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3. 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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4. Warenius H, Kyritsi L, Grierson I, Howarth A, Seabra L, Jones M, Thomas C, Browning P, White R: Spontaneous regression of human cancer cells in vitro: potential role of disruption of Cdk1/Cdk4 co-expression. Anticancer Res; 2009 Jun;29(6):1933-41
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  • [Title] Spontaneous regression of human cancer cells in vitro: potential role of disruption of Cdk1/Cdk4 co-expression.
  • BACKGROUND: Although well-acknowledged in vivo, spontaneous death of cancer cells in vitro is less widely appreciated.
  • MATERIALS AND METHODS: Colony formation was studied in untreated control plates of standard clonogenic assays and measurements of actual and potential doubling times performed in asynchronous cultures of human cancer cells lines.
  • Western blotting of lung large cell carcinoma, COR-L23 cells actively undergoing spontaneous cell death was also carried out.
  • RESULTS: Catastrophic disintegration of mature colonies could be seen in the untreated plates of lung large cell carcinoma, H460 and colon adenocarcinoma, SW620 human cancer cell lines and a significant cell loss factor was present in the cell lines growing as adherent cells in continuous culture.
  • Western blotting demonstrated alterations of relative cyclin dependent kinase (Cdk)1 to Cdk4 protein expression in dying COR-L23 cells.
  • CONCLUSION: The phenomenon of spontaneous cell death should be considered a hallmark of cancer and may be the result of failure to stabilise unstable, fully developed cancer cells due to the disruption of Cdk1/Cdk4 co-expression in those cells.
  • [MeSH-major] CDC2 Protein Kinase / metabolism. Carcinoma, Large Cell / pathology. Cyclin-Dependent Kinase 4 / metabolism. Lung Neoplasms / pathology. Neoplasm Regression, Spontaneous / pathology
  • [MeSH-minor] Blotting, Western. Cell Survival. Colony-Forming Units Assay. Fibroblasts / metabolism. Flow Cytometry. Humans. Skin / cytology. Skin / metabolism. Tumor Cells, Cultured

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  • (PMID = 19528450.001).
  • [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] EC 2.7.11.22 / CDC2 Protein Kinase; EC 2.7.11.22 / CDK4 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 4
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5. Ye L, Li X, Kong X, Wang W, Bi Y, Hu L, Cui B, Li X, Ning G: Hypomethylation in the promoter region of POMC gene correlates with ectopic overexpression in thymic carcinoids. J Endocrinol; 2005 May;185(2):337-43
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  • Using bisulphite sequencing, we identified hypermethylation in the 5' promoter region of the POMC gene in three normal thymuses and one large cell lung cancer, and hypomethylation in five thymic carcinoid tumors resected from patients with ectopic ACTH syndrome.

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  • (PMID = 15845926.001).
  • [ISSN] 0022-0795
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 66796-54-1 / Pro-Opiomelanocortin
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6. 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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7. Le Deley MC, Reiter A, Williams D, Delsol G, Oschlies I, McCarthy K, Zimmermann M, Brugières L, European Intergroup for Childhood Non-Hodgkin Lymphoma: Prognostic factors in childhood anaplastic large cell lymphoma: results of a large European intergroup study. Blood; 2008 Feb 1;111(3):1560-6
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  • [Title] Prognostic factors in childhood anaplastic large cell lymphoma: results of a large European intergroup study.
  • To study prognostic factors of progression/relapse, data concerning 225 children enrolled between 1987 and 1997 in Berlin-Frankfurt-Münster, Société Française d'Oncologie Pédiatrique and United Kingdom Children's Cancer Study Group prospective studies for the treatment of anaplastic large cell lymphoma (ALCL) were merged.
  • In the multivariate analysis, 3 factors remained significant: mediastinal involvement (relative risk [RR] = 2.1 [1.2-3.5]), visceral involvement defined as lung, liver, or spleen involvement (RR = 2.1 [1.3-3.6]), and skin lesions (RR = 1.9 [1.1-3.2]).
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / epidemiology. Lymphoma, Large-Cell, Anaplastic / pathology

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  • (PMID = 17957029.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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8. 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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9. Chen C, Chen P, Zhang CC, Li N, Jin ZL, Li K: [Clinical characteristics and prognosis of large cell lung cancer]. Zhonghua Zhong Liu Za Zhi; 2010 Dec;32(12):932-4
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  • [Title] [Clinical characteristics and prognosis of large cell lung cancer].
  • OBJECTIVE: The aim of this study was to explore the clinical characteristics and analyze the prognostic factors of large cell lung cancer (LCLC).
  • RESULTS: Among the 111 cases, the lesions were in the right lung of 53 patients and 26 of them were located in the superior lobe.
  • The lesions were in the left lung of 58 cases, and 35 of them were in the superior lobe.
  • CONCLUSION: The prognosis of LCLC is worse than other types of non-small cell lung cancer.
  • [MeSH-major] Carcinoma, Large Cell / pathology. Carcinoma, Large Cell / surgery. Lung Neoplasms / pathology. Lung Neoplasms / surgery. Pneumonectomy / methods

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  • (PMID = 21223803.001).
  • [ISSN] 0253-3766
  • [Journal-full-title] Zhonghua zhong liu za zhi [Chinese journal of oncology]
  • [ISO-abbreviation] Zhonghua Zhong Liu Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Taxoids; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; Q20Q21Q62J / Cisplatin; CAP-1 protocol; TP protocol
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10. Kudo K, Sakamoto S, Miyamoto A, Kono T, Motoi N, Yoshimura K: [A case of large cell carcinoma of the lung associated with a sarcoid-like reaction inside the tumor]. Nihon Kokyuki Gakkai Zasshi; 2008 Nov;46(11):889-93
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  • [Title] [A case of large cell carcinoma of the lung associated with a sarcoid-like reaction inside the tumor].
  • An 83 year-old man who was found to have a mass in his left lower lung field on a chest radiograph.
  • The patient was referred to our hospital, and lung biopsy under video-assisted thoracoscopic surgery (VATS) was performed.
  • Since the initial intraoperative pathologic examination showed the presence of non-caseating epithelioid cell granulomas, only partial resection was conducted.
  • However, detailed postoperative histopathological evaluation led to a diagnosis of large cell carcinoma of the lung associated with an internal sarcoid-like reaction.
  • Formation of epithelioid cell granulomas within a tumor is quite rare.
  • [MeSH-major] Carcinoma, Large Cell / pathology. Lung Neoplasms / pathology

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  • (PMID = 19068761.001).
  • [ISSN] 1343-3490
  • [Journal-full-title] Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society
  • [ISO-abbreviation] Nihon Kokyuki Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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11. De P, Abbasi R, Senadhira T, Orr P, Ullah A: Urticaria and large cell undifferentiated carcinoma of lung. Dermatol Online J; 2005;11(3):45
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  • [Title] Urticaria and large cell undifferentiated carcinoma of lung.
  • The association of urticaria with internal cancer is known mostly with lymphoreticular system malignancies.
  • Rarely, it occurs with cancer of lung, mostly with adenocarcinoma or small cell carcinoma.
  • We report a unique occurrence of urticaria on a patient who suffered from large cell undifferentiated carcinoma of lung.
  • [MeSH-major] Carcinoma, Large Cell / complications. Lung Neoplasms / complications. Urticaria / etiology

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  • (PMID = 16409941.001).
  • [ISSN] 1087-2108
  • [Journal-full-title] Dermatology online journal
  • [ISO-abbreviation] Dermatol. Online J.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
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12. 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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13. Goto H, Ito M, Yamaguchi N, Takahashi K, Kawano N, Kaneko T, Ishigatsubo Y: [A case of large cell carcinoma of the lung with rhabdoid phenotype]. Nihon Kokyuki Gakkai Zasshi; 2006 Apr;44(4):325-9
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  • [Title] [A case of large cell carcinoma of the lung with rhabdoid phenotype].
  • A 37-year-old man was admitted to our hospital because of suspicion of the lung cancer in November 2003.
  • Transbronchial tumor biopsy revealed a small number of tumor cells with rhabdoid features, which had eosinophilic cytoplasmic globules.
  • However, a definitive histological diagnosis was not obtained.
  • We considered that a diagnosis of lung malignant tumor was likely according to the findings of chest CT scan and pathology.
  • Immunohistologic staining of the cervical lymph node showed that rhabdoid cells were positive for epithelial membrane antigen (EMA), vimentin, and anticytokeratin antibody (CAM5.2), but not for thyroid transcription factor-1 (TTF-1).
  • From the autopsy findings and clinical course, he was finally diagnosed with large cell carcinoma of the lung with rhabdoid phenotype.
  • Because of its aggressive clinical course, early diagnosis and decision on therapy would be very important for this disease.
  • [MeSH-major] Carcinoma, Large Cell / pathology. Lung Neoplasms / pathology. Neoplasms, Multiple Primary / pathology. Rhabdoid Tumor / pathology
  • [MeSH-minor] Adult. Duodenal Neoplasms / secondary. Humans. Lung / pathology. Lung / radiography. Male. Phenotype. Tomography, X-Ray Computed

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  • (PMID = 16681249.001).
  • [ISSN] 1343-3490
  • [Journal-full-title] Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society
  • [ISO-abbreviation] Nihon Kokyuki Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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14. 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

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  • (PMID = 16100656.001).
  • [ISSN] 0494-1373
  • [Journal-full-title] Tüberküloz ve toraks
  • [ISO-abbreviation] Tuberk Toraks
  • [Language] tur
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Turkey
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15. Takahashi S, Kosaka T, Hattori M, Fujimoto-Ouchi K, Shimonaka Y, Yasuno H, Noguchi M, Mori K, Ogata E: Cancer-related anemia: Correlation analysis among serum levels of hemoglobin, IL-6, hepcidin, albumin, and erythropoietin. J Clin Oncol; 2009 May 20;27(15_suppl):e20655

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cancer-related anemia: Correlation analysis among serum levels of hemoglobin, IL-6, hepcidin, albumin, and erythropoietin.
  • In the present study, we investigated the relationship between cancer-related anemia and inflammatory activity, including the cytokines.
  • The characteristics of anemia in cancer pts were compared with those in mice bearing human lung large cell cancer LC-6-JCK.
  • Correlations were observed between quality of life in cancer pts and anemia parameters including Hb and IL-6.
  • Mice bearing LC-6-JCK tumors developed anemia with characteristic parameters similar to cancer pts with anemia ( Table ).
  • CONCLUSIONS: Present results suggest that cancer-related anemia associates with IL-6, Alb and inflammatory acute phase reaction including hepcidin and ferritin.
  • Further analysis of anemia in cancer pts and murine models would be useful for investigating the mechanisms of cancer anemia.

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  • (PMID = 27961624.001).
  • [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
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. 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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  • [Cites] Radiologe. 1996 Sep;36(9):692-9 [8999444.001]
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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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17. Rekhtman N: Neuroendocrine tumors of the lung: an update. Arch Pathol Lab Med; 2010 Nov;134(11):1628-38
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  • [Title] Neuroendocrine tumors of the lung: an update.
  • CONTEXT: The 2004 World Health Organization (WHO) classification recognizes 4 major types of lung neuroendocrine tumors: typical carcinoid, atypical carcinoid, small cell lung cancer, and large cell neuroendocrine carcinoma.
  • Markedly different prognostic implications and treatment paradigms for these tumors underscore the importance of accurate pathologic diagnosis.
  • OBJECTIVE: To detail the clinical and pathologic features of lung neuroendocrine tumors, with emphasis on diagnostic criteria, differential diagnoses, and application of immunohistochemistry.
  • The emerging evidence for the utility of Ki-67 (MIB1) in the diagnosis of lung neuroendocrine tumors, particularly in small biopsy and cytology, is emphasized.
  • Ki-67 (MIB1) is emerging as a useful ancillary tool in the diagnosis of these tumors.
  • [MeSH-major] Carcinoma, Neuroendocrine / pathology. Lung Neoplasms / pathology
  • [MeSH-minor] Biomarkers, Tumor. Diagnosis, Differential. Humans. Immunohistochemistry. Prognosis

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  • (PMID = 21043816.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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18. 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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19. 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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20. Uzaslan E, Ebsen M, Stuempel T, Freudenberg N, Nakamura S, Costabel U, Guzman J: Surfactant protein A detection in large cell carcinoma of the lung. Appl Immunohistochem Mol Morphol; 2006 Mar;14(1):88-90
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  • [Title] Surfactant protein A detection in large cell carcinoma of the lung.
  • Large cell carcinomas of the lung are undifferentiated malignant epithelial tumors that lack cytologic features of small cell carcinoma, glandular cell carcinoma, or squamous cell differentiation.
  • Lung surfactant protein A (SP-A) is produced by alveolar type II cells and Clara cells.
  • Most bronchioloalveolar carcinomas of the lung react positively for SP-A.
  • Positive SP-A staining of large cell carcinoma of the lung could indicate that at least part of these tumors have the same cellular origin or differentiation as bronchioloalveolar carcinoma.
  • The authors determined the SP-A staining of 63 large cell carcinomas of the lung by IHC.
  • This may imply that about one third of large cell carcinomas of the lung have a similar cellular origin or differentiation as bronchioloalveolar carcinoma.

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  • (PMID = 16540737.001).
  • [ISSN] 1541-2016
  • [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 / Pulmonary Surfactant-Associated Protein A
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21. 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


22. 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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23. 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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24. Mehta H, Bahuva R, Sadikot RT: Lung cancer mimicking as pregnancy with pneumonia. Lung Cancer; 2008 Sep;61(3):416-9
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  • [Title] Lung cancer mimicking as pregnancy with pneumonia.
  • SUMMARY: Lung cancer that presents with secretion of beta HCG is rare.
  • We report a case of a young female patient who presented with symptoms of pneumonia and was found to have a positive pregnancy test.
  • With non-resolution of the consolidation and progression of her symptoms she subsequently was found to have large cell lung cancer with ectopic beta HCG secretion.
  • Ectopic production of a variety of hormones such as ADH, parathyroid hormone, ACTH, insulin-like growth factor thus leading to presentation as endocrine syndromes in patients with lung cancer is well known.
  • The presentation of lung cancer mimicking as pregnancy has not been previously reported.
  • This may prevent a delay in the diagnosis and treatment of malignancy in young women.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / diagnosis. Carcinoma, Non-Small-Cell Lung / metabolism. Chorionic Gonadotropin, beta Subunit, Human / metabolism. Lung Neoplasms / diagnosis. Lung Neoplasms / metabolism
  • [MeSH-minor] Adult. Diagnosis, Differential. Fatal Outcome. Female. Humans. Pneumonia / diagnosis. Pregnancy. Tomography, X-Ray Computed

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  • (PMID = 18304689.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Chorionic Gonadotropin, beta Subunit, Human
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25. 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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26. 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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27. 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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28. Paripati A, Kingsley C, Weiss GJ: Pathway targets to explore in the treatment of small cell and large cell lung cancers. J Thorac Oncol; 2009 Nov;4(11):1313-21
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  • [Title] Pathway targets to explore in the treatment of small cell and large cell lung cancers.
  • INTRODUCTION: With low 5-year survival rates and little progress in therapy, improvements in therapeutic strategies for the treatment of small cell lung cancer (SCLC) and large cell lung cancer (LCC) are warranted.
  • METHODS: Per gene mean expression fold change ratios were calculated from four publicly available microarray data sets consisting of a total of 113 profiled samples.
  • The remaining pathways are targeted by several drugs developed or under development in cancer therapeutics.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Large Cell / genetics. Carcinoma, Non-Small-Cell Lung / genetics. Gene Expression Regulation, Neoplastic. Genes, Neoplasm / genetics. Lung Neoplasms / genetics. Signal Transduction / genetics

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  • (PMID = 19812504.001).
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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29. McDermott U, Iafrate AJ, Gray NS, Shioda T, Classon M, Maheswaran S, Zhou W, Choi HG, Smith SL, Dowell L, Ulkus LE, Kuhlmann G, Greninger P, Christensen JG, Haber DA, Settleman J: Genomic alterations of anaplastic lymphoma kinase may sensitize tumors to anaplastic lymphoma kinase inhibitors. Cancer Res; 2008 May 1;68(9):3389-95
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  • [Title] Genomic alterations of anaplastic lymphoma kinase may sensitize tumors to anaplastic lymphoma kinase inhibitors.
  • Whereas these agents can elicit dramatic clinical responses in some settings, their activity is generally limited to a subset of treated patients whose tumor cells harbor a specific genetic lesion.
  • We have established an automated platform for examining the sensitivity to various molecularly targeted inhibitors across a large panel of human tumor-derived cell lines to identify additional genotype-correlated responses that may be clinically relevant.
  • Among the inhibitors tested in a panel of 602 cell lines derived from a variety of human cancers, we found that a selective inhibitor of the anaplastic lymphoma kinase (ALK) potently suppressed growth of a small subset of tumor cells.
  • This subset included lines derived from anaplastic large cell lymphomas, non-small-cell lung cancers, and neuroblastomas.
  • ALK is a receptor tyrosine kinase that was first identified as part of a protein fusion derived from a chromosomal translocation detected in the majority of anaplastic large cell lymphoma patients, and has recently been implicated as an oncogene in a small fraction of non-small-cell lung cancers and neuroblastomas.
  • Significantly, sensitivity in these cell lines was well correlated with specific ALK genomic rearrangements, including chromosomal translocations and gene amplification.
  • Moreover, in such cell lines, ALK kinase inhibition can lead to potent suppression of downstream survival signaling and an apoptotic response.
  • These findings suggest that a subset of lung cancers, lymphomas, and neuroblastomas that harbor genomic ALK alterations may be clinically responsive to pharmacologic ALK inhibition.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Lymphoma / drug therapy. Neuroblastoma / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Protein-Tyrosine Kinases / genetics. Pyrimidines / therapeutic use
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Benzimidazoles / therapeutic use. Cell Line, Tumor. Cytogenetic Analysis. Drug Evaluation, Preclinical. Gene Amplification / physiology. Genomic Instability / drug effects. Humans. Mutation. Protein Kinase Inhibitors / therapeutic use. Pyridones / therapeutic use. Receptor Protein-Tyrosine Kinases. Translocation, Genetic

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  • (PMID = 18451166.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA115830; United States / NCI NIH HHS / CA / R01 CA115830
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BMS 536924; 0 / Benzimidazoles; 0 / NVP-TAE684; 0 / Protein Kinase Inhibitors; 0 / Pyridones; 0 / Pyrimidines; 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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30. 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

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  • (PMID = 17655697.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antibodies, Neoplasm
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31. Pan Y, Li WX, Li JM, Zhu JQ, Liang YQ, Guo AL: [Correlation of DNA-dependent protein kinase catalytic subunit expression to radiosensitivity of non-small cell lung cancer cell lines]. Ai Zheng; 2009 Jul;28(7):714-7
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  • [Title] [Correlation of DNA-dependent protein kinase catalytic subunit expression to radiosensitivity of non-small cell lung cancer cell lines].
  • BACKGROUND AND OBJECTIVE: DNA-dependent protein kinase catalytic subunit (DNA-PKcs) plays an important role in repairing irradiation-induced DNA double-strand break (DSB), and affects the radiosensitivity of tissue cells.
  • This study was to detect the expression of DNA-PKcs in different non-small cell lung cancer (NSCLC) cell lines and evaluate its correlation to radiosensitivity.
  • METHODS: The content and activity of DNA-PKcs in five NSCLC cell lines A549, H1299, L78, PGCL3 and H460 were measured by Western blot and the DNA-PK activity assay.
  • Cell survival was analyzed using clonogenic formation assay.
  • RESULTS: The radiosensitivities of five NSCLC cell lines were different.
  • The values of survival fraction at 2 Gy (SF2) were 0.74 in A549 cells, 0.25 in H1299 cells, 0.21 in H460 cells, 0.48 in PGCL3 cells, and 0.58 in L78 cells.
  • The protein levels of DNA-PKcs were 3.26+/-0.98 in A549 cells, 0.51+/-0.07 in L78 cells, 0.51+/-0.11 in H1299 cells, 0.86+/-0.23 in H460 cells, and 2.60+/-0.76 in PGCL3 cells.
  • The activity values of DNA-PKcs were 8.30+/-1.03 in A549 cells, 2.45+/-0.52 in H1299 cells, 0.11+/-0.02 in H460 cells, 4.13+/-0.87 in PGCL3 cells, and 0.42+/-0.07 in L78 cells.
  • In adenocarcinoma and large cell carcinoma cell lines, SF2 were correlated to DNA-PKcs content (P<0.05, r=0.95) and activity (P=0.03, r=0.98).
  • CONCLUSION: DNA-PKcs is an important factor to predict the radiosensitivity in adenocarcinoma and large cell lung cancer cell lines.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / pathology. Cell Survival / radiation effects. DNA-Activated Protein Kinase / metabolism. Lung Neoplasms / pathology. Radiation Tolerance
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Carcinoma, Large Cell / metabolism. Carcinoma, Large Cell / pathology. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / pathology. Catalytic Domain. Cell Line, Tumor. Enzyme Activation / radiation effects. Humans. Particle Accelerators

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  • (PMID = 19624897.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] EC 2.7.11.1 / DNA-Activated Protein Kinase
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32. Cutz JC, Guan J, Bayani J, Yoshimoto M, Xue H, Sutcliffe M, English J, Flint J, LeRiche J, Yee J, Squire JA, Gout PW, Lam S, Wang YZ: Establishment in severe combined immunodeficiency mice of subrenal capsule xenografts and transplantable tumor lines from a variety of primary human lung cancers: potential models for studying tumor progression-related changes. Clin Cancer Res; 2006 Jul 1;12(13):4043-54
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  • [Title] Establishment in severe combined immunodeficiency mice of subrenal capsule xenografts and transplantable tumor lines from a variety of primary human lung cancers: potential models for studying tumor progression-related changes.
  • PURPOSE: Lung cancer is a biologically diverse disease and relevant models reflecting its diversity would facilitate the improvement of existing therapies.
  • With a view to establishing such models, we developed and evaluated xenografts of a variety of human lung cancers.
  • EXPERIMENTAL DESIGN: Using nonobese diabetic/severe combined immunodeficiency mice, subrenal capsule xenografts were generated from primary lung cancer tissue, including moderately and poorly differentiated squamous cell carcinoma, adenocarcinoma, adenosquamous carcinoma, small cell carcinoma, large cell undifferentiated carcinoma, and carcinosarcoma.
  • Immunohistochemistry and fluorescence in situ hybridization confirmed the human origin of the tumor cells and development in xenografts of murine supportive stroma.
  • Four transplantable lines were developed from rapidly growing tumors (>5 generations), i.e., a small cell lung carcinoma, large cell undifferentiated carcinoma, pulmonary carcinosarcoma, and squamous cell carcinoma.
  • Analyses including spectral karyotyping, comparative genomic hybridization, and fluorescence in situ hybridization, revealed that the xenografts were genetically similar to the original tumors, showing chromosomal abnormalities consistent with karyotypic changes reported for lung cancer.
  • CONCLUSIONS: The subrenal capsule xenograft approach essentially provides a living tumor bank derived from patient material and a means for isolating and expanding specific cell populations.
  • [MeSH-major] Cell Line, Tumor. Disease Models, Animal. Lung Neoplasms / pathology. Subrenal Capsule Assay


33. 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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34. Lowe EJ, Sposto R, Perkins SL, Gross TG, Finlay J, Zwick D, Abromowitch M, Children's Cancer Group Study 5941: Intensive chemotherapy for systemic anaplastic large cell lymphoma in children and adolescents: final results of Children's Cancer Group Study 5941. Pediatr Blood Cancer; 2009 Mar;52(3):335-9
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  • [Title] Intensive chemotherapy for systemic anaplastic large cell lymphoma in children and adolescents: final results of Children's Cancer Group Study 5941.
  • BACKGROUND: Anaplastic large cell lymphoma (ALCL) is characterized by advanced disease at presentation (70-80% of pediatric cases) and accounts for 10-15% of all childhood lymphomas.
  • METHODS: CCG-5941 used a compressed aggressive multiagent T-cell lineage chemotherapy regimen consisting of a 3-week induction therapy (vincristine, prednisone, cyclophosphamide, daunomycin, asparaginase) followed by a 3-week consolidation period (vincristine, prednisone, etoposide, 6-thioguanine, cytarabine, asparaginase, methotrexate) followed by six courses of maintenance chemotherapy at 7-week intervals (cyclophosphamide, 6-thioguanine, vincristine, prednisone, doxorubicin, asparaginase, methotrexate etoposide, cytarabine).
  • The majority of tumors were positive for ALK (90%) and of T lineage (83%).
  • Extranodal disease was common (mediastinum 35%, skin 15%, lung 14%, bone 12%, bone marrow 13%, liver 6%, and other viscera 17%).
  • Relapse occurred early with 17 (81%) relapses occurring within 2 years of diagnosis and 12 (57%) while receiving therapy.

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  • (PMID = 18985718.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U10 CA098543; None / None / / U10 CA098543-06; United States / NCI NIH HHS / CA / U10 CA098543-06
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS123401; NLM/ PMC2769495
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35. Kelleher FC, McDermott R: The emerging pathogenic and therapeutic importance of the anaplastic lymphoma kinase gene. Eur J Cancer; 2010 Sep;46(13):2357-68
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  • [Title] The emerging pathogenic and therapeutic importance of the anaplastic lymphoma kinase gene.
  • The anaplastic lymphoma kinase gene (ALK) is a gene on chromosome 2p23 that has expression restricted to the brain, testis and small intestine but is not expressed in normal lymphoid tissue.
  • This gene was originally established as being implicated in the pathogenesis of rare diseases including inflammatory myofibroblastic tumour (IMT) and ALK-positive anaplastic large cell lymphoma, which is a subtype of non-Hodgkin's lymphoma.
  • In 2007, an inversion of chromosome 2 involving ALK and a fusion partner gene in a subset of non-small cell lung cancer was discovered.
  • In 2008, publications emerged implicating ALK in familial and sporadic cases of neuroblastoma, a childhood cancer of the sympatho-adrenal system.
  • This has been described in ALK-positive anaplastic large cell lymphoma in which ALK is fused to NPM (nucleolar protein gene) and in non-small cell lung cancer where ALK is fused to EML4 (Echinoderm microtubule-associated protein 4).
  • Point mutations and amplification of the ALK gene occur in the childhood cancer neuroblastoma.
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / therapy. Drug Synergism. Gene Amplification. Humans. Lung Neoplasms / genetics. Lung Neoplasms / therapy. Lymphoma, Large-Cell, Anaplastic / genetics. Lymphoma, Large-Cell, Anaplastic / therapy. Mutation / genetics. Neuroblastoma / genetics. Neuroblastoma / therapy. Pyrimidines / therapeutic use. Pyrroles / therapeutic use. Receptor Protein-Tyrosine Kinases. Receptor, IGF Type 1 / antagonists & inhibitors

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20451371.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / GSK 1838705A; 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 / Receptor, IGF Type 1; EC 2.7.10.1 / anaplastic lymphoma kinase
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36. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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37. 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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38. 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
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
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  • [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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39. Pouniotis DS, Plebanski M, Apostolopoulos V, McDonald CF: Alveolar macrophage function is altered in patients with lung cancer. Clin Exp Immunol; 2006 Feb;143(2):363-72
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  • [Title] Alveolar macrophage function is altered in patients with lung cancer.
  • We examined patients with lung cancer in order to evaluate the immuno-stimulatory potential of AM in lung cancer.
  • Bronchoalveolar lavage fluid samples were obtained from patients with adenocarcinoma, squamous cell carcinoma, large cell undifferentiated lung carcinoma, small cell carcinoma and control subjects.
  • AM from patients with small and squamous cell carcinoma had impaired uptake in vitro of 40 nm fluorescent polystyrene beads.
  • AM from patients with small, squamous and large cell undifferentiated carcinoma showed impaired uptake of 1000 nm fluorescent polystyrene beads.
  • Secreted levels of TNF-alpha and IL-1 from AM of patients with small, squamous, and large cell undifferentiated carcinoma were decreased compared to controls.
  • Secreted AM IL-6 levels were decreased in small and large cell undifferentiated carcinoma.
  • Phenotypic analysis demonstrated that patients with small cell carcinoma were the only group that showed a decrease in MHC class II surface expression.
  • Surface expression of ICAM-1 and CD83 was decreased on AM from patients with large, squamous and small cell carcinoma compared to controls but not adenocarcinoma.
  • Mannose receptor levels were only decreased on AM from patients with squamous and small cell carcinoma but not adenocarcinoma and large cell undifferentiated carcinoma.
  • We conclude that there are type-specific alterations in uptake ability, cytokine secretion and phenotype of AM from lung cancer patients, which may result in an inability to stimulate anti-tumour immunity.
  • The observed differences between lung cancer subgroups may explain previously reported inconsistencies in descriptions of AM characteristics in lung cancer.
  • [MeSH-major] Lung Neoplasms / immunology. Macrophages / immunology. Pulmonary Alveoli / immunology
  • [MeSH-minor] Adenocarcinoma / immunology. Aged. Antigens, CD / analysis. Biomarkers / analysis. Bronchoalveolar Lavage Fluid / immunology. Carcinoma, Large Cell / immunology. Carcinoma, Small Cell / immunology. Carcinoma, Squamous Cell / immunology. Cytokines / immunology. HLA-DR Antigens / analysis. Humans. Immunoglobulins / analysis. Intercellular Adhesion Molecule-1 / analysis. Lectins, C-Type / analysis. Mannose-Binding Lectins / analysis. Membrane Glycoproteins / analysis. Microspheres. Middle Aged. Phenotype. Polystyrenes / pharmacokinetics. Receptors, Cell Surface / analysis

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  • (PMID = 16412062.001).
  • [ISSN] 0009-9104
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers; 0 / CD83 antigen; 0 / Cytokines; 0 / HLA-DR Antigens; 0 / Immunoglobulins; 0 / Lectins, C-Type; 0 / Mannose-Binding Lectins; 0 / Membrane Glycoproteins; 0 / Polystyrenes; 0 / Receptors, Cell Surface; 0 / mannose receptor; 126547-89-5 / Intercellular Adhesion Molecule-1
  • [Other-IDs] NLM/ PMC1809587
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40. Vlastos F, Lacomme S, Wild P, Poulain S, Siat J, Grosdidier G, du Manoir S, Monga B, Hillas G, Varsovie R, Claudot F, Marie B, Vignaud JM, Szymanski N: Do evolving practices improve survival in operated lung cancer patients? A biobank may answer. J Thorac Oncol; 2009 Apr;4(4):505-11
MedlinePlus Health Information. consumer health - Lung Cancer.

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  • [Title] Do evolving practices improve survival in operated lung cancer patients? A biobank may answer.
  • INTRODUCTION: Biobanks may play a pivotal role in lung cancer patients' management, research, and health policy.
  • The Nancy "Centre of Biologic Resources" analyzed the evolving profiles of operated lung cancer patients and their management over 20 years.
  • RESULTS: After 1997, lung cancer was diagnosed at an earlier stage.
  • For Squamous Cell Lung Cancer (SQCLC), stages IA increased from 5.4 to 19.5% and for Adenocarcinoma (ADC), stage IA increased from 9.9 to 24.7%.
  • More patients with Large Cell Lung Cancer were diagnosed recently.
  • CONCLUSION: Overall and stage-adjusted survival of operated lung cancer patients has been improved in the last decade due mainly to earlier diagnosis.
  • [MeSH-major] Lung Neoplasms / mortality

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  • (PMID = 19240651.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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41. 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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42. 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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43. 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
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44. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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45. Weiss J, Sos ML, Seidel D, Peifer M, Zander T, Heuckmann JM, Ullrich RT, Menon R, Maier S, Soltermann A, Moch H, Wagener P, Fischer F, Heynck S, Koker M, Schöttle J, Leenders F, Gabler F, Dabow I, Querings S, Heukamp LC, Balke-Want H, Ansén S, Rauh D, Baessmann I, Altmüller J, Wainer Z, Conron M, Wright G, Russell P, Solomon B, Brambilla E, Brambilla C, Lorimier P, Sollberg S, Brustugun OT, Engel-Riedel W, Ludwig C, Petersen I, Sänger J, Clement J, Groen H, Timens W, Sietsma H, Thunnissen E, Smit E, Heideman D, Cappuzzo F, Ligorio C, Damiani S, Hallek M, Beroukhim R, Pao W, Klebl B, Baumann M, Buettner R, Ernestus K, Stoelben E, Wolf J, Nürnberg P, Perner S, Thomas RK: Frequent and focal FGFR1 amplification associates with therapeutically tractable FGFR1 dependency in squamous cell lung cancer. Sci Transl Med; 2010 Dec 15;2(62):62ra93
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  • [Title] Frequent and focal FGFR1 amplification associates with therapeutically tractable FGFR1 dependency in squamous cell lung cancer.
  • Lung cancer remains one of the leading causes of cancer-related death in developed countries.
  • Although lung adenocarcinomas with EGFR mutations or EML4-ALK fusions respond to treatment by epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) inhibition, respectively, squamous cell lung cancer currently lacks therapeutically exploitable genetic alterations.
  • We conducted a systematic search in a set of 232 lung cancer specimens for genetic alterations that were therapeutically amenable and then performed high-resolution gene copy number analyses.
  • We identified frequent and focal fibroblast growth factor receptor 1 (FGFR1) amplification in squamous cell lung cancer (n = 155), but not in other lung cancer subtypes, and, by fluorescence in situ hybridization, confirmed the presence of FGFR1 amplifications in an independent cohort of squamous cell lung cancer samples (22% of cases).
  • Using cell-based screening with the FGFR inhibitor PD173074 in a large (n = 83) panel of lung cancer cell lines, we demonstrated that this compound inhibited growth and induced apoptosis specifically in those lung cancer cells carrying amplified FGFR1.
  • We validated the FGFR1 dependence of FGFR1-amplified cell lines by FGFR1 knockdown and by ectopic expression of an FGFR1-resistant allele (FGFR1(V561M)), which rescued FGFR1-amplified cells from PD173074-mediated cytotoxicity.
  • Thus, focal FGFR1 amplification is common in squamous cell lung cancer and associated with tumor growth and survival, suggesting that FGFR inhibitors may be a viable therapeutic option in this cohort of patients.
  • [MeSH-major] Lung Neoplasms / genetics. Lung Neoplasms / metabolism. Receptor, Fibroblast Growth Factor, Type 1 / metabolism
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Animals. Apoptosis / genetics. Apoptosis / physiology. Blotting, Western. Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / metabolism. Cell Line. Enzyme Inhibitors / therapeutic use. Gene Expression Regulation, Neoplastic / genetics. Humans. Male. Mice. Mice, Nude. Pyrimidines / therapeutic use. RNA Interference. Xenograft Model Antitumor Assays

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  • [CommentIn] Sci Transl Med. 2010 Dec 15;2(62):62ps56 [21160076.001]
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  • (PMID = 21160078.001).
  • [ISSN] 1946-6242
  • [Journal-full-title] Science translational medicine
  • [ISO-abbreviation] Sci Transl Med
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE25016
  • [Grant] United States / NCI NIH HHS / CA / K08 CA097980; United States / NCI NIH HHS / CA / P01 CA129243; United States / NCI NIH HHS / CA / R01 CA121210
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / PD 173074; 0 / Pyrimidines; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1; Adenocarcinoma of lung
  • [Other-IDs] NLM/ NIHMS569992; NLM/ PMC3990281
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46. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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47. 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


48. Vujanić GM, Kelsey A, Perlman EJ, Sandstedt B, Beckwith JB: Anaplastic sarcoma of the kidney: a clinicopathologic study of 20 cases of a new entity with polyphenotypic features. Am J Surg Pathol; 2007 Oct;31(10):1459-68
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  • [Title] Anaplastic sarcoma of the kidney: a clinicopathologic study of 20 cases of a new entity with polyphenotypic features.
  • We report 20 cases of a distinct, previously unrecognized renal neoplasm, anaplastic sarcoma of the kidney with polyphenotypic features.
  • The tumors were identified by re-reviewing tumors with unusual anaplastic features from the National Wilms Tumor Study Pathology Center, the International Society of Pediatric Oncology and the United Kingdom Children's Cancer Study Group trials.
  • Grossly, most tumors were large, measured 4 to 21 cm (mean 12.7 cm) and weighed 115 to 1820 g (mean 835 g).
  • Histologically, all tumors showed a spindle cell component which contained either multiple foci or diffuse, widespread anaplastic changes with bizarre pleomorphic cells and very atypical mitotic figures.
  • In 2 cases small foci of osteoid were found whereas osteoclast-like giant cells were seen in 4 cases.
  • Cytokeratin, using the antibody CAM5.2, was uniformly negative within the tumor cells.
  • In 4 tumors reverse transcriptase-polymerase chain reaction was performed to detect the SYT-SSX fusion transcript produced by the t(x;18), and the ETV6-NTRK3 fusion transcript using RNA extracted from archived paraffin blocks-results were negative in all 4 specimens.
  • They were usually diagnosed as anaplastic Wilms tumors and treated accordingly.
  • Another stage I patient developed local recurrence after 3 months of diagnosis, but was lost to follow-up.
  • The most common sites of metastases were lung (3 cases), and liver and bones (2 cases each).
  • These tumors showed pathologic features similar to the pleuropulmonary blastoma of childhood and undifferentiated (embryonal) sarcoma of the liver.
  • In the differential diagnosis, anaplastic Wilms tumor, primary renal synovial sarcoma, malignant mesenchymoma, ectomesenchymoma, and mesenchymal chondrosarcomas have been considered but none of these tumors shared the same features as the 20 cases described here which represent a distinct clinicopathologic entity with morphologic features of a polyphenotypic anaplastic sarcoma of the kidney.

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  • (PMID = 17895746.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Desmin; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / SYT-SSX fusion protein; 0 / Vimentin
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49. Sanada H, Hayashi A, Tomimitsu S, Ikeda K, Nakanishi K, Hiyama J, Hidaka D, Sawamoto R, Miyagawa Y, Misumi Y, Fujii A, Nakatsubo S, Tsuru M, Omagari J, Koshizuka H: [Estimation of preoperative induction chemoradiotherapy effectiveness for non small-cell lung cancer]. Gan To Kagaku Ryoho; 2009 Nov;36(12):2012-5
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  • [Title] [Estimation of preoperative induction chemoradiotherapy effectiveness for non small-cell lung cancer].
  • We have performed the clinical evaluations of preoperative induction chemoradiotherapy (CRTx) for 25 patients with non small-cell lung cancer (male: 19, female: 6, mean age: 66.4-year-old).
  • In the histological type of lung cancer, there were 12 patients of adenocarcinoma, 7 of squamous cell carcinoma, 1 of adenosquamous carcinoma, 1 of anaplastic carcinoma, and 4 of large cell carcinoma.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / therapy. Lung Neoplasms / therapy

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  • (PMID = 20037308.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Phytogenic; 0 / Taxoids; 15H5577CQD / docetaxel; BG3F62OND5 / Carboplatin; P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin
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50. Neal JW, Sequist LV: Exciting new targets in lung cancer therapy: ALK, IGF-1R, HDAC, and Hh. Curr Treat Options Oncol; 2010 Jun;11(1-2):36-44
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  • [Title] Exciting new targets in lung cancer therapy: ALK, IGF-1R, HDAC, and Hh.
  • The anaplastic lymphoma kinase (ALK) inhibitor crizotinib will become an integral addition to the treatment of patients with non-small cell lung cancer (NSCLC) harboring genetic ALK translocations.
  • The histone deacetylation (HDAC) inhibitor vorinostat did not demonstrate an improvement in overall survival (OS) compared with placebo in a large randomized trial, but other agents in this class may have greater selectivity and efficacy.
  • Inhibitors of the hedgehog (Hh) signaling pathways have some early clinical promise in both NSCLC and small cell lung cancer (SCLC), and larger studies using these agents are eagerly anticipated.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Hedgehog Proteins / antagonists & inhibitors. Histone Deacetylases / chemistry. Lung Neoplasms / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Receptor, IGF Type 1 / antagonists & inhibitors

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  • (PMID = 20676809.001).
  • [ISSN] 1534-6277
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hedgehog Proteins; 0 / Histone Deacetylase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 3.5.1.98 / Histone Deacetylases
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51. 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

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  • (PMID = 17874719.001).
  • [ISSN] 0042-8450
  • [Journal-full-title] Vojnosanitetski pregled
  • [ISO-abbreviation] Vojnosanit Pregl
  • [Language] srp
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Serbia and Montenegro
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Chromogranin A; 0 / Synaptophysin; EC 4.2.1.11 / Phosphopyruvate Hydratase
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52. 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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53. 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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54. 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


55. Rikova K, Guo A, Zeng Q, Possemato A, Yu J, Haack H, Nardone J, Lee K, Reeves C, Li Y, Hu Y, Tan Z, Stokes M, Sullivan L, Mitchell J, Wetzel R, Macneill J, Ren JM, Yuan J, Bakalarski CE, Villen J, Kornhauser JM, Smith B, Li D, Zhou X, Gygi SP, Gu TL, Polakiewicz RD, Rush J, Comb MJ: Global survey of phosphotyrosine signaling identifies oncogenic kinases in lung cancer. Cell; 2007 Dec 14;131(6):1190-203
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  • [Title] Global survey of phosphotyrosine signaling identifies oncogenic kinases in lung cancer.
  • Despite the success of tyrosine kinase-based cancer therapeutics, for most solid tumors the tyrosine kinases that drive disease remain unknown, limiting our ability to identify drug targets and predict response.
  • Here we present the first large-scale survey of tyrosine kinase activity in lung cancer.
  • Using a phosphoproteomic approach, we characterize tyrosine kinase signaling across 41 non-small cell lung cancer (NSCLC) cell lines and over 150 NSCLC tumors.
  • By focusing on activated cell circuitry, the approach outlined here provides insight into cancer biology not available at the chromosomal and transcriptional levels and can be applied broadly across all human cancers.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / metabolism. Lung Neoplasms / metabolism. Phosphotyrosine / metabolism. Protein-Tyrosine Kinases / metabolism. Signal Transduction / genetics
  • [MeSH-minor] Cell Line, Tumor. Enzyme Activation. Gene Fusion. Humans. Models, Biological. Molecular Sequence Data. Phosphorylation. Receptor Protein-Tyrosine Kinases. Receptor, Platelet-Derived Growth Factor alpha / metabolism


56. Lin E, Li L, Guan Y, Soriano R, Rivers CS, Mohan S, Pandita A, Tang J, Modrusan Z: Exon array profiling detects EML4-ALK fusion in breast, colorectal, and non-small cell lung cancers. Mol Cancer Res; 2009 Sep;7(9):1466-76
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  • [Title] Exon array profiling detects EML4-ALK fusion in breast, colorectal, and non-small cell lung cancers.
  • The echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase (EML4-ALK) fusion gene has been identified as an oncogene in a subset of non-small cell lung cancers (NSCLC).
  • We used profiling of cancer genomes on an exon array to develop a novel computational method for the global search of gene rearrangements.
  • Screening of a large collection of patient tumor samples showed the presence of EML4-ALK fusion in 2.4% of breast (5 of 209), 2.4% of colorectal (2 of 83), and in 11.3% of NSCLC (12 of 106).
  • A20) and 2 (E20; A20), a novel variant E21; A20 was found in colorectal carcinoma.
  • EML4-ALK translocation was also confirmed by fluorescence in situ hybridization assay, which revealed its substantial heterogeneity in both primary tumors and tumor-derived cell lines.
  • To elucidate the functional significance of EML4-ALK, we examined the growth of cell lines harboring the fusion following EML4 and ALK silencing by small interfering RNA.
  • Significant growth inhibition was observed in some but not all cell lines, suggesting their variable dependence on ALK-mediated cell survival signaling.
  • [MeSH-major] Breast Neoplasms / genetics. Carcinoma, Non-Small-Cell Lung / genetics. Colorectal Neoplasms / genetics. Exons. Lung Neoplasms / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Cell Survival / physiology. Chromosome Breakpoints. Female. Gene Rearrangement. Humans. In Situ Hybridization, Fluorescence. Oligonucleotide Array Sequence Analysis / methods. RNA Interference. RNA, Small Interfering / genetics. RNA, Small Interfering / metabolism. Reproducibility of Results. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19737969.001).
  • [ISSN] 1557-3125
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / EML4-ALK fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / RNA, Small Interfering
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57. Rodig SJ, Mino-Kenudson M, Dacic S, Yeap BY, Shaw A, Barletta JA, Stubbs H, Law K, Lindeman N, Mark E, Janne PA, Lynch T, Johnson BE, Iafrate AJ, Chirieac LR: Unique clinicopathologic features characterize ALK-rearranged lung adenocarcinoma in the western population. Clin Cancer Res; 2009 Aug 15;15(16):5216-23
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  • [Title] Unique clinicopathologic features characterize ALK-rearranged lung adenocarcinoma in the western population.
  • PURPOSE: The anaplastic large cell kinase gene (ALK) is rearranged in approximately 5% of lung adenocarcinomas within the Asian population.
  • We evaluated the incidence and the characteristics of ALK-rearranged lung adenocarcinomas within the western population and the optimal diagnostic modality to detect ALK rearrangements in routine clinical practice.
  • EXPERIMENTAL DESIGN: We tested 358 lung adenocarcinomas from three institutions for ALK rearrangements by fluorescent in situ hybridization (FISH) and immunohistochemistry with and without tyramide amplification.
  • RESULTS: We identified 20 (5.6%) lung adenocarcinomas with ALK rearrangements within our cohort of western patients.
  • ALK rearrangement was associated with younger age (P = 0.0002), never smoking (P < 0.0001), advanced clinical stage (P = 0.0001), and a solid histology with signet-ring cells (P < 0.0001).
  • CONCLUSIONS: Lung adenocarcinomas with ALK rearrangements are uncommon in the western population and represent a distinct entity of carcinomas with unique characteristics.
  • For suspected cases, dual diagnostic testing, with FISH and immunohistochemistry, should be considered to accurately identify lung adenocarcinomas with ALK rearrangement.

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  • [CommentIn] Clin Cancer Res. 2015 Dec 1;21(23):5185-7 [26626570.001]
  • [ErratumIn] Clin Cancer Res. 2009 Nov 15;15(22):7110
  • (PMID = 19671850.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA136851-02; United States / PHS HHS / / R01-135257; United States / PHS HHS / / R01-136851; United States / NCI NIH HHS / CA / P50 CA090578; United States / NCI NIH HHS / CA / R01 CA136851-02; United States / NCI NIH HHS / CA / R01 CA136851; United States / NCI NIH HHS / CA / 2P50 CA090578-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Other-IDs] NLM/ NIHMS198972; NLM/ PMC2865649
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58. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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59. 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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60. Attili VS, Reddy CO: An interesting case of lung mass. J Lab Physicians; 2009 Jan;1(1):25-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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  • [Cites] Histopathology. 1995 May;26(5):405-12 [7544761.001]
  • [Cites] Zhonghua Er Ke Za Zhi. 2007 Dec;45(12):949 [18339290.001]
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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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61. Ruffini E, Asioli S, Filosso PL, Lyberis P, Bruna MC, Macrì L, Daniele L, Oliaro A: Clinical significance of tumor-infiltrating lymphocytes in lung neoplasms. Ann Thorac Surg; 2009 Feb;87(2):365-71; discussion 371-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical significance of tumor-infiltrating lymphocytes in lung neoplasms.
  • We examined prevalence, correlations, and prognostic significance of TIL among our patient population of resected lung neoplasms.
  • METHODS: From 1993 to 2006, the presence of TIL was retrospectively evaluated in 1,290 patients operated on for primary lung neoplasms.
  • Tumor-infiltrating lymphocytes were defined as those intraepithelial lymphocytes located within the cancer cell nests.
  • A significant difference was found between prevalence in non-small cell lung carcinomas versus neuroendocrine tumors (290 of 1,208, 24% versus 4 of 82, 5%; p = 0.0001).
  • Prevalence was similar in adenocarcinomas, squamous-cell carcinomas, and large-cell anaplastic carcinomas.
  • A not significantly better survival in the presence of TIL was observed overall (p = 0.20), becoming significant in squamous-cell carcinomas (p = 0.03).
  • In patients with stage I disease, TIL is associated with a significant survival advantage in squamous-cell carcinomas (p = 0.03).
  • CONCLUSIONS: Tumor-infiltrating lymphocytes are observed in about one fourth of resected lung neoplasms: they are rare in neuroendocrine tumors.
  • The presence of TIL correlates with an improved survival in squamous cell carcinomas, particularly at early stage.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Lung Neoplasms / mortality. Lung Neoplasms / pathology. Lymphocytes, Tumor-Infiltrating / metabolism

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  • (PMID = 19161739.001).
  • [ISSN] 1552-6259
  • [Journal-full-title] The Annals of thoracic surgery
  • [ISO-abbreviation] Ann. Thorac. Surg.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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62. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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63. Wang CY, Lin KH, Yang CJ, Tsai JR, Hung JY, Wang PH, Hsu HK, Huang MS: Toona sinensis extracts induced cell cycle arrest and apoptosis in the human lung large cell carcinoma. Kaohsiung J Med Sci; 2010 Feb;26(2):68-75
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Toona sinensis extracts induced cell cycle arrest and apoptosis in the human lung large cell carcinoma.
  • Toona sinensis extracts have been shown to exhibit anti-cancer effects in human ovarian cancer cell lines, human promyelocytic leukemia cells and human lung adenocarcinoma.
  • However, its anti-cancer properties in human lung large cell carcinoma have not been studied.
  • Here, we used a powder obtained by freeze-drying the supernatant of centrifuged crude extract from Toona sinensis leaves (TSL-1) to treat the human lung carcinoma cell line H661.
  • Cell viability was evaluated by the 3-(4-,5-dimethylthiazol-2-yl)-2,5 diphenyl tetrazolium bromide assay.
  • Flow cytometry analysis revealed that TSL-1 blocked H661 cell cycle progression.
  • Western blot analysis showed decreased expression of cell cycle proteins that promote cell cycle progression, including cyclin-dependent kinase 4 and cyclin D1, and increased the expression of proteins that inhibit cell cycle progression, including p27.
  • Furthermore, flow cytometry analysis showed that TSL-1 induced H661 cell apoptosis.
  • Western blot analysis showed that TSL-1 reduced the expression of the anti-apoptotic protein B-cell lymphoma 2, and degraded the DNA repair protein, poly(ADP-ribose) polymerase.
  • TSL-1 shows potential as a novel therapeutic agent or for use as an adjuvant for treating human lung large cell carcinoma.
  • [MeSH-major] Apoptosis / drug effects. Carcinoma, Large Cell / physiopathology. Cell Cycle / drug effects. Lung Neoplasms / physiopathology. Meliaceae / chemistry. Plant Extracts / pharmacology
  • [MeSH-minor] Cell Cycle Proteins / genetics. Cell Cycle Proteins / metabolism. Cell Line, Tumor. Gene Expression Regulation / drug effects. Humans

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  • (PMID = 20123594.001).
  • [ISSN] 1607-551X
  • [Journal-full-title] The Kaohsiung journal of medical sciences
  • [ISO-abbreviation] Kaohsiung J. Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China (Republic : 1949- )
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Plant Extracts
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64. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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65. Mino-Kenudson M, Chirieac LR, Law K, Hornick JL, Lindeman N, Mark EJ, Cohen DW, Johnson BE, Jänne PA, Iafrate AJ, Rodig SJ: A novel, highly sensitive antibody allows for the routine detection of ALK-rearranged lung adenocarcinomas by standard immunohistochemistry. Clin Cancer Res; 2010 Mar 1;16(5):1561-71
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel, highly sensitive antibody allows for the routine detection of ALK-rearranged lung adenocarcinomas by standard immunohistochemistry.
  • PURPOSE: Approximately 5% of lung adenocarcinomas harbor an EML4-ALK gene fusion and define a unique tumor group that may be responsive to targeted therapy.
  • However ALK-rearranged lung adenocarcinomas are difficult to detect by either standard fluorescence in situ hybridization or immunohistochemistry (IHC) assays.
  • In the present study, we used novel antibodies to compare ALK protein expression in genetically defined lung cancers and anaplastic large cell lymphomas.
  • RESULTS: ALK protein is invariably and exclusively expressed in ALK-rearranged lung adenocarcinomas but at much lower levels than in the prototypic ALK-rearranged tumor, anaplastic large cell lymphoma, and as a result, is often not detected by conventional IHC.
  • We further validate a novel IHC that shows excellent sensitivity and specificity (100% and 99%, respectively) for the detection of ALK-rearranged lung adenocarcinomas in biopsy specimens, with excellent interobserver agreement between pathologists (kappa statistic, 0.94).
  • CONCLUSIONS: Low levels of ALK protein expression is a characteristic feature of ALK-rearranged lung adenocarcinomas.
  • However, a novel, highly sensitive IHC assay reliably detects lung adenocarcinomas with ALK rearrangements and obviates the need for fluorescence in situ hybridization analysis for the majority of cases, and therefore could be routinely applicable in clinical practice to detect lung cancers that may be responsive to ALK inhibitors.

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  • (PMID = 20179225.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P20 CA090578; United States / NCI NIH HHS / CA / CA090578; United States / NCI NIH HHS / CA / CA136851-01A1; United States / NCI NIH HHS / CA / R01 CA136851-01A1; United States / NCI NIH HHS / CA / R01CA136851; United States / NCI NIH HHS / CA / P50 CA090578; United States / NCI NIH HHS / CA / R01 CA114465; United States / NCI NIH HHS / CA / R01 CA136851
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / EML4-ALK fusion protein, human; 0 / Oncogene Proteins, Fusion
  • [Other-IDs] NLM/ NIHMS170973; NLM/ PMC2831135
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66. Makdissi A, Zimmerman RS: Humoral hypercalcemia of malignancy in a patient with large cell carcinoma of the lung: report of case and review of literature. Endocr Pract; 2007 Jul-Aug;13(4):389-95
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  • [Title] Humoral hypercalcemia of malignancy in a patient with large cell carcinoma of the lung: report of case and review of literature.
  • OBJECTIVE: To report a case of hypercalcemia associated with parathyroid hormone-related protein (PTHrP) in large cell carcinoma of the lung.
  • METHODS: We present a case of PTHrP-mediated hypercalcemia in a patient with a large cell carcinoma of the lung and review the related literature.
  • Breath sounds were decreased in the left lower lung field.
  • Computed tomographic scans of the chest showed a large complex lesion in the left lower hemithorax, a small right pleural effusion, and extensive pulmonary emphysema bilaterally.
  • Open lung biopsy revealed a large cell undifferentiated carcinoma.
  • CONCLUSION: Although the finding is rare, patients with large cell carcinoma of the lung and hypercalcemia may have humoral hypercalcemia mediated by PTHrP.
  • [MeSH-major] Carcinoma, Large Cell / complications. Hypercalcemia / etiology. Lung Neoplasms / complications. Parathyroid Hormone-Related Protein / blood

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  • (PMID = 17669716.001).
  • [ISSN] 1934-2403
  • [Journal-full-title] Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
  • [ISO-abbreviation] Endocr Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Parathyroid Hormone-Related Protein
  • [Number-of-references] 31
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67. 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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68. Ma L, Zhou Q, Zhu W, Zhu D, Yang X, Wang Y, Chen X, Zhang M, Gao L, Zhap Y: [Effects of nm23-H1 point mutation on activity of GSK-3β in human high-metastatic large cell lung cancer cell line L9981]. Zhongguo Fei Ai Za Zhi; 2006 Feb 20;9(1):30-4
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  • [Title] [Effects of nm23-H1 point mutation on activity of GSK-3β in human high-metastatic large cell lung cancer cell line L9981].
  • BACKGROUND: The results of our previous studies have proven that nm23-H1 gene can suppress metastasis of lung cancer, which may be associated with suppression of the Wnt signal pathway through up-regulating the activity of glycogen synthase kinase 3β (GSK-3β), the key kinase of the Wnt signal pathway.
  • The aim of this study is to investigate the effect of point mutation of nm23-H1 gene on GSK-3β activity in cytoplasm and nucleus in human high-metastatic large cell lung cancer cell line L9981.
  • METHODS: Using immunoprecipitation and a radioactive isotope scintillation counter, the activity of GSK-3β was detected in cytoplasm and nucleus of human low-metastatic large cell lung cancer cell line NL9980, human high-metastatic large cell lung cancer cell line L9981, L9981-pEGFP (transfected with vector), L9981-nm23-H1-pEGFP (transfected with wild type nm23-H1), L9981-nm23-H1 S44A -pEGFP mutant (transfected with serine 44 to alanineon of nm23-H1 gene), L9981-nm23-H1 P96S -pEGFP mutant (transfected with proline 96 to serine of nm23-H1 gene), L9981-nm23-H1 H118F -pEGFP mutant (transfected with histidine 118 to phenylalanine of nm23-H1 gene) and L9981-nm23-H1 S120G -pEGFP mutant (transfected with serine 120 to glycine of nm23-H1 gene).
  • RESULTS: The GSK-3β activity in cytoplasm and nucleus was remarkably decreased in the transgene lung cancer cell lines transfected with mutant nm23-H1 cDNA (L9981-nm23-H1 S44A -pEGFP, L9981-nm23-H1 P96S -pEGFP, L9981-nm23-H1 H118F -pEGFP and L9981-nm23-H1 S120G -pEGFP).
  • Significant differences of GSK-3β activity in cytoplasm and nucleus were observed (P < 0.05) when L9981-nm23-H1-pEGFP cell line was compared with L9981-nm23-H1 S44A -pEGFP, L9981-nm23-H1 P96S -pEGFP, L9981-nm23-H1 H118F -pEGFP and L9981-nm23-H1 S120G -pEGFP lung cancer cell lines.
  • There was a highly significant difference in GSK-3β activity in the cytoplasm between L9981-nm23-H1-pEGFP cell line and L9981-nm23-H1 P96S -pEGFP lung cancer cell line (P < 0.01 ).
  • A highly significant difference in GSK-3β activity in the nucleus was observed (P < 0.01) when L9981-nm23-H1-pEGFP lung cancer cell line was compared with L9981-nm23-H1 S44A -pEGFP, L9981-nm23-H1 P96S -pEGFP and L9981-nm23-H1 H118F -pEGFP lung cancer cell lines. CONCLUSIONS:.
  • (1) Point mutation of nm23-H1 gene can significantly influence the regulating effects on the GSK-3β activity in the cytoplasm and nucleus in the human high-metastatic large cell lung cancer cell line L9981. (2) The effects of nm23-H1 gene on metastatic phenotype may be related to the upregulation of GSK-3β activity in human high-metastatic large cell lung cancer cell line L9981.

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  • (PMID = 21144278.001).
  • [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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69. 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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70. 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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71. 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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72. 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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73. Gao L, Zhu W, Li L, Hou M, Ma L, Zhao Y, Zhou Q: [Comparative proteomics study on human high-metastatic large cell lung cancer cell lines before and after transfecting with nm23-H1 gene]. Zhongguo Fei Ai Za Zhi; 2010 Oct;13(10):928-32
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  • [Title] [Comparative proteomics study on human high-metastatic large cell lung cancer cell lines before and after transfecting with nm23-H1 gene].
  • The aim of this study is to better understand the mechanism of lung cancer metastasis and to find new biomarkers for early diagnosis and new target for therapy by conducting comparative proteomics between the human high-metastatic large cell lung cancer cell lines (L9981) and L9981-nm23-H1 (constructed with transfecting nm23-H1 gene into the L9981 cell line).
  • METHODS: The total proteins of L9981 and L9981-nm23-H1 were separated by immobilized pH gradient (IPG)-based 2-dimensional electrophoresis (2-DE); the significantly differently expressed proteins were examined by mass spectrometry and analyzed by bioinformatics.
  • RESULTS: It was observed that nm23-H1 gene transfection caused remarkable changes of the proteome of L9981 compared with L9981-nm23-H1 cells: 5 proteins were deleted, 9 proteins appeared, 16 proteins downregulated, and 12 proteins up-regulated.
  • These proteins are involved in cell framework, signal transduction, metabolism, proliferation and metastasis.
  • These changes of the proteome could serve as a basis for reversing the invasive and metastatic phenotype in lung cancer and elucidating the mechanisms of the metastasis of lung cancer.
  • [MeSH-major] Carcinoma, Large Cell / metabolism. Carcinoma, Large Cell / pathology. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. NM23 Nucleoside Diphosphate Kinases / genetics. Proteomics / methods. Transfection
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Cell Line, Tumor. Early Detection of Cancer. Humans. Neoplasm Metastasis

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  • (PMID = 20959063.001).
  • [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
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / NM23 Nucleoside Diphosphate Kinases; EC 2.7.4.6 / NME1 protein, human
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74. Liu C, Chen J, Wu Z, Li Y, Zhu Y, Ren Y, Zhou Q: [Selenium compounds induce ROS in human high-metastatic large cell lung cancer cell line L9981.]. Zhongguo Fei Ai Za Zhi; 2008 Jun 20;11(3):354-8

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  • [Title] [Selenium compounds induce ROS in human high-metastatic large cell lung cancer cell line L9981.].
  • BACKGROUND: It has been proved that methylseleninic acid (MSA) is a kind of artificially developed selenium compound, which appeared to be the best candidate for cancer prevention and therapy.
  • METHODS: We confirmed that MSA and selenite have the anticancer effect in the human high-metastatic large cell lung cancer cell line L9981 by growth inhibition detection, we detect the ROS induced by MSA and selenite in L9981 by fluorescence microscopy, and use flow cytometry to quantitate the ROS induced by NAC together with selenium compounds.
  • CONCLUSIONS: (1)MSA and selenite had anti-L9981 effect. (2)Oxidative stress reaction may participate in the induction of apoptosis by MSA and selenite in lung cancer cell line L9981.

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  • (PMID = 20731933.001).
  • [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. Li Y, Zhou Q, Sun Z, Sun Z, Wang Y, Qin Y, Zhu W, Chen X: [Experimental study on molecular mechanism of nm23-H1 gene transfection reversing the malignant phenotype of human high-metastatic large cell lung cancer cell line]. Zhongguo Fei Ai Za Zhi; 2006;9(4):307-11
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  • [Title] [Experimental study on molecular mechanism of nm23-H1 gene transfection reversing the malignant phenotype of human high-metastatic large cell lung cancer cell line].
  • Our previous study has found that transfection of wild type nm23-H1 gene can significantly downregulate the ERK1/2 activity of human high-metastatic large cell lung cancer cell line L9981.
  • The aim of this study is to investigate the influence of nm23-H1 and exogenous ERK1/2 pathway inhibitor U0126 on the extracellular signal-regulated kinase (ERK1/2) of human high-metastatic large cell lung cancer cell line L9981 and its malignant biological behaviors.
  • METHODS: The expressive levels of total-ERK1/2, dually phosphorylated ERK1/2 and ERK1/2 relative activity of the human high-metastatic large cell lung cancer cell lines, L9981 (parent cell line with nm23-H1 gene hetero-deletion), L9981-nm23-H1 (transfected with nm23-H1 gene ) and L9981-PLXSN (transfected with vector) were detected by Western blot and immunoprecipitation technique after treating with U0126 (40μmol/L for 20 minutes).
  • The in vitro proliferative and invasive abilities among the above three lung cancer cell lines were determined by MTT and improved Boyden chamber methods.
  • RESULTS: The phosphorylated ERK1/2 expression level and relative activity in L9981-nm23-H1 lung cancer cell line were remarkably lower than those in L9981 and L9981-PLXSN lung cancer cell lines after being treated with U0126 (P < 0.01), but there was no significant difference between L9981 and L9981-PLXSN lung cancer cell lines.
  • No significant difference of total ERK1/2 expression level was observed among the three lung cancer cell lines (P > 0.05) after being treated with U0126.
  • The in vitro proliferation and invasion of L9981-nm-23H1 lung cancer cell line were remarkably lower than those of L9981 and L9981-PLXSN lung cancer cell lines (P < 0.01 ), but no significant difference was found between L9981 and L9981-PLXSN lung cancer cell lines (P > 0.05 ); U0126 could significantly down-regulate the in vitro proliferation and invasion of L9981 lung cancer cell line (P < 0.01).
  • CONCLUSIONS: Blocking the activity of ERK1/2 in L9981 lung cancer cell line and transfecting the nm23-H1 gene into the L9981 lung cancer cell line may produce similar cell biological behavior changes, namely the significant reduction of in vitro proliferation and invasion of L9981 lung cancer cell line.
  • These results indicate that the molecular mechanism which nm23-H1 gene reverses invasion and proliferation of the human high-metastatic large cell lung cancer cell line may be related to its effects of down-regulating the activity of the key kinase ERK1/2 of Ras-to-MAPK signal transduction pathway.

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  • (PMID = 21176443.001).
  • [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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76. Li Y, Zhou Q, Sun Z, Sun Z, Wang Y, Qin Y, Zhu W, Chen X: [Effects of targeting inhibition of ERK1/2 signal transduction pathway on malignant biological behaviors of human high-metastatic large cell lung cancer cell line L9981]. Zhongguo Fei Ai Za Zhi; 2005 Dec 20;8(6):504-9
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  • [Title] [Effects of targeting inhibition of ERK1/2 signal transduction pathway on malignant biological behaviors of human high-metastatic large cell lung cancer cell line L9981].
  • BACKGROUND: It has been known that oncogenesis and development of lung can- cer is a complex process regulated many genes and involved in multistages.
  • The aim of this study is to investigate the influence of exogenous MEK1/2 pathway inhibitor U0126 on the expression and activity of extracellular signal-regulated kinase (ERK1/2) of human high-metastatic large cell lung cancer cell line L9981 and its malignant biological behaviors.
  • METHODS: The expressive levels of total-ERK1/2, dually phosphorylated ERK1/2 and ERK1/2 relative activity of the human high-metastatic large cell lung cancer cell line L9981 (parent cell line with nm23-H1 gene hetero-deletion ) were detected by Western blot and immuno-precipitation technique after treating with different doses of U0126.
  • The in vitro proliferative and invasive abilities of the lung cancer cell line were determined by MTT and modified Boyden chamber methods.
  • CONCLUSIONS: The inhibition of Ras-to-MAPK pathway by Ras-to-MAPK specific inhibitor U0126 targeting the Ras-to-MAPK pathway of the human high-metastatic large cell lung cancer cell line L9981 is dose-dependent and time-dependent.
  • Suppressing or blocking of Ras-to-MAPK signal transduction pathway can reverse the invasive and metastatic phenotype of the human high-metastatic large cell lung cancer cell line L9981.
  • These results suggest that the key kinase MEK1/2 of the ERK1/2 pathway may be a potent therapeutic target for human lung cancer.


77. 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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78. 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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79. 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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  • [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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80. 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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81. Sugaya M, Takenoyama M, Shigematsu Y, Baba T, Fukuyama T, Nagata Y, Mizukami M, So T, Ichiki Y, Yasuda M, So T, Hanagiri T, Sugio K, Yasumoto K: Identification of HLA-A24 restricted shared antigen recognized by autologous cytotoxic T lymphocytes from a patient with large cell carcinoma of the lung. Int J Cancer; 2007 Mar 1;120(5):1055-62
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  • [Title] Identification of HLA-A24 restricted shared antigen recognized by autologous cytotoxic T lymphocytes from a patient with large cell carcinoma of the lung.
  • The aim of the present study was to elucidate the tumor-specific cellular immunological responses occurring in a patient with large cell carcinoma of the lung who had no evidence of recurrence following surgical resections of both a primary lung lesion and a metastatic adrenal lesion.
  • The F2b possessed T cell receptor (TCR) using the Valpha5 and Vbeta7 gene segment.
  • The existence of precursor CTL (pCTL) against autologous tumor cells (A904L) was analyzed using CTL clone-specific PCR.
  • The F2b recognized 3 out of 7 HLA-A24 positive allogeneic tumor cell lines and in 1 out of 7 HLA-A24 negative allogeneic tumor cell lines when transfected with HLA-A24.
  • This peptide is therefore considered to be potentially useful for performing specific immunotherapy in a significant proportion of lung cancer patients bearing HLA-A24.
  • [MeSH-major] Antigens, Neoplasm / isolation & purification. Carcinoma, Large Cell / immunology. HLA-A Antigens / analysis. Lung Neoplasms / immunology. Microfilament Proteins / genetics. Oligopeptides / isolation & purification. T-Lymphocytes, Cytotoxic / immunology
  • [MeSH-minor] Alternative Splicing. Amino Acid Sequence. Cytotoxicity, Immunologic / genetics. DNA, Complementary / genetics. Gene Expression. HLA-A24 Antigen. Humans. Molecular Sequence Data. Neoplasm Recurrence, Local / diagnosis. Peptides / genetics. Peptides / immunology. Peptides / isolation & purification. Receptors, Antigen, T-Cell / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 17131342.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / DNA, Complementary; 0 / HLA-A Antigens; 0 / HLA-A*24:02 antigen; 0 / HLA-A24 Antigen; 0 / Microfilament Proteins; 0 / NYGFQIHTK; 0 / Oligopeptides; 0 / Peptides; 0 / Receptors, Antigen, T-Cell; 0 / TRIOBP protein, human
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82. 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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83. 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

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  • (PMID = 15854392.001).
  • [ISSN] 1001-0939
  • [Journal-full-title] Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases
  • [ISO-abbreviation] Zhonghua Jie He He Hu Xi Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Multidrug Resistance-Associated Proteins; 0 / P-Glycoprotein; 0 / Tumor Suppressor Protein p53; Q20Q21Q62J / Cisplatin
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84. 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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85. 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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86. 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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87. Hanagiri T, Oka S, Takenaka S, Baba T, Yasuda M, Ono K, So T, Uramoto H, Takenoyama M, Yasumoto K: Results of surgical resection for patients with large cell carcinoma of the lung. Int J Surg; 2010;8(5):391-4
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  • [Title] Results of surgical resection for patients with large cell carcinoma of the lung.
  • PURPOSE: The clinical features of large cell carcinoma (LCC) of the lung have remained unclear due to the low incidence of the disease.
  • SUBJECTS: This study clinicopathologically evaluated 975 patients who had undergone a resection for non-small cell carcinoma between 1994 and 2007.
  • RESULTS: The LCC patients included 49 males and 8 females and included 9 patients with large cell neuroendocrine carcinoma.
  • The mean smoking pack-year index was 49.9 in the patients with LCC, 27.1 in 625 patients with adenocarcinoma, and 52.5 in 266 patients with squamous cell carcinoma, and this was significantly higher in the patients with LCC than in those with adenocarcinoma.
  • The mean tumor diameter was 38 mm for LCC, 28 mm for adenocarcinoma, and 39 mm for squamous cell carcinoma.
  • The post-operative 5-year survival rate was 60.5% for LCC, 64.3% for large cell neuroendocrine carcinoma, 67.0% for adenocarcinoma, and 50.1% for squamous cell carcinoma.
  • CONCLUSION: The tumor diameter was significantly larger for LCC than for adenocarcinoma at the time of diagnosis.
  • The surgical results were similar between LCC and other non-small cell lung carcinomas.
  • [MeSH-major] Carcinoma, Large Cell / surgery. Lung Neoplasms / surgery. Pneumonectomy / methods
  • [MeSH-minor] Bronchoscopy. Diagnosis, Differential. Female. Follow-Up Studies. Humans. Japan / epidemiology. Male. Middle Aged. Neoplasm Staging. Retrospective Studies. Survival Rate / trends. Tomography, X-Ray Computed. Treatment Outcome

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  • [Copyright] Copyright 2010 Surgical Associates Ltd. Published by Elsevier Ltd. All rights reserved.
  • (PMID = 20547250.001).
  • [ISSN] 1743-9159
  • [Journal-full-title] International journal of surgery (London, England)
  • [ISO-abbreviation] Int J Surg
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
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88. Lesniak A, Hodge WG: Large cell carcinoma of the lung and squamous cell carcinoma of the oropharynx presenting as uveitis. Ann Ophthalmol (Skokie); 2009;41(1):52-4
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  • [Title] Large cell carcinoma of the lung and squamous cell carcinoma of the oropharynx presenting as uveitis.
  • Ocular manifestations of systemic malignancy may precede the diagnosis of cancer; some intraocular lymphomas can present initially as chronic uveitis.
  • The two cases described were found to have underlying carcinomas of the lung and oropharynx.
  • [MeSH-major] Carcinoma, Large Cell / diagnosis. Carcinoma, Squamous Cell / diagnosis. Lung Neoplasms / diagnosis. Oropharyngeal Neoplasms / diagnosis. Uveitis / diagnosis

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  • (PMID = 19413230.001).
  • [ISSN] 1530-4086
  • [Journal-full-title] Annals of ophthalmology (Skokie, Ill.)
  • [ISO-abbreviation] Ann Ophthalmol (Skokie)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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89. 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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90. Cannizzo E, Sohani AR, Ferry JA, Hochberg EP, Kluk MJ, Dorn ME, Sadowski C, Bucci JJ, Ackerman AM, Longtine JA, Carulli G, Preffer FI: Carcinoma and multiple lymphomas in one patient: establishing the diagnoses and analyzing risk factors. J Hematop; 2009;2(3):163-70
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  • [Title] Carcinoma and multiple lymphomas in one patient: establishing the diagnoses and analyzing risk factors.
  • We report the case of a patient who showed the sequential occurrence of four different lymphoid neoplasms together with a squamous cell carcinoma of the lung.
  • Two years later, a PET-CT scan showed a left hilar mass in the lung; biopsy showed a squamous cell carcinoma.
  • Simultaneously, he was diagnosed with diffuse large B cell lymphoma in a neck lymph node; after chemo- and radiotherapy, he achieved a complete response.
  • A restaging PET-CT scan 2 years later revealed a retroperitoneal nodule, and biopsy again showed a low-grade follicular lymphoma, while a biopsy of a cutaneous scalp lesion showed a CD30-positive peripheral T cell lymphoma.
  • After some months, a liver biopsy and a right cervical lymph node biopsy showed a CD30-positive peripheral T cell lymphoma consistent with anaplastic lymphoma kinase-negative anaplastic large cell lymphoma.
  • Flow cytometry and cytogenetic and molecular genetic analysis performed at diagnosis and during the patient's follow-up confirmed the presence of two clonally distinct B cell lymphomas, while the two T cell neoplasms were confirmed to be clonally related.

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  • (PMID = 20309424.001).
  • [ISSN] 1865-5785
  • [Journal-full-title] Journal of hematopathology
  • [ISO-abbreviation] J Hematop
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Other-IDs] NLM/ PMC2766444
  • [Keywords] NOTNLM ; Anaplastic large cell lymphoma / Cytogenetics / Diffuse large B cell lymphoma / Follicular lymphoma / Multiple malignancies / Risk factors
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91. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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92. Palanisamy N, Ateeq B, Kalyana-Sundaram S, Pflueger D, Ramnarayanan K, Shankar S, Han B, Cao Q, Cao X, Suleman K, Kumar-Sinha C, Dhanasekaran SM, Chen YB, Esgueva R, Banerjee S, LaFargue CJ, Siddiqui J, Demichelis F, Moeller P, Bismar TA, Kuefer R, Fullen DR, Johnson TM, Greenson JK, Giordano TJ, Tan P, Tomlins SA, Varambally S, Rubin MA, Maher CA, Chinnaiyan AM: Rearrangements of the RAF kinase pathway in prostate cancer, gastric cancer and melanoma. Nat Med; 2010 Jul;16(7):793-8
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  • [Title] Rearrangements of the RAF kinase pathway in prostate cancer, gastric cancer and melanoma.
  • Although recurrent gene fusions involving erythroblastosis virus E26 transformation-specific (ETS) family transcription factors are common in prostate cancer, their products are considered 'undruggable' by conventional approaches.
  • Recently, rare targetable gene fusions involving the anaplastic lymphoma receptor tyrosine kinase (ALK) gene, have been identified in 1-5% of lung cancers, suggesting that similar rare gene fusions may occur in other common epithelial cancers, including prostate cancer.
  • Expression of SLC45A3-BRAF or ESRP1-RAF1 in prostate cells induced a neoplastic phenotype that was sensitive to RAF and mitogen-activated protein kinase kinase (MAP2K1) inhibitors.
  • Screening a large cohort of patients, we found that, although rare, recurrent rearrangements in the RAF pathway tend to occur in advanced prostate cancers, gastric cancers and melanoma.
  • Taken together, our results emphasize the key role of RAF family gene rearrangements in cancer, suggest that RAF and MEK inhibitors may be useful in a subset of gene fusion-harboring solid tumors and demonstrate that sequencing of tumor transcriptomes and genomes may lead to the identification of rare targetable fusions across cancer types.

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  • (PMID = 20526349.001).
  • [ISSN] 1546-170X
  • [Journal-full-title] Nature medicine
  • [ISO-abbreviation] Nat. Med.
  • [Language] ENG
  • [Grant] United States / NIDA NIH HHS / DA / U54 DA21519-01A1; United States / NCI NIH HHS / CA / R01 CA125612-01; United States / NCI NIH HHS / CA / R01 CA132874; United States / NCI NIH HHS / CA / U01 CA111275-01; United States / NCI NIH HHS / CA / P50 CA069568-06A19001; United States / NCI NIH HHS / CA / CA069568-06A19001; United States / NCI NIH HHS / CA / R01 CA125612-01A1; United States / NCI NIH HHS / CA / P50CA69568; United States / NCI NIH HHS / CA / R01 CA125612; Canada / Canadian Institutes of Health Research / / ; United States / NCI NIH HHS / CA / P50 CA069568-06A10016; United States / Howard Hughes Medical Institute / / ; United States / NCI NIH HHS / CA / R01CA132874; United States / NCI NIH HHS / CA / CA069568-06A10016; United States / NIDA NIH HHS / DA / U54 DA021519; United States / NCI NIH HHS / CA / P50 CA069568; United States / NCI NIH HHS / CA / U01 CA111275
  • [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 / ESRP1 protein, human; 0 / Membrane Transport Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA-Binding Proteins; 0 / SLC45a3 protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 2.7.11.1 / Proto-Oncogene Proteins c-raf
  • [Other-IDs] NLM/ NIHMS212353; NLM/ PMC2903732
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93. Ohashi K, Kiura K, Takigawa N, Mizushima T, Ino H, Tabata M, Ueoka H, Tanimoto M: Successful treatment of a patient with gastric and duodenal metastases from large cell carcinoma of the lung with carboplatin and gemcitabine. Anticancer Res; 2006 Nov-Dec;26(6C):4695-6
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  • [Title] Successful treatment of a patient with gastric and duodenal metastases from large cell carcinoma of the lung with carboplatin and gemcitabine.
  • A 62-year-old man with large cell carcinoma of the lung underwent a right upper lobectomy and four months later demonstrated a relapse in the stomach and duodenum.
  • Although the prognosis for patients with gastrointestinal metastases from lung cancer tends to be extremely poor, treatment with chemotherapy and a metastasectomy have resulted in this patient, achieving a long survival.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Large Cell / drug therapy. Duodenal Neoplasms / drug therapy. Lung Neoplasms / pathology. Stomach Neoplasms / drug therapy

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  • (PMID = 17214328.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; BG3F62OND5 / Carboplatin
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94. Che GW, Zhou QH, Zhu W, Wang YP, Qin Y, Liu LX, Chen XH, Sun YL, Sun ZF: [Molecular mechanism of reversing metastatic phenotype in human high-metastatic large cell lung cancer cell line L9981 by nm23-H1]. Ai Zheng; 2005 Mar;24(3):278-84
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  • [Title] [Molecular mechanism of reversing metastatic phenotype in human high-metastatic large cell lung cancer cell line L9981 by nm23-H1].
  • But the molecular mechanism of nm23-H1 in inhibiting or reversing metastasis of lung cancer is unclear.
  • This study was to explore the molecular mechanism of nm23-H1 in reversing metastasis phenotype of lung cancer.
  • METHODS: nm23-H1 gene and pLXSN were separately transfected into human lung cancer cell line L9981.
  • Proliferation of L9981, L9981-pLXSN, and L9981-nm23-H1 cells was detected by MTT assay, cell invasive ability was detected by modified Boyden chamber.
  • Tumorigenesis and experimental lung metastasis were determined in vivo. mRNA and protein levels of beta-catenin, E-Cadherin, CD44S, CD44V6, matrix metalloproteinase-2 (MMP-2), tissue inhibitor of metalloproteinase-1 (TIMP-1), and vascular endothelial growth factor (VEGF) were detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot.
  • RESULTS: (1)Cell proliferation, clone formation, and invasive ability were significantly lower in L9981-nm23-H1 cells than in L9981 cells [(19.5+/-2.9)% vs. 100%, 10.3+/-0.7 vs. 21.7+/-1.3, 31.0+/-3.0 vs. 151.0+/-6.3, P<0.01]. (2) The inhibitory rate of tumorigenesis of nude mice was significantly higher in L8891-nm23-H1 group than in L9981 group (85.6% vs. 0%, P<0.001)u the lung metastatic rate was significantly lower in L9981-nm23-H1 group than in L9981 group (0% vs. 100%, P<0.001). (3)nm23-H1 up-regulated mRNA and protein levels of beta-catenin, E-Cadherin, and TIMP-1, and down-regulated levels of MMP-2, CD44V6, and VEGF (P<0.01). (4) nm23-H1 up-regulated mRNA level of CD44s, protein level of CD44s didn't change (P>0.05).
  • CONCLUSION: nm23-H1 gene can reverse malignant and metastatic phenotype of L9981 cells through regulating the expressions of lung cancer metastasis-related genes.
  • [MeSH-major] Carcinoma, Large Cell / secondary. Lung Neoplasms / pathology. Neoplasm Metastasis. Nucleoside-Diphosphate Kinase / biosynthesis
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation. Gene Expression Regulation, Neoplastic. Humans. Male. Mice. Mice, Inbred BALB C. Mice, Nude. NM23 Nucleoside Diphosphate Kinases. Neoplasm Invasiveness. Neoplasm Transplantation. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Transfection

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  • (PMID = 15757527.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / NM23 Nucleoside Diphosphate Kinases; 0 / RNA, Messenger; EC 2.7.4.6 / NME1 protein, human; EC 2.7.4.6 / Nme1 protein, mouse; EC 2.7.4.6 / Nucleoside-Diphosphate Kinase
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95. 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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96. 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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97. 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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98. 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
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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


99. Ausín P, Gómez-Caro A, Rojo RP, Moradiellos FJ, Díaz-Hellín V, de Nicolás JL: [Spontaneous hemothorax caused by lung cancer]. Arch Bronconeumol; 2005 Jul;41(7):400-1
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Spontaneous hemothorax caused by lung cancer].
  • [Transliterated title] Hemotórax espontáneo por carcinoma broncogénico.
  • We describe the case of a 26-year-old man with spontaneous hemothorax secondary to large-cell carcinoma of the lung, with liver and bone metastases.
  • [MeSH-major] Carcinoma, Bronchogenic / complications. Hemothorax / etiology. Lung Neoplasms / complications

  • Genetic Alliance. consumer health - Lung Cancer.
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  • (PMID = 16029735.001).
  • [ISSN] 0300-2896
  • [Journal-full-title] Archivos de bronconeumología
  • [ISO-abbreviation] Arch. Bronconeumol.
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
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100. 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
Hazardous Substances Data Bank. SODIUM .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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  • MedlinePlus Health Information. consumer health - Lung Cancer.
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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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