[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 221
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
COS Scholar Universe. author profiles.

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

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Cancer Res. 2005 Oct;3(10):585-96 [16254192.001]
  • [Cites] Oncogene. 2005 May 12;24(21):3427-35 [15735694.001]
  • [Cites] J Pathol. 2006 Jun;209(2):206-12 [16521118.001]
  • [Cites] Cancer Res. 2006 Dec 15;66(24):11613-22 [17178855.001]
  • [Cites] Cancer Res. 2007 May 1;67(9):3998-4004 [17483309.001]
  • [Cites] Mol Diagn Ther. 2007;11(3):183-92 [17570740.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Apr 11;97(8):4256-61 [10759549.001]
  • [Cites] Mol Cell Biol. 2000 Aug;20(15):5490-502 [10891489.001]
  • [Cites] Cancer Res. 2000 Aug 1;60(15):4256-61 [10945639.001]
  • [Cites] Clin Cancer Res. 2000 Oct;6(10):3944-8 [11051242.001]
  • [Cites] Mol Cell Biol. 2001 Jan;21(2):575-94 [11134344.001]
  • [Cites] Oncogene. 2000 Dec 27;19(56):6642-50 [11426650.001]
  • [Cites] Gene. 2001 Oct 17;277(1-2):63-81 [11602345.001]
  • [Cites] Nat Rev Cancer. 2002 Mar;2(3):161-74 [11990853.001]
  • [Cites] Breast Cancer Res Treat. 2002 Feb;71(3):181-91 [12002338.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):49-52 [12086887.001]
  • [Cites] Cancer Res. 2004 May 15;64(10):3371-5 [15150086.001]
  • [Cites] Prostate. 2004 Jul 1;60(2):160-7 [15162382.001]
  • [Cites] Nature. 2004 Oct 7;431(7009):707-12 [15361885.001]
  • [Cites] J Natl Cancer Inst. 1977 Jul;59(1):221-6 [327080.001]
  • [Cites] Anticancer Res. 1981;1(6):317-22 [6178358.001]
  • [Cites] FEBS Lett. 1983 Feb 21;152(2):163-7 [6297996.001]
  • [Cites] Nat Rev Cancer. 2007 Dec;7(12):899-910 [18004397.001]
  • [Cites] J Pathol. 2008 Feb;214(3):283-93 [18095256.001]
  • [Cites] Nat Genet. 2008 May;40(5):499-507 [18443585.001]
  • [Cites] Cancer Res. 2008 Dec 15;68(24):10121-7 [19074878.001]
  • [Cites] Nat Genet. 2009 May;41(5):518-20 [19330028.001]
  • [Cites] Mod Pathol. 2010 Jan;23(1):98-104 [19820691.001]
  • [Cites] Cancer Res. 1985 Mar;45(3):1187-97 [2578876.001]
  • [Cites] Cancer Res. 1985 Jun;45(6):2913-23 [2985257.001]
  • [Cites] Cancer Res. 1986 Feb;46(2):798-806 [3940644.001]
  • [Cites] J Biol Chem. 1990 Jul 5;265(19):11077-82 [2162831.001]
  • [Cites] Biochim Biophys Acta. 1990 Jul 30;1049(3):231-43 [2200521.001]
  • [Cites] Cancer Res. 1990 Sep 1;50(17):5481-7 [2386953.001]
  • [Cites] J Biol Chem. 1991 Oct 25;266(30):19945-52 [1939057.001]
  • [Cites] Genomics. 1992 Mar;12(3):503-9 [1559701.001]
  • [Cites] Chest. 1992 Dec;102(6):1808-14 [1446493.001]
  • [Cites] Nucleic Acids Res. 1993 Sep 11;21(18):4259-67 [8414980.001]
  • [Cites] Anticancer Res. 1994 Jan-Feb;14(1B):261-7 [8166465.001]
  • [Cites] J Eukaryot Microbiol. 1996 Jan-Feb;43(1):34-43 [8563708.001]
  • [Cites] J Biol Chem. 1998 Jan 9;273(2):1216-22 [9422789.001]
  • [Cites] Clin Cancer Res. 1996 Apr;2(4):623-33 [9816212.001]
  • [Cites] Cancer Res. 1998 Dec 15;58(24):5690-4 [9865724.001]
  • [Cites] Mol Cell Biol. 1999 Aug;19(8):5237-46 [10409715.001]
  • [Cites] Oncogene. 2004 Nov 4;23(52):8557-62 [15378028.001]
  • [Cites] Pancreas. 2005 Mar;30(2):158-67 [15714138.001]
  • [Cites] Nat Rev Cancer. 2006 Mar;6(3):227-39 [16498445.001]
  • (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
  •  go-up   go-down


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
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Implications of ALK (anaplastic lymphoma kinase) in oncohematology].
  • [Transliterated title] Implications d'ALK (anaplastic lymphoma kinase) en oncohématologie.
  • The anaplastic lymphoma kinase gene (ALK) code for a receptor tyrosine-kinase.
  • The fusion proteins from the ALK gene have been identified in oncohaematology malignancies including ALK positive anaplastic lymphoma large cell and non small cells lung cancer with EML4-ALK fusion gene.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / enzymology. Lung Neoplasms / enzymology. Lymphoma, Large-Cell, Anaplastic / enzymology. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


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
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] 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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


Advertisement
4. Califano L, Sanguedolce F, Staibano S, Pannone G, Tortorella S, Serpico R, Lo Muzio L, Bufo P: Large oral soft tissue metastasis from anaplastic carcinoma of the lung mimicking a primitive malignancy: case report and brief review of the literature. Minerva Stomatol; 2008 Sep;57(9):447-51
MedlinePlus Health Information. consumer health - Oral Cancer.

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

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


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
MedlinePlus Health Information. consumer health - Thymus Cancer.

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

  • MedlinePlus Health Information. consumer health - Carcinoid Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


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
The Lens. Cited by Patents in .

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

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. FLUOROURACIL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


7. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


8. 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
Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .

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

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


9. 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
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] [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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


10. 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
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] 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

  • MedlinePlus Health Information. consumer health - Hives.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


11. 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
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] [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

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Gallbladder Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


12. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


13. 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
Genetic Alliance. consumer health - Lung Cancer.

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

  • Genetic Alliance. consumer health - Lambert Eaton myasthenic syndrome.
  • Genetic Alliance. consumer health - Lambert syndrome.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


14. 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.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


15. Schmid I, Fliegner M: [Digital ischemia of a patient with undifferentiated large cell lung cancer]. Internist (Berl); 2008 Mar;49(3):346-8
MedlinePlus Health Information. consumer health - Raynaud's Disease.

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

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Radiologe. 1996 Sep;36(9):692-9 [8999444.001]
  • [Cites] Clin Dermatol. 1993 Jan-Mar;11(1):11-3 [8339184.001]
  • [Cites] Am J Med. 1995 Dec;99(6):662-71 [7503090.001]
  • [Cites] Br J Dermatol. 1996 Dec;135(6):995-8 [8977727.001]
  • [Cites] Am J Med. 1992 May;92(5):571-2 [1580306.001]
  • [Cites] J Am Acad Dermatol. 2002 Jul;47(1):47-52 [12077580.001]
  • [Cites] Scand J Rheumatol. 2004;33(4):253-6 [15370722.001]
  • [Cites] Curr Opin Rheumatol. 1992 Feb;4(1):90-3 [1543670.001]
  • [Cites] Mund Kiefer Gesichtschir. 2002 Sep;6(5):331-5 [12448236.001]
  • [Cites] Dtsch Med Wochenschr. 2006 May 26;131(21):1223-7 [16721713.001]
  • [Cites] Dtsch Med Wochenschr. 1994 Aug 26;119(34-35):1162-6 [8076504.001]
  • (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
  •  go-up   go-down


16. Rekhtman N: Neuroendocrine tumors of the lung: an update. Arch Pathol Lab Med; 2010 Nov;134(11):1628-38
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] 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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


17. Ricciardelli L, Rapicano G, Pinto A, Napolitano G, Feleppa C, Martino G, Martino A: [Small bowel intussusception caused by metastasis from anaplastic thyroid carcinoma: case report and literature review]. Ann Ital Chir; 2006 Jan-Feb;77(1):63-7
MedlinePlus Health Information. consumer health - Thyroid Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Small bowel intussusception caused by metastasis from anaplastic thyroid carcinoma: case report and literature review].
  • [Transliterated title] Invaginazione ileo-ileale da metastasi di carcinoma anaplastico tiroideo. Caso clinico e revisione della letteratura.
  • Symptomatic involvement of the small bowel by metastasis from an extra-abdominal primary malignancy is rare, most commonly resulting from malignant melanoma and lung cancer; very rarely is small bowel involvement as first metastatic site.
  • The Authors report a case of anaplastic thyroid carcinoma with lung metastasis, brain metastasis and an isolated metastasis to the small bowel leading intestinal obstruction due to small bowel intussusception.
  • The Authors review the international literature about frequency, etiopathogenesis, clinical and diagnostic features and therapy of small bowel metastasis by extra-abdominal malignancies, especially by primary anaplastic thyroid carcinoma.
  • Small bowel metastasis from extra-abdominal malignancies are very unusual, especially from anaplastic thyroid carcinoma, and the etiopathogenesis is still unknown.
  • Clinical findings are typical for abdominal urgency, especially by small bowel obstruction from anaplastic thyroid carcinoma.
  • [MeSH-major] Carcinoma / complications. Carcinoma / diagnosis. Ileal Neoplasms / complications. Ileal Neoplasms / diagnosis. Intussusception / etiology. Thyroid Neoplasms / pathology
  • [MeSH-minor] Aged. Brain Neoplasms / secondary. Female. Humans. Ileal Diseases / etiology. Lung Neoplasms / secondary. Tomography, X-Ray Computed

  • MedlinePlus Health Information. consumer health - Intestinal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16910363.001).
  • [ISSN] 0003-469X
  • [Journal-full-title] Annali italiani di chirurgia
  • [ISO-abbreviation] Ann Ital Chir
  • [Language] ita
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 37
  •  go-up   go-down


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
Hazardous Substances Data Bank. Calcitonin .

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

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


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
COS Scholar Universe. author profiles.

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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


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
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] 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.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


21. 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
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] 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

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


22. Majima T, Komatsu Y, Doi K, Shigemoto M, Takagi C, Fukao A, Kojima M, Tamaki H, Ito J, Nakao K: Anaplastic thyroid carcinoma associated with Graves' disease. Endocr J; 2005 Oct;52(5):551-7
MedlinePlus Health Information. consumer health - Thyroid Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anaplastic thyroid carcinoma associated with Graves' disease.
  • This report concerns a 79-year-old woman with coexisting anaplastic thyroid carcinoma (ATC) and Graves' disease (GD).
  • These findings led to a diagnosis of GD.
  • On the other hand, the thyroid nodule could not be definitely diagnosed even after fine needle aspiration biopsy (FNAB) which produced findings suggestive of both papillary thyroid carcinoma and ATC.
  • Regional lymph node metastases as well as multiple lung metastases, which could not be found at the initial visit, had been already developed by that time.
  • Our case is pathophysiologically interesting because it suggests that GD or thyroid-stimulating antibodies (TSAb) may stimulate malignant transformation of differentiated carcinoma.
  • [MeSH-major] Carcinoma / complications. Graves Disease / complications. Thyroid Neoplasms / complications

  • Genetic Alliance. consumer health - Graves' Disease.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16284432.001).
  • [ISSN] 0918-8959
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


23. Ogawa M, Hori H, Hirayama M, Kobayashi M, Shiraishi T, Watanabe Y, Komada Y: Anaplastic transformation from papillary thyroid carcinoma with increased serum CA19-9. Pediatr Blood Cancer; 2005 Jul;45(1):64-7
MedlinePlus Health Information. consumer health - Thyroid Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anaplastic transformation from papillary thyroid carcinoma with increased serum CA19-9.
  • A 24-year-old woman presented with anaplastic transformation from papillary thyroid carcinoma with increased serum CA19-9.
  • The patient had been diagnosed as having papillary thyroid carcinoma with lung metastasis at 11 years of age.
  • Elevated serum CA19-9 was detected in the terminal stage, and anaplastic transformation was confirmed by post-mortem examination.
  • Although there are few clinical reports suggesting a prognostic indicator for anaplastic thyroid carcinoma, CA19-9 may be a useful serum marker for this tumor.
  • [MeSH-major] CA-19-9 Antigen / blood. Carcinoma / blood. Carcinoma, Papillary / pathology. Thyroid Neoplasms / blood. Thyroid Neoplasms / pathology
  • [MeSH-minor] Adult. Anaplasia / blood. Cell Transformation, Neoplastic. Fatal Outcome. Female. Humans

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Pediatr Blood Cancer. 2006 Aug;47(2):229-30 [16526055.001]
  • (PMID = 15770642.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CA-19-9 Antigen
  •  go-up   go-down


24. Mehta H, Bahuva R, Sadikot RT: Lung cancer mimicking as pregnancy with pneumonia. Lung Cancer; 2008 Sep;61(3):416-9
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] 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

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Pregnancy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


25. Martin AC, Friedlander M, Kiernan MC: Paraneoplastic mononeuritis multiplex in non-small-cell lung carcinoma. J Clin Neurosci; 2006 Jun;13(5):595-8
COS Scholar Universe. author profiles.

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

  • Genetic Alliance. consumer health - Mononeuritis multiplex.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


26. 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
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] 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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


27. 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
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] 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 / pathology. Echinococcosis / radiography. Echinococcosis / surgery. Echinococcus granulosus. Humans. Male. Prognosis. Tomography, X-Ray Computed

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


28. Ito Y, Higashiyama T, Hirokawa M, Fukushima M, Inoue H, Yabuta T, Tomoda C, Uruno T, Kihara M, Takamura Y, Miya A, Kobayashi K, Matsuzuka F, Miyauchi A: Prognosis of patients with papillary carcinoma showing anaplastic transformation in regional lymph nodes that were curatively resected. Endocr J; 2008 Dec;55(6):985-9
MedlinePlus Health Information. consumer health - Thyroid Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognosis of patients with papillary carcinoma showing anaplastic transformation in regional lymph nodes that were curatively resected.
  • Anaplastic carcinoma arises from differentiated carcinoma and generally shows a dire prognosis.
  • Anaplastic transformation may occur not only in primary tumors but also in metastatic lymph nodes.
  • We encountered 5 cases of papillary carcinoma showing anaplastic transformation in lymph nodes that were curatively resected.
  • Two of these patients showed anaplastic transformation at the initial surgery and the remaining 3 showed anaplastic transformation after repeated recurrence to the lymph nodes.
  • After resection of anaplastic lesions of the nodes, 2 patients underwent radiation therapy, whereas the remaining 3 did not receive any adjuvant therapy.
  • One patient died of rapid growth of lung metastasis 5 months after the resection.
  • One patient died of carcinoma 63 months after surgery.
  • It is therefore suggested that long-term survival can be expected for patients with differentiated carcinoma showing anaplastic transformation in the lymph node if the lesions can be curatively resected.
  • [MeSH-major] Carcinoma / secondary. Carcinoma, Papillary / diagnosis. Lymph Nodes / surgery. Thyroid Neoplasms / diagnosis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18612180.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


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
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] 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

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lymphoma.
  • MedlinePlus Health Information. consumer health - Neuroblastoma.
  • COS Scholar Universe. author profiles.
  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


30. 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
COS Scholar Universe. author profiles.

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

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


31. 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
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] 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


32. Al-Qsous W, Miller ID: Anaplastic transformation in lung metastases of differentiated papillary thyroid carcinoma: an autopsy case report and review of the literature. Ann Diagn Pathol; 2010 Feb;14(1):41-3
MedlinePlus Health Information. consumer health - Thyroid Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anaplastic transformation in lung metastases of differentiated papillary thyroid carcinoma: an autopsy case report and review of the literature.
  • Anaplastic transformation of papillary thyroid carcinoma is a rare condition and is associated with an aggressive behavior.
  • We report a case of an 83-year-old man who, 10 years after being treated for a conventional papillary thyroid carcinoma, presented with widespread metastases in his lungs.
  • At autopsy, he was found to have extensive metastatic deposits in both lungs, which histologically and immunohistochemically were consistent with papillary thyroid carcinoma.
  • An unusual finding was the presence of solid pleomorphic foci within tumor deposits, consistent with anaplastic transformation.
  • [MeSH-major] Carcinoma / pathology. Carcinoma, Papillary / secondary. Cell Transformation, Neoplastic / pathology. Lung Neoplasms / secondary. Thyroid Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20123456.001).
  • [ISSN] 1532-8198
  • [Journal-full-title] Annals of diagnostic pathology
  • [ISO-abbreviation] Ann Diagn Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 12
  •  go-up   go-down


33. Kwak EL, Bang YJ, Camidge DR, Shaw AT, Solomon B, Maki RG, Ou SH, Dezube BJ, Jänne PA, Costa DB, Varella-Garcia M, Kim WH, Lynch TJ, Fidias P, Stubbs H, Engelman JA, Sequist LV, Tan W, Gandhi L, Mino-Kenudson M, Wei GC, Shreeve SM, Ratain MJ, Settleman J, Christensen JG, Haber DA, Wilner K, Salgia R, Shapiro GI, Clark JW, Iafrate AJ: Anaplastic lymphoma kinase inhibition in non-small-cell lung cancer. N Engl J Med; 2010 Oct 28;363(18):1693-703
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 inhibition in non-small-cell lung cancer.
  • BACKGROUND: Oncogenic fusion genes consisting of EML4 and anaplastic lymphoma kinase (ALK) are present in a subgroup of non-small-cell lung cancers, representing 2 to 7% of such tumors.
  • METHODS: After screening tumor samples from approximately 1500 patients with non-small-cell lung cancer for the presence of ALK rearrangements, we identified 82 patients with advanced ALK-positive disease who were eligible for the clinical trial.
  • CONCLUSIONS: The inhibition of ALK in lung tumors with the ALK rearrangement resulted in tumor shrinkage or stable disease in most patients. (Funded by Pfizer and others; ClinicalTrials.gov number, NCT00585195.).
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrazoles / therapeutic use. Pyridines / therapeutic use
  • [MeSH-minor] Administration, Oral. Adult. Aged. Cell Cycle Proteins / genetics. Disease Progression. Female. Humans. In Situ Hybridization, Fluorescence. Kaplan-Meier Estimate. Male. Microtubule-Associated Proteins / genetics. Middle Aged. Mutation. Oncogene Proteins, Fusion / genetics. Proto-Oncogene Proteins c-met / antagonists & inhibitors. Receptor Protein-Tyrosine Kinases. Receptors, Growth Factor / antagonists & inhibitors. Serine Endopeptidases / genetics

  • Genetic Alliance. consumer health - Anaplastic Small Cell Lymphoma.
  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cell Mol Life Sci. 2004 Dec;61(23):2939-53 [15583856.001]
  • [Cites] Am J Clin Oncol. 1982 Dec;5(6):649-55 [7165009.001]
  • [Cites] Br J Cancer. 2006 Oct 23;95(8):998-1004 [17047648.001]
  • [Cites] Nature. 2007 Aug 2;448(7153):561-6 [17625570.001]
  • [Cites] Mol Cancer Ther. 2007 Dec;6(12 Pt 1):3314-22 [18089725.001]
  • [Cites] Neoplasia. 2008 Mar;10(3):298-302 [18320074.001]
  • [Cites] J Thorac Oncol. 2008 Apr;3(4):430-40 [18379366.001]
  • [Cites] Cancer Res. 2008 May 1;68(9):3389-95 [18451166.001]
  • [Cites] J Clin Oncol. 2008 May 20;26(15):2442-9 [18458038.001]
  • [Cites] Cancer Res. 2008 Jul 1;68(13):4971-6 [18593892.001]
  • [Cites] Clin Cancer Res. 2008 Jul 1;14(13):4275-83 [18594010.001]
  • [Cites] Nature. 2008 Oct 16;455(7215):930-5 [18724359.001]
  • [Cites] Nature. 2008 Oct 16;455(7215):975-8 [18923525.001]
  • [Cites] Clin Cancer Res. 2008 Oct 15;14(20):6618-24 [18927303.001]
  • [Cites] Cancer Sci. 2008 Dec;99(12):2349-55 [19032370.001]
  • [Cites] J Clin Oncol. 2009 Apr 10;27(11):1836-43 [19273711.001]
  • [Cites] Cancer. 2009 Apr 15;115(8):1723-33 [19170230.001]
  • [Cites] Clin Cancer Res. 2009 May 1;15(9):3143-9 [19383809.001]
  • [Cites] Clin Cancer Res. 2009 Aug 15;15(16):5216-23 [19671850.001]
  • [Cites] N Engl J Med. 2009 Sep 3;361(10):947-57 [19692680.001]
  • [Cites] J Clin Oncol. 2009 Sep 10;27(26):4247-53 [19667264.001]
  • [Cites] Clin Cancer Res. 2010 Mar 1;16(5):1561-71 [20179225.001]
  • [Cites] J Clin Oncol. 2006 Jul 20;24(21):3340-6 [16785471.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Sep 7;101(36):13306-11 [15329413.001]
  • [Cites] Science. 2004 Jun 4;304(5676):1497-500 [15118125.001]
  • [Cites] N Engl J Med. 2004 May 20;350(21):2129-39 [15118073.001]
  • [Cites] J Clin Oncol. 2002 Sep 1;20(17):3691-702 [12202671.001]
  • [CommentIn] Expert Opin Ther Targets. 2011 Mar;15(3):351-3 [21208134.001]
  • [CommentIn] N Engl J Med. 2011 Feb 24;364(8):776-7; author reply 778 [21345113.001]
  • [CommentIn] N Engl J Med. 2010 Oct 28;363(18):1760-2 [20979477.001]
  • [CommentIn] Nat Rev Cancer. 2010 Dec;10(12):817 [21155181.001]
  • [ErratumIn] N Engl J Med. 2011 Feb 10;364(6):588
  • (PMID = 20979469.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00585195
  • [Grant] United States / NCI NIH HHS / CA / P20 CA090578; United States / NCI NIH HHS / CA / P20 CA090578-04; United States / NCI NIH HHS / CA / P50 CA058187; United States / NCI NIH HHS / CA / CA58187; United States / NCI NIH HHS / CA / CA090578; United States / NCI NIH HHS / CA / P30 CA046934-21; United States / NCI NIH HHS / CA / R01 CA136851-02; United States / NCI NIH HHS / CA / P30 CA006516-45; United States / NCI NIH HHS / CA / R01CA136851; United States / NCI NIH HHS / CA / P50 CA058187-13; United States / NCI NIH HHS / CA / CA46934; United States / NCI NIH HHS / CA / P30 CA046934; United States / NCI NIH HHS / CA / P01 CA047179-18; United States / NCI NIH HHS / CA / P50 CA090578; United States / NCI NIH HHS / CA / CA47179; United States / NCI NIH HHS / CA / P30 CA062203; United States / NCI NIH HHS / CA / CA06516; United States / NCI NIH HHS / CA / P30 CA006516; United States / NCI NIH HHS / CA / R01 CA136851; United States / NCI NIH HHS / CA / P01 CA047179
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Microtubule-Associated Proteins; 0 / Oncogene Proteins, Fusion; 0 / Protein Kinase Inhibitors; 0 / Pyrazoles; 0 / Pyridines; 0 / Receptors, Growth Factor; 53AH36668S / crizotinib; EC 2.7.10.1 / MET protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; 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; EC 3.4.21.- / EML4 protein, human; EC 3.4.21.- / Serine Endopeptidases
  • [Other-IDs] NLM/ NIHMS249183; NLM/ PMC3014291
  •  go-up   go-down


34. Bogsrud TV, Karantanis D, Nathan MA, Mullan BP, Wiseman GA, Kasperbauer JL, Reading CC, Hay ID, Lowe VJ: 18F-FDG PET in the management of patients with anaplastic thyroid carcinoma. Thyroid; 2008 Jul;18(7):713-9
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 18F-FDG PET in the management of patients with anaplastic thyroid carcinoma.
  • BACKGROUND: Anaplastic thyroid carcinoma (ATC) is one of the most aggressive solid tumors in humans.
  • True-positive PET findings were seen for all primary tumors, in all nine patients with lymph node metastases, in five out of eight patients with lung metastases, and in two patients with distant metastases other than lung metastases.
  • [MeSH-major] Carcinoma / radiotherapy. Fluorodeoxyglucose F18 / pharmacokinetics. Positron-Emission Tomography / methods. Thyroid Neoplasms / radiotherapy

  • MedlinePlus Health Information. consumer health - Thyroid Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18630999.001).
  • [ISSN] 1050-7256
  • [Journal-full-title] Thyroid : official journal of the American Thyroid Association
  • [ISO-abbreviation] Thyroid
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
  •  go-up   go-down


35. Kohli PS, Soni NK: Nasal tip metastasis: an unusual site and mode of spread in anaplastic thyroid carcinoma. Indian J Otolaryngol Head Neck Surg; 2008 Sep;60(3):269-70

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nasal tip metastasis: an unusual site and mode of spread in anaplastic thyroid carcinoma.
  • Anaplastic thyroid carcinoma (ATC) is the most aggressive and lethal form of thyroid malignancy which is difficult to treat.
  • At the time of diagnosis, majority of patients have distant metastases most commonly in lung, bone, and liver.
  • Implantation of malignant cells on nasal tip is also unknown.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Am Acad Dermatol. 1990 Jan;22(1):19-26 [2298962.001]
  • [Cites] Surg Gynecol Obstet. 1971 Oct;133(4):673-7 [4938079.001]
  • [Cites] Otolaryngol Head Neck Surg. 1997 Jul;117(1):139 [9230343.001]
  • [Cites] Can J Surg. 2002 Jun;45(3):224-5 [12067183.001]
  • (PMID = 23120560.001).
  • [ISSN] 2231-3796
  • [Journal-full-title] Indian journal of otolaryngology and head and neck surgery : official publication of the Association of Otolaryngologists of India
  • [ISO-abbreviation] Indian J Otolaryngol Head Neck Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC3450640
  • [Keywords] NOTNLM ; Implantation metastasis / Nasal metastasis / Thyroid carcinoma
  •  go-up   go-down


36. 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
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] [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

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


37. 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
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] [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

  • Genetic Alliance. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


38. 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
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 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


39. Boland JM, Erdogan S, Vasmatzis G, Yang P, Tillmans LS, Johnson MR, Wang X, Peterson LM, Halling KC, Oliveira AM, Aubry MC, Yi ES: Anaplastic lymphoma kinase immunoreactivity correlates with ALK gene rearrangement and transcriptional up-regulation in non-small cell lung carcinomas. Hum Pathol; 2009 Aug;40(8):1152-8
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anaplastic lymphoma kinase immunoreactivity correlates with ALK gene rearrangement and transcriptional up-regulation in non-small cell lung carcinomas.
  • Recently, the fusion gene EML4-ALK was identified in non-small cell lung carcinoma, which could be a potential therapeutic target.
  • We investigated the prevalence of anaplastic lymphoma kinase protein expression in these tumors by immunohistochemistry and correlated the results with data from ALK molecular studies.
  • Immunohistochemistry was also performed on an independent cohort consisting of 150 adenocarcinomas and 150 squamous cell carcinomas to evaluate the utility of anaplastic lymphoma kinase immunostaining as a screening tool.
  • Florescence in situ hybridization for the ALK locus and reverse transcriptase-polymerase chain reaction for EML4-ALK were performed on tumors positive for anaplastic lymphoma kinase by immunohistochemistry.
  • These 2 cases were positive for anaplastic lymphoma kinase by immunohistochemistry, whereas the remaining 33 cases were completely negative.
  • In the independent cohort, anaplastic lymphoma kinase immunostaining was positive in 1 of 150 squamous cell carcinomas and in 3 of 150 adenocarcinomas.
  • The 6 cases positive for anaplastic lymphoma kinase by immunohistochemistry showed evidence of ALK locus rearrangement by florescence in situ hybridization but were negative for EGFR and KRAS mutation.
  • In conclusion, anaplastic lymphoma kinase immunoreactivity in non-small cell lung carcinomas was associated with transcriptional up-regulation, ALK locus rearrangement, and the presence of EML4-ALK fusion transcript.
  • Anaplastic lymphoma kinase immunohistochemistry may have utility as a screening tool or as a surrogate marker for the molecular techniques to detect the EML4-ALK fusion gene in these tumors.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Gene Expression Regulation, Neoplastic. Gene Rearrangement. Lung Neoplasms / genetics. Protein-Tyrosine Kinases / genetics. Up-Regulation / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Aged. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / pathology. Cohort Studies. Female. Gene Expression Profiling. Humans. In Situ Hybridization, Fluorescence. Male. Oncogene Proteins, Fusion / genetics. Receptor Protein-Tyrosine Kinases. Sequence Analysis, DNA. Transcription, Genetic

  • Genetic Alliance. consumer health - Anaplastic Small Cell Lymphoma.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Hum Pathol. 2010 Apr;41(4):614-5; author reply 615-616 [20163822.001]
  • (PMID = 19386350.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / EML4-ALK fusion protein, human; 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  •  go-up   go-down


40. Zhou ZY, Sun RC, Yang GY, Yang SD, Yu MH, Liang JB: Giant-cell anaplastic carcinoma with osteoclastic giant cells of the chest cavity: a distinctive form of thymic carcinoma? Int J Surg Pathol; 2010 Oct;18(5):363-8
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Giant-cell anaplastic carcinoma with osteoclastic giant cells of the chest cavity: a distinctive form of thymic carcinoma?
  • Here, the authors describe a case of giant-cell anaplastic carcinoma with osteoclastic giant cells of the chest cavity-which could be a distinctive form of thymic carcinoma-which expressed CD5 and CD45.
  • Palliative resection of a mediastinal tumor was performed.
  • During the operation, it was found that the mass occupied most of the chest invading the chest wall, aorta, vena cava, and lung tissue.
  • The tumor was composed of large areas of necrosis and anaplastic neoplastic giant cells with high mitotic activity, and osteoclast-like cells; there was marked inflammatory cell infiltration.
  • The anaplastic neoplastic giant cells were immunoreactive for CKpan, CD5, CD45, VIM, and p53.
  • Approximately 50% to 60% of the tumor cells showed immunoreactivity for Ki-67.
  • In situ hybridization for Epstein-Barr virus-encoded RNA was negative for tumor cells and nonneoplastic osteoclastic giant cells.
  • Because this tumor is very rare, extensive clinical, radiological, and morphological examinations as well as immunohistochemical studies are essential to make the diagnosis.
  • [MeSH-major] Carcinoma / pathology. Osteoclasts / pathology. Thoracic Cavity / pathology. Thoracic Neoplasms / pathology. Thymus Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Thymus Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20667924.001).
  • [ISSN] 1940-2465
  • [Journal-full-title] International journal of surgical pathology
  • [ISO-abbreviation] Int. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD5; 0 / Biomarkers, Tumor; EC 3.1.3.48 / Antigens, CD45; EC 3.1.3.48 / PTPRC protein, human
  •  go-up   go-down


41. Lee DH, Lee GK, Kong SY, Kook MC, Yang SK, Park SY, Park SH, Keam B, Park DJ, Cho BY, Kim SW, Chung KW, Lee ES, Kim SW: Epidermal growth factor receptor status in anaplastic thyroid carcinoma. J Clin Pathol; 2007 Aug;60(8):881-4
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] Epidermal growth factor receptor status in anaplastic thyroid carcinoma.
  • BACKGROUND: The epidermal growth factor receptor (EGFR) has been reported to be overexpressed in anaplastic thyroid carcinoma (ATC).
  • In vitro studies have shown that EGFR tyrosine kinase inhibitors (TKIs) greatly inhibit cellular growth and induced apoptosis in the ATC cell lines, while somatic mutations in the tyrosine kinase domain or an increased gene copy number are associated with increased sensitivity to TKIs in non-small cell lung cancer.
  • High polysomy was observed in all 10 cases with giant cell subtype, but in only 4/11 (36.3%) with squamoid and 0/2 with spindle cell sarcomatoid subtype.
  • CONCLUSION: Despite the low incidence of somatic EGFR gene mutation and amplification in the study samples, in view of the fact that high polysomy was often identified by FISH, as well as the current lack of therapeutic options, EGFR TKIs are worth investigating for treating the patients with ATC who have at least giant cell subtype.

  • MedlinePlus Health Information. consumer health - Thyroid Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Pathol. 2006 Aug;209(4):445-53 [16739104.001]
  • [Cites] Surgery. 2001 Dec;130(6):1028-34 [11742333.001]
  • [Cites] CA Cancer J Clin. 2003 Jan-Feb;53(1):5-26 [12568441.001]
  • [Cites] J Clin Oncol. 2003 Jun 15;21(12):2237-46 [12748244.001]
  • [Cites] J Mol Diagn. 2003 Aug;5(3):155-9 [12876205.001]
  • [Cites] J Clin Oncol. 2003 Oct 15;21(20):3798-807 [12953099.001]
  • [Cites] JAMA. 2003 Oct 22;290(16):2149-58 [14570950.001]
  • [Cites] Annu Rev Pharmacol Toxicol. 2004;44:195-217 [14744244.001]
  • [Cites] Clin Gastroenterol Hepatol. 2003 Nov;1(6):438-45 [15017643.001]
  • [Cites] J Neuropathol Exp Neurol. 2004 Apr;63(4):314-22 [15099021.001]
  • [Cites] N Engl J Med. 2004 May 20;350(21):2129-39 [15118073.001]
  • [Cites] Diagn Mol Pathol. 2004 Mar;13(1):1-8 [15163002.001]
  • [Cites] Science. 2004 Jun 4;304(5676):1497-500 [15118125.001]
  • [Cites] Mod Pathol. 2004 Aug;17(8):895-904 [15143334.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Sep 7;101(36):13306-11 [15329413.001]
  • [Cites] Clin Cancer Res. 2004 Dec 15;10(24):8594-602 [15623643.001]
  • [Cites] Ann N Y Acad Sci. 2004 Dec;1030:69-77 [15659782.001]
  • [Cites] Br J Cancer. 2005 Mar 28;92(6):1110-6 [15785737.001]
  • [Cites] J Natl Cancer Inst. 2005 May 4;97(9):643-55 [15870435.001]
  • [Cites] N Engl J Med. 2005 Jul 14;353(2):123-32 [16014882.001]
  • [Cites] Mod Pathol. 2005 Aug;18(8):1027-33 [15920544.001]
  • [Cites] J Clin Oncol. 2005 Oct 1;23(28):6838-45 [15998906.001]
  • [Cites] N Engl J Med. 2005 Nov 10;353(19):2012-24 [16282176.001]
  • [ErratumIn] J Clin Pathol. 2007 Oct;60(10):1184
  • (PMID = 17079354.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Other-IDs] NLM/ PMC1994497
  •  go-up   go-down


42. Oktay MH, Smolkin MB, Williams M, Cajigas A: Metastatic anaplastic carcinoma of the thyroid mimicking squamous cell carcinoma: report of a case of a challenging cytologic diagnosis. Acta Cytol; 2006 Mar-Apr;50(2):201-4
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Metastatic anaplastic carcinoma of the thyroid mimicking squamous cell carcinoma: report of a case of a challenging cytologic diagnosis.
  • BACKGROUND: The probability of anaplastic transformation in a differentiated thyroid carcinoma (DTC) is <2%.
  • Admixture of DTC and undifferentiated carcinoma can occasionally be found in thyroidectomy specimens, or the undifferentiated tumor may develop in metastatic foci months or years after removal of the primary tumor.
  • CASE: Anaplastic transformation of a metastatic DTC was diagnosed at autopsy in a 71-year-old female.
  • At the time of her total thyroidectomy for follicular carcinoma, she already had several lung nodules, which diminished in size upon 131I treatment.
  • Five years later the patient developed a new, pleura-based lung mass.
  • Fine needle aspiration biopsy of the paraspinal mass resulted in a diagnosis of metastatic squamous cell carcinoma.
  • Histologic evaluation of the lung nodules and pleura-based mass revealed areas of follicular carcinoma intermixed with a various patterns of undifferentiated carcinoma.
  • The paraspinal and kidney mass consisted entirely of anaplastic tumor, including areas of squamoid differentiation.
  • CONCLUSION: In patients with a history of DTC who develop a rapidly growing mass elsewhere, a possibility of metastatic DTC with anaplastic transformation must be considered.
  • [MeSH-major] Carcinoma / diagnosis. Carcinoma, Squamous Cell / diagnosis. Kidney Neoplasms / secondary. Lung Neoplasms / secondary. Spinal Neoplasms / secondary. Thyroid Neoplasms / diagnosis
  • [MeSH-minor] Aged. Biopsy, Fine-Needle / methods. Diagnosis, Differential. Disease Progression. Fatal Outcome. Female. Humans. Sensitivity and Specificity


43. 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
COS Scholar Universe. author profiles.

  • [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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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 / 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
  •  go-up   go-down


44. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Clin Cancer Res. 2002 Nov;8(11):3480-6 [12429638.001]
  • [Cites] J Clin Oncol. 2005 Feb 10;23(5):953-64 [15598976.001]
  • [Cites] Clin Cancer Res. 2003 Feb;9(2):729-37 [12576442.001]
  • [Cites] Scand J Immunol. 2003 Feb;57(2):173-8 [12588664.001]
  • [Cites] J Immunol. 1984 Jan;132(1):181-6 [6228577.001]
  • [Cites] Cancer Immunol Immunother. 1985;20(2):158-66 [3849978.001]
  • [Cites] Cancer Res. 1987 Apr 15;47(8):2199-202 [3829005.001]
  • [Cites] J Biol Response Mod. 1988 Oct;7(5):483-7 [3183685.001]
  • [Cites] Chest. 1990 Oct;98(4):881-5 [2119952.001]
  • [Cites] Cancer Res. 1991 Feb 1;51(3):857-62 [1988125.001]
  • [Cites] Chest. 1991 Nov;100(5):1277-80 [1935281.001]
  • [Cites] Clin Exp Immunol. 1993 Jan;91(1):126-30 [8093433.001]
  • [Cites] J Immunother Emphasis Tumor Immunol. 1993 Jan;13(1):1-6 [8435427.001]
  • [Cites] J Leukoc Biol. 1994 Apr;55(4):437-42 [8145013.001]
  • [Cites] Cancer Res. 1994 Oct 15;54(20):5455-63 [7923179.001]
  • [Cites] Am J Respir Cell Mol Biol. 1994 Nov;11(5):631-7 [7946392.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Oct 24;92(22):10128-32 [7479739.001]
  • [Cites] J Leukoc Biol. 1996 Mar;59(3):397-402 [8604018.001]
  • [Cites] Immunology. 1996 Feb;87(2):250-8 [8698387.001]
  • [Cites] Respir Med. 1999 Sep;93(9):666-71 [10542982.001]
  • [Cites] Chest. 2000 Feb;117(2):365-73 [10669676.001]
  • [Cites] Vaccine. 2000 Jul 15;18(27):3174-84 [10856797.001]
  • [Cites] Respiration. 2000;67(3):280-6 [10867596.001]
  • [Cites] Eur J Immunol. 2000 Jun;30(6):1733-9 [10898511.001]
  • [Cites] Cytokine. 2000 Sep;12(9):1348-55 [10975994.001]
  • [Cites] Vaccine. 1996 Jun;14(9):930-8 [8843637.001]
  • [Cites] Immunology. 1997 Jul;91(3):369-74 [9301525.001]
  • [Cites] Am J Respir Cell Mol Biol. 1997 Sep;17(3):279-83 [9308913.001]
  • [Cites] Cancer Immunol Immunother. 1997 Oct;45(1):37-44 [9353425.001]
  • [Cites] Ann Oncol. 2000 Jul;11(7):815-9 [10997808.001]
  • [Cites] Jpn J Clin Oncol. 2000 Jul;30(7):295-300 [11007161.001]
  • [Cites] Folia Histochem Cytobiol. 2000;38(4):185-8 [11185724.001]
  • [Cites] Clin Exp Allergy. 2001 Apr;31(4):625-36 [11359432.001]
  • [Cites] Biol Neonate. 2001 Aug;80(2):124-32 [11509812.001]
  • [Cites] Lung Cancer. 2001 Dec;34 Suppl 2:S79-82 [11720746.001]
  • [Cites] Anticancer Res. 2001 Jul-Aug;21(4A):2609-15 [11724329.001]
  • [Cites] J Pathol. 2002 Mar;196(3):254-65 [11857487.001]
  • [Cites] Curr Mol Med. 2001 Sep;1(4):469-74 [11899091.001]
  • [Cites] Int J Cancer. 2002 Sep 20;101(3):287-92 [12209981.001]
  • [Cites] Am J Respir Crit Care Med. 2002 Nov 1;166(9):1166-96 [12403687.001]
  • [Cites] Br J Cancer. 1998 May;77(10):1696-703 [9635852.001]
  • [Cites] Histopathology. 1998 Jul;33(1):55-63 [9726050.001]
  • [Cites] Am J Physiol. 1999 Jul;277(1 Pt 1):L49-57 [10409230.001]
  • [Cites] J Lab Clin Med. 2002 Nov;140(5):320-8 [12434133.001]
  • (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
  •  go-up   go-down


45. 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.

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

  • Genetic Alliance. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


46. 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
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] 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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


47. Sato K, Waseda R, Tatsuzawa Y, Soma R, Ueda Y, Katsuda S: Papillary thyroid carcinoma with anaplastic transformation showing a rhabdoid phenotype solely in the cervical lymph node metastasis. Pathol Res Pract; 2006;202(1):55-9
MedlinePlus Health Information. consumer health - Thyroid Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Papillary thyroid carcinoma with anaplastic transformation showing a rhabdoid phenotype solely in the cervical lymph node metastasis.
  • We describe a rare case of anaplastically transformed papillary thyroid carcinoma with a rhabdoid phenotype appearing solely in a metastatic focus.
  • Examination of surgically resected specimens disclosed that the thyroid tumor was a well-differentiated papillary carcinoma (2.0 cm in diameter), and the right lateral cervical mass was an anaplastic carcinoma (2.4 cm in diameter) showing a rhabdoid phenotype with scant amounts of a papillary carcinoma component in the periphery, considered to be transformed through the metastasis of the papillary thyroid carcinoma in a cervical lymph node.
  • The rhabdoid cells had eccentric nuclei with conspicuous nucleoli and spherical hyaline cytoplasmic inclusions, which are immunoreactive for vimentin and sarcomeric actin.
  • [MeSH-major] Carcinoma, Papillary / pathology. Thyroid Neoplasms / diagnosis. Thyroid Neoplasms / pathology. Thyroid Neoplasms / surgery
  • [MeSH-minor] Aged. Biomarkers, Tumor. Follow-Up Studies. Humans. Lung Neoplasms / secondary. Lymph Nodes. Lymphatic Metastasis. Male. Rhabdoid Tumor

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16310972.001).
  • [ISSN] 0344-0338
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  •  go-up   go-down


48. 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 .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Genet Cytogenet. 2007 Jul 15;176(2):107-14 [17656252.001]
  • [Cites] Exp Hematol. 2007 Aug;35(8):1240-8 [17560012.001]
  • [Cites] Blood. 2004 Sep 1;104(5):1580-1 [15317731.001]
  • [Cites] J Cell Sci. 2004 Oct 15;117(Pt 22):5405-15 [15466886.001]
  • [Cites] Blood. 1985 Oct;66(4):848-58 [3876124.001]
  • [Cites] J Antibiot (Tokyo). 1989 Apr;42(4):571-6 [2656615.001]
  • [Cites] Eur J Biochem. 1989 Dec 22;186(3):733-40 [2558016.001]
  • [Cites] J Biol Chem. 1990 Jun 25;265(18):10765-70 [2355021.001]
  • [Cites] EMBO J. 1990 Jul;9(7):2279-87 [2357970.001]
  • [Cites] J Biol Chem. 1990 Oct 5;265(28):16721-4 [2170351.001]
  • [Cites] Biochem Biophys Res Commun. 1990 Oct 30;172(2):850-4 [1700712.001]
  • [Cites] Biochem Biophys Res Commun. 1990 Nov 30;173(1):246-51 [1701634.001]
  • [Cites] Biochem Biophys Res Commun. 1991 Oct 15;180(1):145-51 [1819274.001]
  • [Cites] Anat Embryol (Berl). 1992 Sep;186(4):387-406 [1416088.001]
  • [Cites] Biochem Int. 1992 Oct;28(1):1-9 [1445382.001]
  • [Cites] Trends Biochem Sci. 1993 Feb;18(2):40-1 [8387703.001]
  • [Cites] Science. 1994 Mar 4;263(5151):1281-4 [8122112.001]
  • [Cites] J Biol Chem. 1994 Apr 29;269(17):12999-3004 [8175719.001]
  • [Cites] Oncogene. 1994 Jun;9(6):1567-74 [8183550.001]
  • [Cites] Cancer. 1994 Sep 1;74(5):1584-90 [7520350.001]
  • [Cites] Biochem Biophys Res Commun. 1994 Sep 15;203(2):1131-9 [8093031.001]
  • [Cites] Neurosci Lett. 1994 Sep 12;178(2):216-20 [7824199.001]
  • [Cites] Development. 1995 Jan;121(1):37-51 [7867507.001]
  • [Cites] Breast Cancer Res Treat. 1994;31(2-3):309-14 [7533562.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Mar 28;92(7):2558-62 [7708684.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Jul 3;92(14):6334-8 [7603991.001]
  • [Cites] Am J Surg Pathol. 1995 Aug;19(8):859-72 [7611533.001]
  • [Cites] Blood. 1995 Sep 1;86(5):1954-60 [7655022.001]
  • [Cites] Nat Med. 1996 May;2(5):561-6 [8616716.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Apr 30;93(9):4181-6 [8633037.001]
  • [Cites] Hum Pathol. 1996 Jun;27(6):590-4 [8666370.001]
  • [Cites] J Biol Chem. 1996 Aug 30;271(35):21446-52 [8702927.001]
  • [Cites] Oncogene. 1997 Jan 30;14(4):439-49 [9053841.001]
  • [Cites] Blood. 1997 Feb 15;89(4):1394-404 [9028963.001]
  • [Cites] Blood. 1997 Mar 1;89(5):1483-90 [9057627.001]
  • [Cites] Mol Cell Biol. 1997 Apr;17(4):2312-25 [9121481.001]
  • [Cites] J Biochem. 1997 Feb;121(2):197-205 [9089390.001]
  • [Cites] Oncogene. 1997 May 8;14(18):2175-88 [9174053.001]
  • [Cites] J Biol Chem. 1997 Jul 4;272(27):16733-6 [9201975.001]
  • [Cites] Nature. 1997 Aug 14;388(6643):691-3 [9262405.001]
  • [Cites] Blood. 1997 Oct 15;90(8):2901-10 [9376569.001]
  • [Cites] Science. 1998 Jan 23;279(5350):577-80 [9438854.001]
  • [Cites] Adv Exp Med Biol. 1998;431:221-6 [9598063.001]
  • [Cites] Mol Cell Biol. 1998 Dec;18(12):6951-61 [9819383.001]
  • [Cites] EMBO Rep. 2003 Aug;4(8):781-6 [12855999.001]
  • [Cites] Oncogene. 2003 Aug 21;22(35):5399-407 [12934099.001]
  • [Cites] Br J Haematol. 1998 Dec;103(4):1138-44 [9886332.001]
  • [Cites] Genes Cells. 1998 Dec;3(12):811-22 [10096022.001]
  • [Cites] Blood. 1999 Apr 15;93(8):2697-706 [10194450.001]
  • [Cites] Blood. 1999 May 1;93(9):3088-95 [10216106.001]
  • [Cites] Blood. 1999 Jun 1;93(11):3913-21 [10339500.001]
  • [Cites] Cancer Res. 1999 Jun 15;59(12):2776-80 [10383129.001]
  • [Cites] J Thorac Surg. 1954 Jul;28(1):55-63 [13175281.001]
  • [Cites] Blood. 2005 Jan 15;105(2):827-9 [15374880.001]
  • [Cites] Nat Biotechnol. 2005 Jan;23(1):94-101 [15592455.001]
  • [Cites] Mutat Res. 2005 Feb 15;570(1):9-15 [15680399.001]
  • [Cites] Nat Med. 2005 Jun;11(6):623-9 [15895073.001]
  • [Cites] Biochemistry. 2005 Jun 14;44(23):8533-42 [15938644.001]
  • [Cites] Am J Pathol. 2005 Jul;167(1):213-22 [15972965.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Aug 5;333(3):714-21 [15985215.001]
  • [Cites] Haematologica. 2005 Jul;90(7):988-90 [15996942.001]
  • [Cites] J Biol Chem. 2005 Jul 15;280(28):26039-48 [15886198.001]
  • [Cites] Cell. 2005 Jul 15;122(1):45-57 [16009132.001]
  • [Cites] J Biol Chem. 2005 Jul 22;280(29):26953-64 [15908427.001]
  • [Cites] Leukemia. 2005 Jul;19(7):1128-34 [15902287.001]
  • [Cites] Anticancer Res. 2005 Sep-Oct;25(5):3191-6 [16101126.001]
  • [Cites] Hum Pathol. 2005 Sep;36(9):939-44 [16153455.001]
  • [Cites] Pediatr Blood Cancer. 2005 Nov;45(6):796-801 [15602716.001]
  • [Cites] Int J Cancer. 2005 Dec 20;117(6):942-51 [15986444.001]
  • [Cites] J Pharmacol Exp Ther. 2005 Dec;315(3):971-9 [16002463.001]
  • [Cites] Lab Invest. 2005 Dec;85(12):1544-54 [16170336.001]
  • [Cites] J Cell Sci. 2005 Dec 15;118(Pt 24):5811-23 [16317043.001]
  • [Cites] Dev Genes Evol. 2006 Jan;216(1):10-8 [16220264.001]
  • [Cites] Int J Cancer. 2006 Mar 1;118(5):1181-6 [16161041.001]
  • [Cites] Blood. 2006 Jan 15;107(2):689-97 [16189272.001]
  • [Cites] J Comp Neurol. 2006 Mar 10;495(2):202-12 [16435287.001]
  • [Cites] J Med Chem. 2006 Feb 9;49(3):1006-15 [16451066.001]
  • [Cites] Blood. 2006 Feb 15;107(4):1617-23 [16254137.001]
  • [Cites] J Clin Oncol. 2006 May 10;24(14):2137-50 [16682732.001]
  • [Cites] Gene Expr Patterns. 2006 Jun;6(5):448-61 [16458083.001]
  • [Cites] Lab Invest. 2006 Jul;86(7):645-53 [16619002.001]
  • [Cites] Cancer Res. 2006 Jul 1;66(13):6589-97 [16818631.001]
  • [Cites] Mol Cell Biol. 2006 Aug;26(16):6209-22 [16880530.001]
  • [Cites] Br J Haematol. 2006 Oct;135(1):26-32 [16939498.001]
  • [Cites] Blood. 2006 Oct 1;108(7):2407-15 [16763206.001]
  • [Cites] Blood. 2006 Oct 15;108(8):2796-803 [16825495.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Dec 29;351(4):839-46 [17094947.001]
  • [Cites] Genes Cells. 2006 Dec;11(12):1405-17 [17121547.001]
  • [Cites] World J Gastroenterol. 2006 Nov 28;12(44):7104-12 [17131471.001]
  • [Cites] J Clin Invest. 2006 Dec;116(12):3171-82 [17111047.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jan 2;104(1):270-5 [17185414.001]
  • [Cites] Oncogene. 2007 Feb 8;26(6):859-69 [16878150.001]
  • [Cites] Oncogene. 2007 Feb 8;26(6):813-21 [16909118.001]
  • [Cites] FEBS Lett. 2007 Feb 20;581(4):727-34 [17274988.001]
  • [Cites] Blood. 2007 Mar 1;109(5):2156-64 [17077326.001]
  • [Cites] Mod Pathol. 2007 Mar;20(3):310-9 [17277765.001]
  • [Cites] Cell. 2007 Mar 9;128(5):961-75 [17350579.001]
  • [Cites] Am J Surg Pathol. 2007 Apr;31(4):509-20 [17414097.001]
  • [Cites] Oncogene. 2007 May 3;26(20):2950-4 [17086210.001]
  • [Cites] Cancer Res. 2007 May 1;67(9):4278-86 [17483340.001]
  • [Cites] Cancer Res. 2007 May 1;67(9):4408-17 [17483355.001]
  • [Cites] J Exp Zool B Mol Dev Evol. 2007 May 15;308(3):269-82 [17285636.001]
  • [Cites] Hum Pathol. 2007 Jun;38(6):940-5 [17509395.001]
  • [Cites] Biochem Biophys Res Commun. 2007 Jun 29;358(2):399-403 [17490616.001]
  • [Cites] Differentiation. 2007 Jun;75(5):418-26 [17286600.001]
  • [Cites] Lancet. 2007 Jun 23;369(9579):2106-20 [17586306.001]
  • [Cites] N Engl J Med. 2007 Jul 5;357(1):39-51 [17611206.001]
  • [Cites] J Mol Med (Berl). 2007 Aug;85(8):863-75 [17318615.001]
  • [Cites] Cancer Res. 2009 Mar 15;69(6):2550-8 [19244133.001]
  • [Cites] Blood. 2009 Mar 19;113(12):2776-90 [18845790.001]
  • [Cites] Nature. 2007 Aug 2;448(7153):561-6 [17625570.001]
  • [Cites] Oncogene. 2007 Aug 16;26(38):5606-14 [17353907.001]
  • [Cites] Blood. 2007 Sep 1;110(5):1621-30 [17416736.001]
  • [Cites] Blood. 1999 Nov 1;94(9):3265-8 [10556217.001]
  • [Cites] Blood. 1999 Nov 15;94(10):3614-7 [10610119.001]
  • [Cites] J Biol Chem. 2000 Feb 25;275(8):5600-5 [10681541.001]
  • [Cites] Ann Oncol. 2000 Jan;11(1):53-8 [10690387.001]
  • [Cites] Cancer Res. 2000 Feb 15;60(4):793-8 [10706082.001]
  • [Cites] Am J Pathol. 2000 Mar;156(3):781-9 [10702393.001]
  • [Cites] Blood. 2000 Mar 15;95(6):2144-9 [10706887.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Mar 14;97(6):2603-8 [10706604.001]
  • [Cites] Biochem Biophys Res Commun. 2000 Apr 21;270(3):936-41 [10772929.001]
  • [Cites] J Biol Chem. 2000 May 5;275(18):13564-70 [10788472.001]
  • [Cites] Am J Pathol. 2000 May;156(5):1711-21 [10793082.001]
  • [Cites] Blood. 2000 May 15;95(10):3204-7 [10807789.001]
  • [Cites] Dev Growth Differ. 2000 Apr;42(2):113-9 [10830434.001]
  • [Cites] Am J Pathol. 2000 Aug;157(2):377-84 [10934142.001]
  • [Cites] J Pharmacol Exp Ther. 2000 Oct;295(1):139-45 [10991971.001]
  • [Cites] Blood. 2000 Dec 1;96(12):3681-95 [11090048.001]
  • [Cites] Blood. 2000 Dec 15;96(13):4319-27 [11110708.001]
  • [Cites] J Biol Chem. 2001 Mar 23;276(12):9526-31 [11121404.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1052-6 [11287975.001]
  • [Cites] Cancer Res. 2001 Mar 1;61(5):2194-9 [11280786.001]
  • [Cites] J Clin Oncol. 2001 Apr 15;19(8):2319-33 [11304786.001]
  • [Cites] Lab Invest. 2001 Mar;81(3):419-26 [11310834.001]
  • [Cites] J Biol Chem. 2001 May 18;276(20):16772-9 [11278720.001]
  • [Cites] Am J Pathol. 2001 Jun;158(6):2185-93 [11395396.001]
  • [Cites] Mod Pathol. 2001 Jun;14(6):569-76 [11406658.001]
  • [Cites] Genes Cells. 2001 Jun;6(6):531-44 [11442633.001]
  • [Cites] Am J Pathol. 2001 Aug;159(2):411-5 [11485898.001]
  • [Cites] Blood. 2001 Aug 15;98(4):1209-16 [11493472.001]
  • [Cites] Cancer Res. 2001 Sep 1;61(17):6517-23 [11522649.001]
  • [Cites] Development. 2001 Sep;128(17):3331-8 [11546749.001]
  • [Cites] Am J Surg Pathol. 2001 Nov;25(11):1364-71 [11684952.001]
  • [Cites] Cell. 2001 Nov 2;107(3):387-98 [11701128.001]
  • [Cites] Lancet. 2001 Oct 27;358(9291):1421-3 [11705489.001]
  • [Cites] Mech Dev. 2002 Jan;110(1-2):85-96 [11744371.001]
  • [Cites] J Immunol. 2002 Jan 1;168(1):466-74 [11751994.001]
  • [Cites] Oncogene. 2002 Feb 7;21(7):1038-47 [11850821.001]
  • [Cites] Cancer Res. 2002 Mar 1;62(5):1559-66 [11888936.001]
  • [Cites] Am J Pathol. 2002 Apr;160(4):1487-94 [11943732.001]
  • [Cites] J Biol Chem. 2002 Apr 19;277(16):14153-8 [11809760.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4540-6 [12036886.001]
  • [Cites] Cell. 2002 May 31;109(5):639-49 [12062106.001]
  • [Cites] J Biol Chem. 2002 Jun 21;277(25):22231-9 [11919185.001]
  • [Cites] Genes Chromosomes Cancer. 2002 Aug;34(4):354-62 [12112524.001]
  • [Cites] Int J Cancer. 2002 Jul 1;100(1):49-56 [12115586.001]
  • [Cites] N Engl J Med. 2002 Aug 15;347(7):472-80 [12181401.001]
  • [Cites] Oncogene. 2002 Aug 29;21(38):5823-34 [12185581.001]
  • [Cites] J Biochem. 2002 Sep;132(3):359-71 [12204104.001]
  • [Cites] Mod Pathol. 2002 Sep;15(9):931-8 [12218210.001]
  • [Cites] J Biol Chem. 2002 Sep 27;277(39):35862-8 [12107166.001]
  • [Cites] J Biol Chem. 2002 Sep 27;277(39):35990-8 [12122009.001]
  • [Cites] Histopathology. 2002 Nov;41(5):461-7 [12405914.001]
  • [Cites] Oncogene. 2003 Jan 30;22(4):517-27 [12555065.001]
  • [Cites] Blood. 2003 Mar 1;101(5):1919-27 [12424201.001]
  • [Cites] Nat Rev Cancer. 2003 Mar;3(3):203-16 [12612655.001]
  • [Cites] Exp Hematol. 2003 Mar;31(3):226-33 [12644020.001]
  • [Cites] Genes Chromosomes Cancer. 2003 May;37(1):98-105 [12661011.001]
  • [Cites] Clin Cancer Res. 2003 Jun;9(6):2213-20 [12796388.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Aug;37(4):427-32 [12800156.001]
  • [Cites] J Biol Chem. 2003 Aug 8;278(32):30028-36 [12748172.001]
  • [Cites] Cancer. 2009 Apr 15;115(8):1723-33 [19170230.001]
  • [Cites] Pediatr Dev Pathol. 2009 Jul-Aug;12(4):275-83 [18788887.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Oct;38(2):187-90 [12939746.001]
  • [Cites] Lab Invest. 2003 Sep;83(9):1255-65 [13679433.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2638-41 [12750159.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2642-4 [12816858.001]
  • [Cites] Clin Cancer Res. 2003 Sep 1;9(10 Pt 1):3692-9 [14506160.001]
  • [Cites] Nature. 2003 Oct 2;425(6957):507-12 [14523446.001]
  • [Cites] Nature. 2003 Oct 2;425(6957):512-6 [14523447.001]
  • [Cites] Am J Surg Pathol. 2003 Nov;27(11):1473-6 [14576483.001]
  • [Cites] Oncogene. 2003 Oct 30;22(49):7750-61 [14586401.001]
  • [Cites] Blood. 2004 Feb 15;103(4):1464-71 [14563642.001]
  • [Cites] Development. 2004 Feb;131(4):743-54 [14757637.001]
  • [Cites] Cancer Lett. 2004 Feb 20;204(2):127-43 [15013213.001]
  • [Cites] Oncogene. 2004 Apr 8;23(15):2617-29 [14968112.001]
  • [Cites] J Cell Physiol. 2004 Jun;199(3):330-58 [15095281.001]
  • [Cites] J Clin Oncol. 2004 May 1;22(9):1682-8 [15117990.001]
  • [Cites] Blood. 2004 Jun 15;103(12):4622-9 [14962911.001]
  • [Cites] Science. 2004 Jun 4;304(5676):1497-500 [15118125.001]
  • [Cites] Hum Pathol. 2004 Jun;35(6):711-21 [15188137.001]
  • [Cites] Cancer. 2004 Jul 1;101(1):3-27 [15221985.001]
  • [Cites] J Cell Sci. 2004 Jul 1;117(Pt 15):3319-29 [15226403.001]
  • [Cites] Nature. 2004 Jul 15;430(6997):345-50 [15208641.001]
  • [Cites] Oncogene. 2004 Jul 15;23(32):5426-34 [15184887.001]
  • [Cites] Oncogene. 2004 Aug 12;23(36):6071-82 [15208656.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2259-67 [17519389.001]
  • [Cites] J Biol Chem. 2007 Sep 28;282(39):28683-90 [17681947.001]
  • [Cites] Cell Signal. 2007 Dec;19(12):2434-43 [17904822.001]
  • [Cites] Nat Med. 2007 Nov;13(11):1341-8 [17922009.001]
  • [Cites] Cell. 2007 Dec 14;131(6):1190-203 [18083107.001]
  • [Cites] Mol Cancer Ther. 2007 Dec;6(12 Pt 1):3314-22 [18089725.001]
  • [Cites] J Thorac Oncol. 2008 Jan;3(1):13-7 [18166835.001]
  • [Cites] Neuropsychopharmacology. 2008 Feb;33(3):685-700 [17487225.001]
  • [Cites] J Biol Chem. 2008 Feb 15;283(7):3743-50 [18070884.001]
  • [Cites] Annu Rev Physiol. 2008;70:431-57 [17850209.001]
  • [Cites] Neoplasia. 2008 Mar;10(3):298-302 [18320074.001]
  • [Cites] J Biochem. 2008 Apr;143(4):441-8 [18024471.001]
  • [Cites] PLoS Genet. 2008 Mar;4(3):e1000026 [18369445.001]
  • [Cites] J Clin Pathol. 2008 Apr;61(4):428-37 [17938159.001]
  • [Cites] Med Res Rev. 2008 May;28(3):372-412 [17694547.001]
  • [Cites] Oncogene. 2008 Apr 24;27(19):2728-36 [17998938.001]
  • [Cites] Cancer Res. 2008 May 1;68(9):3389-95 [18451166.001]
  • [Cites] Br J Cancer. 2008 May 6;98(9):1536-9 [18414414.001]
  • [Cites] Korean J Lab Med. 2008 Apr;28(2):89-94 [18458503.001]
  • [Cites] Hematol Oncol. 2008 Jun;26(2):108-13 [18220322.001]
  • [Cites] Nat Med. 2008 Jun;14(6):676-80 [18469826.001]
  • [Cites] Blood. 2008 Jun 15;111(12):5496-504 [18385450.001]
  • [Cites] Clin Cancer Res. 2008 Jul 1;14(13):4275-83 [18594010.001]
  • [Cites] Lung Cancer. 2008 Aug;61(2):163-9 [18242762.001]
  • [Cites] Curr Biol. 2008 Aug 5;18(15):1101-9 [18674914.001]
  • [Cites] Nature. 2008 Oct 16;455(7215):930-5 [18724359.001]
  • [Cites] Nature. 2008 Oct 16;455(7215):967-70 [18923523.001]
  • [Cites] Nature. 2008 Oct 16;455(7215):971-4 [18923524.001]
  • [Cites] Nature. 2008 Oct 16;455(7215):975-8 [18923525.001]
  • [Cites] Cancer Res. 2008 Nov 1;68(21):8899-907 [18974134.001]
  • [Cites] Neuroreport. 2008 Nov 19;19(17):1733-8 [18849880.001]
  • [Cites] Biochem J. 2008 Dec 1;416(2):153-9 [18990089.001]
  • [Cites] Hum Pathol. 2009 Jan;40(1):75-82 [18755494.001]
  • [Cites] Blood. 2008 Dec 15;112(13):4808-17 [19064740.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Dec 16;105(50):19893-7 [19064915.001]
  • [Cites] Am J Pathol. 2009 Feb;174(2):361-70 [19131589.001]
  • [Cites] Am J Pathol. 2009 Feb;174(2):661-70 [19147828.001]
  • [Cites] Neoplasia. 2009 Feb;11(2):145-56 [19177199.001]
  • [Cites] Eur J Neurosci. 2009 Jan;29(2):275-86 [19200234.001]
  • (PMID = 19459784.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / EML4-ALK fusion protein, human; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Number-of-references] 237
  • [Other-IDs] NLM/ PMC2708929
  •  go-up   go-down


49. Lin SF, Price DL, Chen CH, Brader P, Li S, Gonzalez L, Zhang Q, Yu YA, Chen N, Szalay AA, Fong Y, Wong RJ: Oncolytic vaccinia virotherapy of anaplastic thyroid cancer in vivo. J Clin Endocrinol Metab; 2008 Nov;93(11):4403-7
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] Oncolytic vaccinia virotherapy of anaplastic thyroid cancer in vivo.
  • CONTEXT: Anaplastic thyroid carcinoma (ATC) is a fatal disease with a median survival of only 6 months.
  • OBJECTIVE: A mutated, replication-competent, vaccinia virus (GLV-1h68) has oncolytic effects on human ATC cell lines in vitro.
  • We assessed the utility of GLV-1h68 in treating anaplastic thyroid cancer in vivo.
  • At d 10, tumor viral recovery was increased more than 50-fold as compared with the injected dose, and minimal virus was recovered from the lung, liver, brain, heart, spleen, and kidneys.
  • [MeSH-major] Cancer Vaccines / therapeutic use. Carcinoma / immunology. Thyroid Neoplasms / immunology. Vaccinia virus / immunology. Viral Vaccines / therapeutic use
  • [MeSH-minor] Animals. Cell Division / drug effects. Cell Line, Tumor. Genetic Markers. Humans. Mice. Mice, Nude. Neoplasm Transplantation. Transplantation, Heterologous. Viral Plaque Assay

  • Genetic Alliance. consumer health - Thyroid cancer, anaplastic.
  • Genetic Alliance. consumer health - Thyroid Cancer.
  • MedlinePlus Health Information. consumer health - Thyroid Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Thyroid. 2000 Jul;10(7):587-94 [10958311.001]
  • [Cites] Surgery. 2001 Dec;130(6):1028-34 [11742333.001]
  • [Cites] Surgery. 2002 Mar;131(3):245-8 [11894027.001]
  • [Cites] Br J Cancer. 2002 Jun 17;86(12):1848-53 [12085174.001]
  • [Cites] Nat Biotechnol. 2004 Mar;22(3):313-20 [14990953.001]
  • [Cites] Expert Opin Biol Ther. 2004 Aug;4(8):1307-21 [15268664.001]
  • [Cites] World J Surg. 1998 Jul;22(7):725-30 [9606289.001]
  • [Cites] Lancet. 1973 Mar 24;1(7804):656-9 [4121857.001]
  • [Cites] Cancer. 1985 Nov 1;56(9):2155-60 [3902203.001]
  • [Cites] J Endocrinol Invest. 1991 Jun;14(6):475-80 [1723086.001]
  • [Cites] Surgery. 2007 Dec;142(6):976-83; discussion 976-83 [18063085.001]
  • [Cites] Mol Ther. 2005 Feb;11(2):180-95 [15668130.001]
  • [Cites] Cancer Res. 2007 Oct 15;67(20):10038-46 [17942938.001]
  • [Cites] Int J Cancer. 2004 Nov 10;112(3):525-32 [15382081.001]
  • (PMID = 18697871.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / T32 CA009685
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / Genetic Markers; 0 / Viral Vaccines
  • [Other-IDs] NLM/ PMC3728375
  •  go-up   go-down


50. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


51. Camidge DR, Kono SA, Flacco A, Tan AC, Doebele RC, Zhou Q, Crino L, Franklin WA, Varella-Garcia M: Optimizing the detection of lung cancer patients harboring anaplastic lymphoma kinase (ALK) gene rearrangements potentially suitable for ALK inhibitor treatment. Clin Cancer Res; 2010 Nov 15;16(22):5581-90
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] Optimizing the detection of lung cancer patients harboring anaplastic lymphoma kinase (ALK) gene rearrangements potentially suitable for ALK inhibitor treatment.
  • PURPOSE: Anaplastic lymphoma kinase (ALK) rearrangements, associated with sensitivity to an experimental ALK/MET inhibitor, occur in 3% to 5% of non-small cell lung cancers.
  • EXPERIMENTAL DESIGN: Lung cancer patients were screened by ALK and MET FISH and for EGFR and KRAS mutations.
  • ALK FISH positivity was heterogeneous, but mean values in tumor areas from ALK-positive patients (54% of cells; range, 22-87%) were significantly higher than in adjacent normal tissue or tumor/normal areas from ALK-negative patients (mean, 5-7%).
  • One hundred percent sensitivity and specificity occurred when four or more fields (∼60 cells) were counted.

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Genetic Testing.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] ©2010 AACR.
  • [Cites] Nature. 2007 Aug 2;448(7153):561-6 [17625570.001]
  • [Cites] Cancer Cell. 2010 Jan 19;17(1):77-88 [20129249.001]
  • [Cites] Cell. 2007 Dec 14;131(6):1190-203 [18083107.001]
  • [Cites] Neoplasia. 2008 Mar;10(3):298-302 [18320074.001]
  • [Cites] Cancer Res. 2008 May 1;68(9):3389-95 [18451166.001]
  • [Cites] Clin Cancer Res. 2008 May 15;14(10):2895-9 [18483355.001]
  • [Cites] Cancer Res. 2008 Jul 1;68(13):4971-6 [18593892.001]
  • [Cites] Clin Cancer Res. 2008 Jul 1;14(13):4275-83 [18594010.001]
  • [Cites] N Engl J Med. 2008 Sep 25;359(13):1367-80 [18815398.001]
  • [Cites] Clin Cancer Res. 2008 Oct 15;14(20):6618-24 [18927303.001]
  • [Cites] Cancer Sci. 2008 Dec;99(12):2349-55 [19032370.001]
  • [Cites] Am J Pathol. 2009 Feb;174(2):661-70 [19147828.001]
  • [Cites] J Clin Oncol. 2009 Apr 1;27(10):1667-74 [19255323.001]
  • [Cites] Mod Pathol. 2009 Apr;22(4):508-15 [19234440.001]
  • [Cites] Cancer. 2009 Apr 15;115(8):1723-33 [19170230.001]
  • [Cites] Clin Cancer Res. 2009 May 1;15(9):3143-9 [19383809.001]
  • [Cites] Biochem J. 2009 Jun 15;420(3):345-61 [19459784.001]
  • [Cites] Clin Cancer Res. 2009 Aug 15;15(16):5216-23 [19671850.001]
  • [Cites] Oncogene. 2009 Aug;28 Suppl 1:S24-31 [19680293.001]
  • [Cites] N Engl J Med. 2009 Sep 3;361(10):947-57 [19692680.001]
  • [Cites] J Clin Oncol. 2009 Sep 10;27(26):4232-5 [19667260.001]
  • [Cites] J Clin Oncol. 2009 Sep 10;27(26):4247-53 [19667264.001]
  • [Cites] J Thorac Oncol. 2009 Dec;4(12):1450-4 [20009909.001]
  • [Cites] J Mol Diagn. 2010 Jan;12(1):43-50 [20007845.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 11;104(50):19936-41 [18077425.001]
  • (PMID = 21062932.001).
  • [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 / P50 CA058187; United States / NCI NIH HHS / CA / P50CA58187
  • [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 / Protein Kinase Inhibitors; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Other-IDs] NLM/ NIHMS375238; NLM/ PMC3395226
  •  go-up   go-down


52. 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
MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


53. Kawada K, Kitagawa K, Kamei S, Inada M, Mitsuma A, Sawaki M, Kikumori T, Fujimoto Y, Arima H, Imai T, Ando Y: The feasibility study of docetaxel in patients with anaplastic thyroid cancer. Jpn J Clin Oncol; 2010 Jun;40(6):596-9
Hazardous Substances Data Bank. DOCETAXEL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The feasibility study of docetaxel in patients with anaplastic thyroid cancer.
  • There is no established chemotherapy for anaplastic thyroid cancer.
  • We conducted a prospective feasibility study at a single center to explore the antitumor activity of docetaxel against anaplastic thyroid cancer.
  • Docetaxel was administered intravenously at a dose of 60 mg/m(2) over the course of 1 h every 3 weeks in patients with anaplastic thyroid cancer who had received no prior chemotherapy.
  • A total of seven patients with anaplastic thyroid cancer were enrolled over the course of 30 months and received docetaxel.
  • Docetaxel could be an effective drug for the treatment of anaplastic thyroid cancer, with tolerable toxicity.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Carcinoma / drug therapy. Taxoids / administration & dosage. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Aged. Disease Progression. Feasibility Studies. Female. Humans. Infusions, Intravenous. Lung Neoplasms / secondary. Male

  • Genetic Alliance. consumer health - Thyroid cancer, anaplastic.
  • Genetic Alliance. consumer health - Thyroid Cancer.
  • MedlinePlus Health Information. consumer health - Thyroid Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20200039.001).
  • [ISSN] 1465-3621
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Taxoids; 15H5577CQD / docetaxel
  •  go-up   go-down


54. Khan N, Oriuchi N, Higuchi T, Endo K: Review of fluorine-18-2-fluoro-2-deoxy-D-glucose positron emission tomography (FDG-PET) in the follow-up of medullary and anaplastic thyroid carcinomas. Cancer Control; 2005 Oct;12(4):254-60
MedlinePlus Health Information. consumer health - Thyroid Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Review of fluorine-18-2-fluoro-2-deoxy-D-glucose positron emission tomography (FDG-PET) in the follow-up of medullary and anaplastic thyroid carcinomas.
  • BACKGROUND: The goal of posttreatment follow-up for medullary and anaplastic thyroid cancer (MTC and ATC) is the early diagnosis of recurrence or metastases.
  • However, the PET technique is limited by less accurate spatial assignment of small lesions, especially in the lung and liver.
  • [MeSH-major] Carcinoma / radionuclide imaging. Carcinoma, Medullary / radionuclide imaging. Fluorodeoxyglucose F18. Radiopharmaceuticals. Thyroid Neoplasms / radionuclide imaging

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16258498.001).
  • [ISSN] 1073-2748
  • [Journal-full-title] Cancer control : journal of the Moffitt Cancer Center
  • [ISO-abbreviation] Cancer Control
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
  • [Number-of-references] 45
  •  go-up   go-down


55. 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
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] 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

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


56. Franks TJ, Galvin JR: Sarcomatoid carcinoma of the lung: histologic criteria and common lesions in the differential diagnosis. Arch Pathol Lab Med; 2010 Jan;134(1):49-54
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] Sarcomatoid carcinoma of the lung: histologic criteria and common lesions in the differential diagnosis.
  • CONTEXT: Sarcomatoid carcinoma of the lung is a subset of poorly differentiated non-small cell lung cancers that are diagnostically challenging because they are uncommon, may reveal little of their parent cell of origin, and overlap morphologically with other anaplastic epithelioid and spindle cell tumors that can be primary in, or metastatic to, the lung and pleura.
  • OBJECTIVE: To review the current histologic classification and diagnostic criteria that identify the 5 subtypes of sarcomatoid carcinoma of the lung and to discuss the most common tumors in the differential diagnosis.
  • CONCLUSIONS: Identification of sarcomatoid carcinoma of the lung requires knowledge of specific histologic criteria that define the 5 subgroups, targeted immunohistochemical studies, and correlation with chest imaging to assess distribution of disease and to avoid misdiagnosis.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / diagnosis. Carcinoma, Non-Small-Cell Lung / pathology. Lung Neoplasms / diagnosis. Lung Neoplasms / pathology
  • [MeSH-minor] Diagnosis, Differential. Humans. Sarcoma / diagnosis. Sarcoma / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20073605.001).
  • [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
  • [Number-of-references] 27
  •  go-up   go-down


57. Swann MH, Yoon J: Merkel cell carcinoma. Semin Oncol; 2007 Feb;34(1):51-6
MedlinePlus Health Information. consumer health - Skin Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Merkel cell carcinoma.
  • Merkel cell carcinoma (MCC) is a rare, aggressive cutaneous cancer that predominately affects elderly Caucasians with fair skin and has a propensity for local recurrence and regional lymph node metastases.
  • A variety of terms have been used to describe this tumor, including trabecular cell carcinoma, neuroendocrine or primary small cell carcinoma of the skin, and anaplastic cancer of the skin.
  • It may be difficult to accurately diagnose MCC by light microscopy alone and ancillary techniques, including electron microscopy and immunohistochemistry, may be necessary to make a definitive diagnosis.
  • Systemic chemotherapy, akin to regimens for small cell carcinoma of the lung, may be considered as an adjuvant following surgery or to treat locoregional or distant disease.
  • Successful outcomes are most often seen in patients with early diagnosis and complete excision.
  • [MeSH-major] Carcinoma, Merkel Cell. Skin Neoplasms
  • [MeSH-minor] Aged. Combined Modality Therapy. Humans. Lymphatic Metastasis. Neoplasm Recurrence, Local / diagnosis. Prognosis. Treatment Outcome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17270666.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 48
  •  go-up   go-down


58. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


59. Kalac M, Ostojić S, Gasparov S, Planinc-Peraica A, Dominis M, Jaksić B: [Microcellular lung carcinoma in patient with hepatosplenic T-cell lymphoma: a case report]. Lijec Vjesn; 2006 Mar-Apr;128(3-4):76-8
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Microcellular lung carcinoma in patient with hepatosplenic T-cell lymphoma: a case report].
  • Hepatosplenic T-cell lymphoma (HSTCL) is a rare form of extranodal non-Hodgkin lymphoma derived from cytotoxic T-cells, usually manifesting by sinusoidal infiltration of spleen, liver and bone marrow.
  • In 1997 World Health Organization classified malignant lymphomas and placed HSTCL among peripheral T-cell neoplasms.
  • We present a case of a 48-year-old male patient whose initial symptoms were fatigue, weight loss and night sweats, which were followed by splenomegaly and pancytopenia.
  • Upon the completion of the 6th course of therapy he was diagnosed with lung anaplastic microcellular carcinoma and was treated with 3 course of PE therapy (cisplatin, etoposide).
  • [MeSH-major] Carcinoma, Small Cell / pathology. Liver Neoplasms / pathology. Lung Neoplasms / pathology. Lymphoma, T-Cell / pathology. Neoplasms, Second Primary / pathology. Splenic Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16808095.001).
  • [ISSN] 0024-3477
  • [Journal-full-title] Lijec̆nic̆ki vjesnik
  • [ISO-abbreviation] Lijec Vjesn
  • [Language] hrv
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Croatia
  •  go-up   go-down


60. Marlow LA, Reynolds LA, Cleland AS, Cooper SJ, Gumz ML, Kurakata S, Fujiwara K, Zhang Y, Sebo T, Grant C, McIver B, Wadsworth JT, Radisky DC, Smallridge RC, Copland JA: Reactivation of suppressed RhoB is a critical step for the inhibition of anaplastic thyroid cancer growth. Cancer Res; 2009 Feb 15;69(4):1536-44
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] Reactivation of suppressed RhoB is a critical step for the inhibition of anaplastic thyroid cancer growth.
  • Anaplastic thyroid carcinoma (ATC) is a highly aggressive form of the disease for which new therapeutic options are desperately needed.
  • Previously, we showed that the high-affinity peroxisome proliferator-activated receptor gamma (PPARgamma) agonist, RS5444, inhibits cell proliferation of ATC cells via induction of the cyclin-dependent kinase inhibitor p21(WAF1/CIP1) (p21).
  • We show here that up-regulation of RhoB is a critical step in PPARgamma-mediated activation of p21-induced cell stasis.
  • Using multiple independently derived ATC cell lines, we found that treatment with RS5444 leads to the up-regulation of RhoB and subsequent activation of p21, and that silencing of RhoB by RNAi blocks the ability of RS5444 to induce p21 and to inhibit cell proliferation.
  • We further implicate RhoB as a key signaling effector for the growth inhibition of ATC, as treatment with a histone deacetylase inhibitor shown to increase RhoB expression in lung cancer cells caused the up-regulation of RhoB in ATC cells accompanied by increased expression of p21 and inhibition of cell proliferation; this effect occurred even in ATC cells that were unresponsive to RS5444 due to a lack of expression of PPARgamma.

  • Genetic Alliance. consumer health - Thyroid cancer, anaplastic.
  • Genetic Alliance. consumer health - Thyroid Cancer.
  • MedlinePlus Health Information. consumer health - Thyroid Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 1999 Nov 1;59(21):5492-6 [10554025.001]
  • [Cites] Endocr Relat Cancer. 2009 Mar;16(1):17-44 [18987168.001]
  • [Cites] J Biol Chem. 2000 Jun 16;275(24):17974-8 [10770919.001]
  • [Cites] Int J Oncol. 2000 Dec;17(6):1157-64 [11078801.001]
  • [Cites] Semin Cancer Biol. 2000 Dec;10(6):443-52 [11170866.001]
  • [Cites] J Mol Med (Berl). 2001;79(1):30-47 [11327101.001]
  • [Cites] Hepatology. 2001 May;33(5):1087-97 [11343236.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 May 22;98(11):6192-7 [11353846.001]
  • [Cites] Methods. 2001 Dec;25(4):402-8 [11846609.001]
  • [Cites] Nat Rev Cancer. 2001 Nov;1(2):162-8 [11905808.001]
  • [Cites] Clin Exp Metastasis. 2002;19(1):9-15 [11918088.001]
  • [Cites] Clin Cancer Res. 2002 Jul;8(7):2225-32 [12114424.001]
  • [Cites] Mol Cancer Ther. 2001 Dec;1(2):141-9 [12467231.001]
  • [Cites] Clin Cancer Res. 2003 Jan;9(1):1-9 [12538445.001]
  • [Cites] Cell Cycle. 2002 Nov-Dec;1(6):430-7 [12548020.001]
  • [Cites] Endocrinology. 2003 Sep;144(9):3852-9 [12933658.001]
  • [Cites] Oncogene. 2003 Sep 18;22(40):6204-13 [13679859.001]
  • [Cites] Oncogene. 2004 Feb 5;23(5):1136-45 [14647415.001]
  • [Cites] J Cell Sci. 2004 Mar 15;117(Pt 8):1301-12 [15020670.001]
  • [Cites] Clin Cancer Res. 2004 Apr 15;10(8):2742-50 [15102679.001]
  • [Cites] Endocrinology. 2004 Jun;145(6):2865-75 [14976143.001]
  • [Cites] Mol Cell Biol. 2004 Jun;24(12):5565-76 [15169915.001]
  • [Cites] J Clin Invest. 1993 Jan;91(1):179-84 [8423216.001]
  • [Cites] Mol Cell Biol. 1995 Nov;15(11):6443-53 [7565796.001]
  • [Cites] Mol Cell Biol. 1998 Aug;18(8):4689-97 [9671479.001]
  • [Cites] Mol Cell. 1999 Jun;3(6):799-804 [10394368.001]
  • [Cites] Endocrinology. 2004 Dec;145(12):5774-85 [15345676.001]
  • [Cites] Cancer Res. 2004 Nov 15;64(22):8389-96 [15548709.001]
  • [Cites] Oncogene. 2005 Jan 13;24(3):502-11 [15543229.001]
  • [Cites] J Biol Chem. 2005 May 13;280(19):19243-9 [15713677.001]
  • [Cites] Clin Cancer Res. 2005 May 15;11(10):3958-65 [15897598.001]
  • [Cites] Histol Histopathol. 2006 Feb;21(2):213-8 [16329046.001]
  • [Cites] Oncogene. 2006 Apr 13;25(16):2304-17 [16331265.001]
  • [Cites] Oncogene. 2006 May 4;25(19):2736-47 [16314832.001]
  • [Cites] Mol Cell Endocrinol. 2006 Jun 7;251(1-2):17-32 [16574311.001]
  • [Cites] J Cell Biochem. 2006 Jul 1;98(4):1021-35 [16795079.001]
  • [Cites] Cancer Chemother Pharmacol. 2006 Oct;58(4):460-70 [16435154.001]
  • [Cites] Endocrinology. 2006 Sep;147(9):4463-75 [16777971.001]
  • [Cites] Thyroid. 2006 Dec;16(12):1293-302 [17199440.001]
  • [Cites] CA Cancer J Clin. 2007 Jan-Feb;57(1):43-66 [17237035.001]
  • [Cites] J Cell Physiol. 2007 Jul;212(1):1-12 [17443682.001]
  • [Cites] J Biol Chem. 2007 Aug 10;282(32):23387-401 [17565986.001]
  • [Cites] BMC Cancer. 2007;7:220 [18047684.001]
  • [Cites] Annu Rev Biochem. 2008;77:289-312 [18518822.001]
  • [Cites] Cancer Gene Ther. 2008 Jul;15(7):456-64 [18340357.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Nov;93(11):4331-41 [18713817.001]
  • [Cites] Cancer Res. 2000 Feb 15;60(4):1129-38 [10706135.001]
  • (PMID = 19208833.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA015083-34; United States / NCI NIH HHS / CA / P30 CA015083; United States / NCI NIH HHS / CA / P30 CA015083-34; United States / NCI NIH HHS / CA / P30CA15083
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / PPAR gamma; 0 / Thiazolidinediones; EC 3.6.5.2 / rhoB GTP-Binding Protein; M17ILL71MC / efatutazone
  • [Other-IDs] NLM/ NIHMS83531; NLM/ PMC2644344
  •  go-up   go-down


61. 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
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] 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.

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Am J Surg Pathol. 2001 Dec;25(12):1515-9 [11717541.001]
  • [Cites] J Surg Oncol. 2002 Jul;80(3):119-20 [12115792.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2568-73 [12763927.001]
  • [Cites] J Clin Oncol. 2004 Mar 15;22(6):1103-9 [15020612.001]
  • [Cites] N Engl J Med. 2004 May 20;350(21):2129-39 [15118073.001]
  • [Cites] Science. 2004 Jun 4;304(5676):1497-500 [15118125.001]
  • [Cites] Hum Pathol. 1990 Apr;21(4):459-60 [2156774.001]
  • [Cites] Science. 1994 Mar 4;263(5151):1281-4 [8122112.001]
  • [Cites] Cancer. 1995 Jun 15;75(12):2844-52 [7773933.001]
  • [Cites] Blood. 1996 Jan 1;87(1):284-91 [8547653.001]
  • [Cites] J Histochem Cytochem. 1996 Dec;44(12):1353-62 [8985127.001]
  • [Cites] J Clin Pathol. 1998 Jul;51(7):506-11 [9797726.001]
  • [Cites] Hum Pathol. 1999 Apr;30(4):378-83 [10208457.001]
  • [Cites] Cancer Res. 1999 Jun 15;59(12):2776-80 [10383129.001]
  • [Cites] Chest. 2005 Jul;128(1):317-21 [16002952.001]
  • [Cites] Semin Respir Crit Care Med. 2005 Jun;26(3):342-52 [16052436.001]
  • [Cites] Int J Cancer. 2006 May 15;118(10):2498-504 [16353158.001]
  • [Cites] J Mol Diagn. 2007 Jul;9(3):320-6 [17591931.001]
  • [Cites] J Thorac Oncol. 2007 Jul;2(7):581-2 [17607109.001]
  • [Cites] Nature. 2007 Aug 2;448(7153):561-6 [17625570.001]
  • [Cites] Chest. 2007 Sep;132(3 Suppl):29S-55S [17873159.001]
  • [Cites] Cell. 2007 Dec 14;131(6):1190-203 [18083107.001]
  • [Cites] J Thorac Oncol. 2008 Jan;3(1):13-7 [18166835.001]
  • [Cites] Neoplasia. 2008 Mar;10(3):298-302 [18320074.001]
  • [Cites] CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96 [18287387.001]
  • [Cites] Lung Cancer. 2006 Apr;52(1):47-52 [16503085.001]
  • [Cites] J Natl Compr Canc Netw. 2006 Jul;4(6):548-82 [16813724.001]
  • [Cites] Cancer Res. 2006 Sep 1;66(17):8337-41 [16951139.001]
  • [Cites] N Engl J Med. 2006 Oct 26;355(17):1763-71 [17065637.001]
  • [Cites] Ann Thorac Surg. 2007 Jan;83(1):209-14 [17184664.001]
  • [Cites] Med Res Rev. 2008 May;28(3):372-412 [17694547.001]
  • [Cites] Am J Surg Pathol. 2008 Jun;32(6):810-27 [18391747.001]
  • [Cites] Clin Cancer Res. 2008 Jul 1;14(13):4275-83 [18594010.001]
  • [Cites] Lung Cancer. 2008 Aug;61(2):163-9 [18242762.001]
  • [Cites] Nature. 2008 Oct 16;455(7215):971-4 [18923524.001]
  • [Cites] Nature. 2008 Oct 16;455(7215):975-8 [18923525.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Dec 16;105(50):19893-7 [19064915.001]
  • [Cites] Genes Chromosomes Cancer. 2009 Apr;48(4):366-80 [19156837.001]
  • [Cites] Mod Pathol. 2009 Apr;22(4):508-15 [19234440.001]
  • [Cites] Cancer. 2009 Apr 15;115(8):1723-33 [19170230.001]
  • [Cites] J Clin Oncol. 2009 Sep 10;27(26):4247-53 [19667264.001]
  • [Cites] J Cell Mol Med. 2009 Aug;13(8B):1977-86 [19040416.001]
  • [Cites] Am J Pathol. 2000 May;156(5):1711-21 [10793082.001]
  • [Cites] Am J Pathol. 2000 Aug;157(2):377-84 [10934142.001]
  • [Cites] Histopathology. 2001 Oct;39(4):397-401 [11683941.001]
  • [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
  •  go-up   go-down


62. Martelli MP, Sozzi G, Hernandez L, Pettirossi V, Navarro A, Conte D, Gasparini P, Perrone F, Modena P, Pastorino U, Carbone A, Fabbri A, Sidoni A, Nakamura S, Gambacorta M, Fernández PL, Ramirez J, Chan JK, Grigioni WF, Campo E, Pileri SA, Falini B: EML4-ALK rearrangement in non-small cell lung cancer and non-tumor lung tissues. Am J Pathol; 2009 Feb;174(2):661-70
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] EML4-ALK rearrangement in non-small cell lung cancer and non-tumor lung tissues.
  • A fusion gene, echinoderm microtubule associated protein like 4-anaplastic lymphoma kinase (EML4-ALK), with transforming activity has recently been identified in a subset of non-small cell lung cancer (NSCLC), but its pathogenetic, diagnostic, and therapeutic roles remain unclear.
  • Both frequency and type of EML4-ALK transcripts were investigated by reverse transcription PCR in 120 frozen NSCLC specimens from Italy and Spain; non-neoplastic lung tissues taken far from the tumor were used as controls.
  • EML4-ALK transcripts (variants 1 and 3) were detected in 9 of 120 NSCLC samples but were not specific for NSCLC since they were also found in non-cancerous lung tissues taken far from the tumor.
  • Fluorescence in situ hybridization analysis of cases expressing EML4-ALK transcripts showed that only a minority of cells harbored the EML4-ALK gene.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Lung Neoplasms / genetics. Oncogene Proteins, Fusion / biosynthesis
  • [MeSH-minor] Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Blotting, Western. Female. Gene Rearrangement. Humans. Immunohistochemistry. Immunoprecipitation. In Situ Hybridization, Fluorescence. Lung / metabolism. Male. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic


63. 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
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] 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

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 2010 Mar 1;70(5):2085-94 [20179196.001]
  • [Cites] Nature. 2010 Feb 18;463(7283):899-905 [20164920.001]
  • [Cites] N Engl J Med. 2010 Oct 28;363(18):1693-703 [20979469.001]
  • [Cites] Chem Biol. 2010 Mar 26;17(3):285-95 [20338520.001]
  • [Cites] Cancer Res. 2010 Feb 1;70(3):868-74 [20103621.001]
  • [Cites] Nat Rev Cancer. 2010 Feb;10(2):116-29 [20094046.001]
  • [Cites] Cancer Biol Ther. 2009 Nov;8(21):2042-50 [19755855.001]
  • [Cites] Lung Cancer. 2001 Feb-Mar;31(2-3):139-48 [11165392.001]
  • [Cites] N Engl J Med. 2001 Mar 15;344(11):783-92 [11248153.001]
  • [Cites] J Clin Oncol. 2003 Dec 1;21(23):4342-9 [14645423.001]
  • [Cites] N Engl J Med. 2004 May 20;350(21):2129-39 [15118073.001]
  • [Cites] Chem Biol. 2004 May;11(5):691-701 [15157880.001]
  • [Cites] Science. 2004 Jun 4;304(5676):1497-500 [15118125.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Sep 7;101(36):13306-11 [15329413.001]
  • [Cites] EMBO J. 1998 Oct 15;17(20):5896-904 [9774334.001]
  • [Cites] Cancer Res. 2005 Jul 1;65(13):5561-70 [15994928.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jul 5;102(27):9625-30 [15983384.001]
  • [Cites] Clin Cancer Res. 2006 Nov 15;12(22):6652-62 [17121884.001]
  • [Cites] N Engl J Med. 2006 Dec 14;355(24):2542-50 [17167137.001]
  • [Cites] Nature. 2007 Mar 8;446(7132):153-8 [17344846.001]
  • [Cites] Nature. 2007 Aug 2;448(7153):561-6 [17625570.001]
  • [Cites] Nature. 2007 Dec 6;450(7171):893-8 [17982442.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 11;104(50):19936-41 [18077425.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 11;104(50):20007-12 [18077431.001]
  • [Cites] Cell. 2007 Dec 14;131(6):1190-203 [18083107.001]
  • [Cites] J Pathol. 2009 Jan;217(1):65-72 [18932182.001]
  • [Cites] Mol Pharmacol. 2009 Jan;75(1):196-207 [18849352.001]
  • [Cites] Cancer Res. 2009 May 1;69(9):3937-46 [19366796.001]
  • [Cites] Lancet. 2009 May 2;373(9674):1525-31 [19410716.001]
  • [Cites] J Clin Invest. 2009 Jun;119(6):1727-40 [19451690.001]
  • [Cites] N Engl J Med. 2009 Sep 3;361(10):947-57 [19692680.001]
  • [Cites] Nat Genet. 2009 Nov;41(11):1238-42 [19801978.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Oct 27;106(43):18351-6 [19805051.001]
  • [CommentIn] Sci Transl Med. 2010 Dec 15;2(62):62ps56 [21160076.001]
  • [CommentIn] Nat Rev Drug Discov. 2011 Feb;10(2):98-9 [21283102.001]
  • [ErratumIn] Sci Transl Med. 2012 Apr 18;4(130):130er2
  • [ErratumIn] Sci Transl Med. 2011 Jan 19;3(66):66er2
  • (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
  •  go-up   go-down


64. Soda M, Choi YL, Enomoto M, Takada S, Yamashita Y, Ishikawa S, Fujiwara S, Watanabe H, Kurashina K, Hatanaka H, Bando M, Ohno S, Ishikawa Y, Aburatani H, Niki T, Sohara Y, Sugiyama Y, Mano H: Identification of the transforming EML4-ALK fusion gene in non-small-cell lung cancer. Nature; 2007 Aug 2;448(7153):561-6
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] Identification of the transforming EML4-ALK fusion gene in non-small-cell lung cancer.
  • Improvement in the clinical outcome of lung cancer is likely to be achieved by identification of the molecular events that underlie its pathogenesis.
  • Here we show that a small inversion within chromosome 2p results in the formation of a fusion gene comprising portions of the echinoderm microtubule-associated protein-like 4 (EML4) gene and the anaplastic lymphoma kinase (ALK) gene in non-small-cell lung cancer (NSCLC) cells.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Cell Cycle Proteins / genetics. Cell Transformation, Neoplastic / genetics. Lung Neoplasms / genetics. Microtubule-Associated Proteins / genetics. Oncogene Proteins, Fusion / genetics. Oncogene Proteins, Fusion / metabolism. Protein-Tyrosine Kinases / genetics. Serine Endopeptidases / genetics
  • [MeSH-minor] 3T3 Cells. Amino Acid Sequence. Animals. Cell Proliferation / drug effects. Chromosome Inversion / genetics. Chromosomes, Human, Pair 2 / genetics. Humans. Mice. Molecular Sequence Data. Mutation / genetics. Receptor Protein-Tyrosine Kinases


65. Shinmura K, Kageyama S, Tao H, Bunai T, Suzuki M, Kamo T, Takamochi K, Suzuki K, Tanahashi M, Niwa H, Ogawa H, Sugimura H: EML4-ALK fusion transcripts, but no NPM-, TPM3-, CLTC-, ATIC-, or TFG-ALK fusion transcripts, in non-small cell lung carcinomas. Lung Cancer; 2008 Aug;61(2):163-9
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] EML4-ALK fusion transcripts, but no NPM-, TPM3-, CLTC-, ATIC-, or TFG-ALK fusion transcripts, in non-small cell lung carcinomas.
  • EML4-ALK gene fusions have recently been discovered in a subset of human lung carcinomas, and fusions of the ALK tyrosine kinase gene with the NPM, TPM3, CLTC, ATIC, and TFG genes have been found in hematological malignancies.
  • To elucidate the role of fusions between ALK and other genes in pulmonary carcinogenesis, we examined 77 non-small cell lung carcinomas (NSCLCs) for EML4-, NPM-, TPM3-, CLTC-, ATIC-, and TFG-ALK fusion transcripts by RT-PCR and subsequent sequencing analysis.
  • No somatic mutations were detected in the mutation cluster regions of the EGFR, K-RAS, and PIK3CA genes in these two carcinomas, however, a Pro177Ser mutation of the p53 gene was detected in the carcinoma that contained the variant 1 EML4-ALK fusion transcripts.
  • In situ PCR of a paraffin block section showed that the carcinoma with expression of the variant 1 actually contained an EML4-ALK fusion gene.
  • These results suggested that the EML4-ALK fusion gene product is involved in the carcinogenesis of a subset of NSCLCs.
  • [MeSH-major] Adenocarcinoma / genetics. Carcinoma, Non-Small-Cell Lung / genetics. Lung Neoplasms / genetics. Oncogene Proteins, Fusion / genetics


66. 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
COS Scholar Universe. author profiles.

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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Obstet Gynecol. 2002 Nov;100(5 Pt 2):1079-82 [12423812.001]
  • [Cites] J Chemother. 2003 Aug;15(4):406-8 [12962371.001]
  • [Cites] J Clin Oncol. 2007 Apr 20;25(12):1489-97 [17372278.001]
  • [Cites] Haematologica. 2008 Mar;93(3):398-404 [18268277.001]
  • [Cites] Am J Surg Pathol. 2002 May;26(5):630-6 [11979093.001]
  • [Cites] J Exp Clin Cancer Res. 1998 Jun;17(2):239-42 [9700587.001]
  • [Cites] Leuk Lymphoma. 1999 Mar;33(1-2):161-8 [10194134.001]
  • [Cites] Eur J Haematol. 2000 Aug;65(2):123-7 [10966173.001]
  • [Cites] Br J Cancer. 2001 Sep 28;85(7):997-1005 [11592772.001]
  • [Cites] Rinsho Ketsueki. 1986 Dec;27(12):2313-8 [3573322.001]
  • (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
  •  go-up   go-down


67. 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
Hazardous Substances Data Bank. CARBOPLATIN .

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

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. TAXOL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


68. Buendia AJ, Sánchez J, Martinez CM, Navarro JA: Immunohistochemical characterization of a pulmonary large-cell carcinoma in a dog. Vet Pathol; 2008 Jul;45(4):484-8
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] Immunohistochemical characterization of a pulmonary large-cell carcinoma in a dog.
  • Pulmonary large-cell carcinoma is considered extremely rare in domestic animals, and some of the few reported cases actually may have been cases of malignant pulmonary histiocytosis.
  • Histologically, pulmonary alveolar spaces contained clusters of large round anaplastic cells with ample eosinophilic cytoplasm and large irregularly shaped nuclei with prominent nucleoli.
  • Immunohistochemistry was used to distinguish large-cell carcinoma from malignant pulmonary histiocytosis.
  • Tumor cells had strong immunoreactivity for cytokeratin, consistent with epithelial origin.
  • However, a substantial percentage of the neoplastic cells co-expressed vimentin and MHC-II.
  • The type II alveolar epithelial cell was considered the cell of origin of the neoplasm based on the presence of lamellar bodies in some neoplastic cells and immunoreactivity for surfactant protein A and thyroid transcription factor-1.
  • [MeSH-major] Carcinoma, Large Cell / veterinary. Dog Diseases / pathology. Lung Neoplasms / veterinary

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18587094.001).
  • [ISSN] 0300-9858
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


69. 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
MedlinePlus Health Information. consumer health - Lung Diseases.

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

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


70. Lin JD, Chao TC: Follicular thyroid carcinoma: From diagnosis to treatment. Endocr J; 2006 Aug;53(4):441-8
SciCrunch. KEGG: Data: Disease Annotation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Follicular thyroid carcinoma: From diagnosis to treatment.
  • Unusual presentations with bone, lung or soft tissue metastases in initial diagnosis of follicular thyroid carcinoma have been reported occasionally.
  • This implies how difficult it is to diagnosis this type of cancer at the pre-operative or intra-operative stage of treatment.
  • Fine needle aspiration cytology has been shown to be an ineffective method for diagnosing vascular or capsule invasion of follicular thyroid cancer.
  • Although radioactive iodide (131I) has been used as the standard treatment for follicular thyroid carcinoma with distant metastases, the effectiveness of 131I treatment for follicular thyroid carcinoma depends on the differentiation of cancer cells.
  • The possibility of 131I for thyroid remnant ablation replacing a secondary operation for follicular thyroid carcinoma has been debated.
  • Recent studies applied more expressions of sodium iodide symporters to attain the effect of 131I treatment and slow the proliferation of thyroid cancer cell which, in turn, slows the progression of follicular carcinoma.
  • Consensus for the surgical procedures for the specific prognostic risks for follicular thyroid carcinoma is needed.
  • Dedifferentiated, anti-angiogenic, or gene therapies for follicular thyroid cancer with distant metastases or anaplastic transformation comprise the principal directions in future research for this cancer.
  • [MeSH-major] Adenocarcinoma, Follicular / diagnosis. Adenocarcinoma, Follicular / therapy. Thyroid Neoplasms / diagnosis. Thyroid Neoplasms / therapy
  • [MeSH-minor] Biomarkers, Tumor / analysis. Biopsy, Fine-Needle. Carcinoma, Papillary / diagnosis. Carcinoma, Papillary / pathology. Carcinoma, Papillary / therapy. Diagnostic Imaging. Humans. Iodine Radioisotopes / therapeutic use. Predictive Value of Tests. Thyroidectomy

  • MedlinePlus Health Information. consumer health - Thyroid Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16807500.001).
  • [ISSN] 0918-8959
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Iodine Radioisotopes
  • [Number-of-references] 72
  •  go-up   go-down


71. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [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

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


72. 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
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] 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

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


73. Kim IM, Ackerson T, Ramakrishna S, Tretiakova M, Wang IC, Kalin TV, Major ML, Gusarova GA, Yoder HM, Costa RH, Kalinichenko VV: The Forkhead Box m1 transcription factor stimulates the proliferation of tumor cells during development of lung cancer. Cancer Res; 2006 Feb 15;66(4):2153-61
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] The Forkhead Box m1 transcription factor stimulates the proliferation of tumor cells during development of lung cancer.
  • The proliferation-specific Forkhead Box m1 (Foxm1 or Foxm1b) transcription factor (previously called HFH-11B, Trident, Win, or MPP2) regulates expression of cell cycle genes essential for progression into DNA replication and mitosis.
  • Expression of Foxm1 is found in a variety of distinct human cancers including hepatocellular carcinomas, intrahepatic cholangiocarcinomas, basal cell carcinomas, ductal breast carcinomas, and anaplastic astrocytomas and glioblastomas.
  • In this study, we show that human Foxm1 protein is abundantly expressed in highly proliferative human non-small cell lung cancers (NSCLC) as well as in mouse lung tumors induced by urethane.
  • To determine the role of Foxm1 during the development of mouse lung tumors, we used IFN-inducible Mx-Cre recombinase transgene to delete mouse Foxm1 fl/fl-targeted allele before inducing lung tumors with urethane.
  • We show that Mx-Cre Foxm1-/- mice exhibit diminished proliferation of lung tumor cells causing a significant reduction in number and size of lung adenomas.
  • Transient transfection experiments with A549 lung adenocarcinoma cells show that depletion of Foxm1 levels by short interfering RNA caused diminished DNA replication and mitosis and reduced anchorage-independent growth of cell colonies on soft agar.
  • Foxm1-depleted A549 cells exhibit reduced expression of cell cycle-promoting cyclin A2 and cyclin B1 genes.
  • These data show that Foxm1 stimulates the proliferation of tumor cells during progression of NSCLC.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / pathology. Forkhead Transcription Factors / physiology. Lung Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / chemically induced. Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Alleles. Animals. Cell Adhesion. Cell Growth Processes / physiology. Cyclin A / biosynthesis. Cyclin A / genetics. Cyclin A2. Cyclin B / biosynthesis. Cyclin B / genetics. Cyclin B1. DNA Replication. DNA, Neoplasm / biosynthesis. Gene Deletion. Humans. Mice. Mice, Inbred C57BL. Mice, Transgenic. Mitosis. RNA, Small Interfering / genetics. Urethane

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ETHYL CARBAMATE .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16489016.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK 54687-06
  • [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 / CCNA2 protein, human; 0 / CCNB1 protein, human; 0 / Ccnb1 protein, mouse; 0 / Cyclin A; 0 / Cyclin A2; 0 / Cyclin B; 0 / Cyclin B1; 0 / DNA, Neoplasm; 0 / FOXM1 protein, human; 0 / Forkhead Transcription Factors; 0 / Foxm1 protein, mouse; 0 / RNA, Small Interfering; 3IN71E75Z5 / Urethane
  •  go-up   go-down


74. 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.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


75. Roberts PJ, Stinchcombe TE, Der CJ, Socinski MA: Personalized medicine in non-small-cell lung cancer: is KRAS a useful marker in selecting patients for epidermal growth factor receptor-targeted therapy? J Clin Oncol; 2010 Nov 1;28(31):4769-77
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Personalized medicine in non-small-cell lung cancer: is KRAS a useful marker in selecting patients for epidermal growth factor receptor-targeted therapy?
  • In patients with metastatic colorectal cancer, the predictive value of KRAS mutational status in the selection of patients for treatment with anti-epidermal growth factor (EGFR) monoclonal antibodies is established.
  • In patients with non-small-cell lung cancer (NSCLC), the utility of determining KRAS mutational status to predict clinical benefit to anti-EGFR therapies remains unclear.
  • Unlike colorectal cancer, KRAS mutations do not seem to identify patients who do not benefit from anti-EGFR monoclonal antibodies in NSCLC.
  • The future value of testing for KRAS mutational status may be to exclude the possibility of an EGFR mutation or anaplastic lymphoma kinase translocation or to identify a molecular subset of patients with NSCLC in whom to pursue a drug development strategy that targets the KRAS pathway.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Biomarkers, Tumor / metabolism. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Mutation. Precision Medicine. Proto-Oncogene Proteins / metabolism. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / metabolism. ras Proteins / metabolism
  • [MeSH-minor] Antibodies, Monoclonal / pharmacology. Antibodies, Monoclonal, Humanized. Carboplatin / pharmacology. Cell Cycle Proteins / genetics. Cetuximab. Cisplatin / pharmacology. Clinical Trials as Topic. Deoxycytidine / analogs & derivatives. Deoxycytidine / pharmacology. Erlotinib Hydrochloride. Humans. Microtubule-Associated Proteins / genetics. Paclitaxel / pharmacology. Patient Selection. Predictive Value of Tests. Protein-Tyrosine Kinases / genetics. Quinazolines / pharmacology. Receptor Protein-Tyrosine Kinases. Serine Endopeptidases / genetics. Signal Transduction. Survival Analysis. Translocation, Genetic

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. CETUXIMAB .
  • Hazardous Substances Data Bank. TAXOL .
  • Hazardous Substances Data Bank. CARBOPLATIN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20921461.001).
  • [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; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Cell Cycle Proteins; 0 / KRAS protein, human; 0 / Microtubule-Associated Proteins; 0 / Proto-Oncogene Proteins; 0 / Quinazolines; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; BG3F62OND5 / Carboplatin; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 3.4.21.- / EML4 protein, human; EC 3.4.21.- / Serine Endopeptidases; EC 3.6.5.2 / ras Proteins; P88XT4IS4D / Paclitaxel; PQX0D8J21J / Cetuximab; Q20Q21Q62J / Cisplatin; S65743JHBS / gefitinib
  •  go-up   go-down


76. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


77. Vassilatou E, Fisfis M, Morphopoulos G, Savva S, Voucouti E, Stefanoudaki K, Tzavara I: Papillary thyroid carcinoma producing granulocyte-macrophage colony-stimulating factor is associated with neutrophilia and eosinophilia. Hormones (Athens); 2006 Oct-Dec;5(4):303-9
MedlinePlus Health Information. consumer health - Thyroid Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Papillary thyroid carcinoma producing granulocyte-macrophage colony-stimulating factor is associated with neutrophilia and eosinophilia.
  • Thyroid tumors producing colony-stimulating factors associated with neutrophilia and/or eosinophilia are very rare and almost all of them concern anaplastic thyroid cancer.
  • Only one case of papillary thyroid carcinoma associated with neutrophilia and one case of medullary thyroid carcinoma associated with eosinophilia have been reported.
  • In this report a 72-year old male patient with metastatic papillary thyroid carcinoma associated with neutrophilia and eosinophilia is described.
  • While investigating the cause of neutrophilia and eosinophilia, a blind bone marrow biopsy of the posterior iliac crest was performed, which showed infiltration by papillary thyroid carcinoma.
  • As other causes of neutrophilia and eosinophilia were excluded, we assumed that these were paraneoplastic manifestations induced by GM-csF produced by the thyroid tumor. the disease progressed rapidly, despite appropriate treatment which included thyroidectomy and postoperative radioactive (131)I administration. the patient died 11 months after diagnosis because of extensive lung metastasis.
  • Neutrophilia and eosinophilia were stable findings, while serum thyroglobulin levels remained elevated throughout the follow-up period. to our knowledge, this is the first report of a patient with metastatic papillary thyroid carcinoma in whom neutrophilia and eosinophilia associated with high circulating levels of GM-csF were detected.
  • [MeSH-major] Carcinoma, Papillary / pathology. Eosinophils / pathology. Granulocyte-Macrophage Colony-Stimulating Factor / blood. Neutrophils / pathology. Thyroid Neoplasms / pathology
  • [MeSH-minor] Aged. Eosinophilia / diagnosis. Eosinophilia / etiology. Eosinophilia / pathology. Humans. Male

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17178706.001).
  • [ISSN] 1109-3099
  • [Journal-full-title] Hormones (Athens, Greece)
  • [ISO-abbreviation] Hormones (Athens)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
  •  go-up   go-down


78. Gurbuz Y, Kose N, Aydin O, Ozturk M: An immunohistochemical profile of giant cell carcinoma of the larynx. Auris Nasus Larynx; 2007 Sep;34(3):413-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An immunohistochemical profile of giant cell carcinoma of the larynx.
  • OBJECTIVE: This report describes a case of a 62-year-old male with giant cell carcinoma of the larynx that presented as a neck mass and hoarseness.
  • Microscopical examination showed that the tumor was composed of solid masses of anaplastic small cells with hyperchromatic nuclei.
  • There were multinucleated giant cells with huge nuclei, prominent nucleoli, and clear or eosinophylic cytoplasm.
  • The diagnosis of giant cell carcinoma of the larynx was made.
  • CONCLUSION: Giant cell carcinoma of the larynx is an extremely rare tumor the origin of which is not clearly understood.
  • It is believed to be the counterpart of giant cell carcinoma of the lung in larynx.
  • In conclusion, giant cell carcinoma of the larynx is confirmed to be a specific entity of simple epithelial origin and it is the counterpart of giant cell carcinoma of the lung.
  • [MeSH-major] Carcinoma, Giant Cell / pathology. Laryngeal Neoplasms / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17376621.001).
  • [ISSN] 0385-8146
  • [Journal-full-title] Auris, nasus, larynx
  • [ISO-abbreviation] Auris Nasus Larynx
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  •  go-up   go-down


79. Choi YL, Takeuchi K, Soda M, Inamura K, Togashi Y, Hatano S, Enomoto M, Hamada T, Haruta H, Watanabe H, Kurashina K, Hatanaka H, Ueno T, Takada S, Yamashita Y, Sugiyama Y, Ishikawa Y, Mano H: Identification of novel isoforms of the EML4-ALK transforming gene in non-small cell lung cancer. Cancer Res; 2008 Jul 1;68(13):4971-6
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] Identification of novel isoforms of the EML4-ALK transforming gene in non-small cell lung cancer.
  • The genome of a subset of non-small-cell lung cancers (NSCLC) harbors a small inversion within chromosome 2 that gives rise to a transforming fusion gene, EML4-ALK, which encodes an activated protein tyrosine kinase.
  • Although breakpoints within EML4 have been identified in introns 13 and 20, giving rise to variants 1 and 2, respectively, of EML4-ALK, it has remained unclear whether other isoforms of the fusion gene are present in NSCLC cells.
  • A lung cancer cell line expressing endogenous variant 3 of EML4-ALK underwent cell death on exposure to a specific inhibitor of ALK catalytic activity.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Cell Transformation, Neoplastic / genetics. Lung Neoplasms / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] 3T3 Cells. Amino Acid Sequence. Animals. Cell Death / drug effects. Cells, Cultured. Humans. Mice. Mice, Nude. Molecular Sequence Data. Protein Isoforms / genetics. Protein Isoforms / physiology. Protein Kinase Inhibitors / pharmacology. Protein-Tyrosine Kinases / antagonists & inhibitors. Protein-Tyrosine Kinases / metabolism. Receptor Protein-Tyrosine Kinases

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18593892.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / EML4-ALK fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Protein Isoforms; 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
  •  go-up   go-down


80. 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
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] 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


81. Wong DW, Leung EL, So KK, Tam IY, Sihoe AD, Cheng LC, Ho KK, Au JS, Chung LP, Pik Wong M, University of Hong Kong Lung Cancer Study Group: The EML4-ALK fusion gene is involved in various histologic types of lung cancers from nonsmokers with wild-type EGFR and KRAS. Cancer; 2009 Apr 15;115(8):1723-33
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] The EML4-ALK fusion gene is involved in various histologic types of lung cancers from nonsmokers with wild-type EGFR and KRAS.
  • BACKGROUND: The echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase (EML4-ALK) fusion gene resulting from the chromosome inversion inv(2)(p21;p23) recently was identified in nonsmall cell lung cancer (NSCLC).
  • METHODS: EML4-ALK was investigated in 266 resected primary NSCLC, including adenocarcinomas (AD), lymphoepithelioma-like carcinomas, squamous cell carcinomas, mucoepidermoid carcinomas, and adenosquamous carcinomas, by reverse transcriptase-polymerase chain reaction and was verified by sequencing.
  • Immunohistochemistry demonstrated diffuse ALK fusion proteins in the tumor cell cytoplasm.
  • The authors concluded that EML4-ALK may be useful for predicting the potential response to ALK inhibitors as a therapeutic option for patients with lung cancer.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Genes, ras. Lung Neoplasms / genetics. Oncogene Proteins, Fusion / genetics. Receptor, Epidermal Growth Factor / genetics. Smoking


82. Takeuchi K, Choi YL, Togashi Y, Soda M, Hatano S, Inamura K, Takada S, Ueno T, Yamashita Y, Satoh Y, Okumura S, Nakagawa K, Ishikawa Y, Mano H: KIF5B-ALK, a novel fusion oncokinase identified by an immunohistochemistry-based diagnostic system for ALK-positive lung cancer. Clin Cancer Res; 2009 May 1;15(9):3143-9
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] KIF5B-ALK, a novel fusion oncokinase identified by an immunohistochemistry-based diagnostic system for ALK-positive lung cancer.
  • PURPOSE: EML4-ALK is a transforming fusion tyrosine kinase, several isoforms of which have been identified in lung cancer.
  • Four tumors were also found to be positive for ALK in an archive of lung adenocarcinoma (n = 130) and another 4 among fresh cases analyzed in a diagnostic laboratory.
  • Multiplex reverse transcription-PCR analysis of additional archival tumor specimens identified another case of lung adenocarcinoma positive for KIF5B-ALK.
  • [MeSH-major] Adenocarcinoma / enzymology. Carcinoma, Non-Small-Cell Lung / enzymology. Kinesin / metabolism. Lung Neoplasms / enzymology. Oncogene Proteins, Fusion / metabolism. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] 3T3 Cells. Animals. Antibodies, Monoclonal. Cell Transformation, Neoplastic. Fibroblasts / cytology. Fibroblasts / metabolism. Genetic Variation. Humans. Immunoenzyme Techniques. Mice. Mice, Nude. Molecular Sequence Data. Polymers / chemistry. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptor Protein-Tyrosine Kinases. Reverse Transcriptase Polymerase Chain Reaction

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19383809.001).
  • [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
  • [Databank-accession-numbers] GENBANK/ AB462411/ AB462412/ AB462413
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / EML4-ALK fusion protein, human; 0 / KIF5B protein, human; 0 / Oncogene Proteins, Fusion; 0 / Polymers; 0 / RNA, Messenger; 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 3.6.1.- / Kinesin
  •  go-up   go-down


83. Sasaki T, Rodig SJ, Chirieac LR, Jänne PA: The biology and treatment of EML4-ALK non-small cell lung cancer. Eur J Cancer; 2010 Jul;46(10):1773-80
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] The biology and treatment of EML4-ALK non-small cell lung cancer.
  • The fusion between echinoderm microtubule-associated protein-like 4 (EML4) and anaplastic lymphoma kinase (ALK) has recently been identified in a subset of non-small cell lung cancers (NSCLCs).
  • EML4-ALK is most often detected in never smokers with lung cancer and has unique pathologic features.
  • This review will focus on the biology, clinical characteristics, diagnosis and treatment of EML4-ALK NSCLC.

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • [Cites] J Clin Oncol. 2008 Feb 20;26(6):983-94 [18281673.001]
  • [Cites] Mol Cancer Ther. 2007 Dec;6(12 Pt 1):3314-22 [18089725.001]
  • [Cites] Cancer Res. 2008 May 1;68(9):3389-95 [18451166.001]
  • [Cites] Br J Cancer. 2008 May 6;98(9):1536-9 [18414414.001]
  • [Cites] Cancer Res. 2008 Jul 1;68(13):4971-6 [18593892.001]
  • [Cites] Clin Cancer Res. 2008 Jul 1;14(13):4275-83 [18594010.001]
  • [Cites] Br J Cancer. 2008 Jul 22;99(2):245-52 [18594528.001]
  • [Cites] Lung Cancer. 2008 Aug;61(2):163-9 [18242762.001]
  • [Cites] Clin Cancer Res. 2008 Oct 15;14(20):6618-24 [18927303.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Dec 16;105(50):19893-7 [19064915.001]
  • [Cites] Am J Pathol. 2009 Feb;174(2):661-70 [19147828.001]
  • [Cites] Mod Pathol. 2009 Apr;22(4):508-15 [19234440.001]
  • [Cites] Cancer. 2009 Apr 15;115(8):1723-33 [19170230.001]
  • [Cites] Clin Cancer Res. 2009 May 1;15(9):3143-9 [19383809.001]
  • [Cites] Clin Cancer Res. 2009 Aug 15;15(16):5216-23 [19671850.001]
  • [Cites] N Engl J Med. 2009 Sep 3;361(10):947-57 [19692680.001]
  • [Cites] J Clin Oncol. 2009 Sep 10;27(26):4247-53 [19667264.001]
  • [Cites] Mol Cancer Res. 2009 Sep;7(9):1466-76 [19737969.001]
  • [Cites] Carcinogenesis. 2010 Jan;31(1):100-10 [19934210.001]
  • [Cites] Ann Surg Oncol. 2010 Mar;17(3):889-97 [20183914.001]
  • [Cites] Clin Cancer Res. 2010 Mar 1;16(5):1561-71 [20179225.001]
  • [Cites] J Thorac Oncol. 2008 Jan;3(1):13-7 [18166835.001]
  • [Cites] Am J Surg Pathol. 1999 Nov;23(11):1386-92 [10555007.001]
  • [Cites] Blood. 1999 Nov 1;94(9):3265-8 [10556217.001]
  • [Cites] Dev Cell. 2001 Jul;1(1):63-72 [11703924.001]
  • [Cites] Cancer. 2001 Sep 15;92(6):1525-30 [11745231.001]
  • [Cites] N Engl J Med. 2002 Jan 10;346(2):92-8 [11784875.001]
  • [Cites] Cancer Res. 2004 Oct 15;64(20):7241-4 [15492241.001]
  • [Cites] Clin Cancer Res. 2005 Feb 1;11(3):1167-73 [15709185.001]
  • [Cites] J Natl Cancer Inst. 2005 Mar 2;97(5):339-46 [15741570.001]
  • [Cites] Cancer Res. 2005 Mar 1;65(5):1642-6 [15753357.001]
  • [Cites] Cancer Res. 2005 Jun 15;65(12):5076-83 [15958551.001]
  • [Cites] Chest. 2005 Jul;128(1):317-21 [16002952.001]
  • [Cites] Clin Cancer Res. 2005 Oct 1;11(19 Pt 1):6816-22 [16203769.001]
  • [Cites] Int J Cancer. 2006 Feb 15;118(4):963-9 [16152581.001]
  • [Cites] Clin Cancer Res. 2006 Mar 1;12(5):1647-53 [16533793.001]
  • [Cites] Am J Surg Pathol. 2006 Oct;30(10):1309-15 [17001163.001]
  • [Cites] Cancer Res. 2007 Jun 15;67(12):5667-72 [17575133.001]
  • [Cites] Nature. 2007 Aug 2;448(7153):561-6 [17625570.001]
  • [Cites] Nat Rev Cancer. 2007 Oct;7(10):778-90 [17882278.001]
  • [Cites] Cell. 2007 Dec 14;131(6):1190-203 [18083107.001]
  • [Cites] Neoplasia. 2008 Mar;10(3):298-302 [18320074.001]
  • (PMID = 20418096.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA136851-02; United States / NCI NIH HHS / CA / R01 CA136851; United States / NCI NIH HHS / CA / R01 CA136851-02; United States / NCI NIH HHS / CA / R01CA136851
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / EML4-ALK fusion protein, human; 0 / Enzyme Inhibitors; 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
  • [Other-IDs] NLM/ NIHMS195408; NLM/ PMC2888755
  •  go-up   go-down


84. Solomon B, Varella-Garcia M, Camidge DR: ALK gene rearrangements: a new therapeutic target in a molecularly defined subset of non-small cell lung cancer. J Thorac Oncol; 2009 Dec;4(12):1450-4
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] ALK gene rearrangements: a new therapeutic target in a molecularly defined subset of non-small cell lung cancer.
  • Transforming rearrangements of the ALK (anaplastic lymphoma kinase) gene have recently been described in non-small cell lung cancer (NSCLC).
  • Although ALK gene rearrangements affect only about 4% of all lung cancers, they are more frequent in adenocarcinomas, in never or light smokers, and seem almost mutually exclusive with activating EGFR or KRAS mutations.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / genetics. Gene Rearrangement. Lung Neoplasms / genetics. Oncogene Proteins, Fusion / antagonists & inhibitors. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] J Thorac Oncol. 2012 Mar;7(3):482-4 [22334010.001]
  • (PMID = 20009909.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 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
  •  go-up   go-down


85. Mano H: Non-solid oncogenes in solid tumors: EML4-ALK fusion genes in lung cancer. Cancer Sci; 2008 Dec;99(12):2349-55
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] Non-solid oncogenes in solid tumors: EML4-ALK fusion genes in lung cancer.
  • However, chromosome translocations involving the e26 transformation-specific sequence transcription factor loci have been demonstrated recently in many prostate cancer cases.
  • Furthermore, through a functional screening with retroviral cDNA expression libraries, we have discovered the fusion-type protein tyrosine kinase echinoderm microtubule-associated protein like-4 (EML4)-anaplastic lymphoma kinase (ALK) in non-small cell lung cancer (NSCLC) specimens.
  • EML4-ALK oligomerizes constitutively in cells through the coiled coil domain within the EML4 region, and becomes activated to exert a marked oncogenicity both in vitro and in vivo.
  • Break and fusion points within the EML4 locus may diverge in NSCLC cells to generate various isoforms of EML4-ALK, which may constitute approximately 5% of NSCLC cases, at least in the Asian ethnic group.
  • In the present review I summarize how detection of EML4-ALK cDNA may become a sensitive diagnostic means for NSCLC cases that are positive for the fusion gene, and discuss whether suppression of ALK enzymatic activity could be an effective treatment strategy against this intractable disorder.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Lung Neoplasms / genetics. Neoplasms / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Carcinoma, Adenosquamous / genetics. Cell Transformation, Neoplastic. Chromosomes, Human, Pair 2. Exons. Gene Rearrangement. Humans. Male. Middle Aged. Models, Genetic. Translocation, Genetic

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19032370.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [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 / Oncogene Proteins, Fusion
  • [Number-of-references] 71
  •  go-up   go-down


86. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • The Weizmann Institute of Science GeneCards and MalaCards databases. gene/protein/disease-specific - MalaCards for large cell carcinoma .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


87. 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
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

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

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


88. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


89. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


90. Gressner O, Popp H, Mey U, Friedrichs N, Strehl J, Sauerbruch T, Schmidt-Wolf IG, Gorschlüter M: Long-term survival of a patient with small cell lung cancer after nine lines of chemotherapy and radiation. Onkologie; 2008 Sep;31(8-9):469-72
Hazardous Substances Data Bank. CARBOPLATIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term survival of a patient with small cell lung cancer after nine lines of chemotherapy and radiation.
  • BACKGROUND: Small cell lung cancer (SCLC) results in death within 1-2 months if left untreated.
  • CASE REPORT: We present a 52-year-old man with confirmed anaplastic SCLC who survived 10 years while receiving 9 lines of chemotherapy including high-dose chemotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Lung Neoplasms / drug therapy. Lung Neoplasms / radiotherapy. Small Cell Lung Carcinoma / drug therapy. Small Cell Lung Carcinoma / radiotherapy

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • Hazardous Substances Data Bank. Topotecan .
  • Hazardous Substances Data Bank. TAXOL .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2008 S. Karger AG, Basel.
  • (PMID = 18787355.001).
  • [ISSN] 1423-0240
  • [Journal-full-title] Onkologie
  • [ISO-abbreviation] Onkologie
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 6PLQ3CP4P3 / Etoposide; 7M7YKX2N15 / Topotecan; BG3F62OND5 / Carboplatin; P88XT4IS4D / Paclitaxel
  •  go-up   go-down


91. 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
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] 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

  • Genetic Alliance. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


92. Shaw AT, Yeap BY, Mino-Kenudson M, Digumarthy SR, Costa DB, Heist RS, Solomon B, Stubbs H, Admane S, McDermott U, Settleman J, Kobayashi S, Mark EJ, Rodig SJ, Chirieac LR, Kwak EL, Lynch TJ, Iafrate AJ: Clinical features and outcome of patients with non-small-cell lung cancer who harbor EML4-ALK. J Clin Oncol; 2009 Sep 10;27(26):4247-53
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] Clinical features and outcome of patients with non-small-cell lung cancer who harbor EML4-ALK.
  • PURPOSE: The EML4-ALK fusion oncogene represents a novel molecular target in a small subset of non-small-cell lung cancers (NSCLC).
  • Eighteen of the 19 EML4-ALK tumors were adenocarcinomas, predominantly the signet ring cell subtype.


93. 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
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] [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

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Metastatic cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


94. Sequist LV, Gettinger S, Senzer NN, Martins RG, Jänne PA, Lilenbaum R, Gray JE, Iafrate AJ, Katayama R, Hafeez N, Sweeney J, Walker JR, Fritz C, Ross RW, Grayzel D, Engelman JA, Borger DR, Paez G, Natale R: Activity of IPI-504, a novel heat-shock protein 90 inhibitor, in patients with molecularly defined non-small-cell lung cancer. J Clin Oncol; 2010 Nov 20;28(33):4953-60
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] Activity of IPI-504, a novel heat-shock protein 90 inhibitor, in patients with molecularly defined non-small-cell lung cancer.
  • We studied the activity of IPI-504 after epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) therapy in patients with advanced, molecularly defined non-small-cell lung cancer (NSCLC).
  • RESULTS: Seventy-six patients were enrolled between December 2007 and May 2009 from 10 United States cancer centers.
  • [MeSH-major] Benzoquinones / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. HSP90 Heat-Shock Proteins / antagonists & inhibitors. Lactams, Macrocyclic / therapeutic use. Lung Neoplasms / drug therapy

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20940188.001).
  • [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] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzoquinones; 0 / HSP90 Heat-Shock Proteins; 0 / Lactams, Macrocyclic; 4GY0AVT3L4 / tanespimycin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Other-IDs] NLM/ PMC4676802
  •  go-up   go-down


95. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Metastatic cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


96. Liang HH, Wu CH, Tam KW, Chai CY, Lin SE, Chen SC: Thyroid metastasis in a patient with hepatocellular carcinoma: case report and review of literature. World J Surg Oncol; 2007;5:144
MedlinePlus Health Information. consumer health - Thyroid Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Thyroid metastasis in a patient with hepatocellular carcinoma: case report and review of literature.
  • BACKGROUND: Despite the apparent low incidence of cancer metastatic to the thyroid, autopsy and clinical series suggest it is more common than generally.
  • Although lung, renal, and breast cancer are probably the most common primary sites, a number of cancers have been reported to metastasize to the thyroid synchronously with diagnosis of primary tumor or years after apparently curative treatment.
  • CASE PRESENTATION: We report a rare case of a hepatocellular carcinoma metasatic to the thyroid.
  • The patient presented seven months after original diagnosis and treatment with hepatic lobectomy with multiple neck lesions producing a mass effect on the trachea and bilateral lymphadenopathy.
  • Fine-needle aspiration revealed highly anaplastic carcinoma, and immunohistochemistry confirmed hepatocellular carcinoma.
  • CONCLUSION: Clinicians should consider the possibility of metastatic cancer in each patient who presents with a new thyroid mass, especially those with a history of cancer, however remote.
  • In cases where cytology or histology is not diagnostic, immunohistochemistry may be definitive in making the diagnosis.
  • [MeSH-major] Carcinoma / diagnosis. Carcinoma, Hepatocellular / secondary. Liver Neoplasms / pathology. Thyroid Neoplasms / secondary

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Int J Clin Oncol. 2004 Dec;9(6):515-9 [15616884.001]
  • [Cites] Ann Surg. 1960 Apr;151:551-61 [13820008.001]
  • [Cites] Thyroid. 1998 Feb;8(2):149-53 [9510123.001]
  • [Cites] Int J Clin Oncol. 2007 Feb;12(1):63-7 [17380445.001]
  • [Cites] Cancer. 1997 Feb 1;79(3):574-8 [9028370.001]
  • [Cites] Eur J Surg Oncol. 2004 Aug;30(6):583-8 [15256229.001]
  • [Cites] Radiat Med. 2001 Jan-Feb;19(1):43-6 [11305618.001]
  • [Cites] J Formos Med Assoc. 2001 Feb;100(2):106-12 [11393097.001]
  • [Cites] Am J Clin Pathol. 2002 Dec;118(6):911-21 [12472285.001]
  • [Cites] J Am Coll Surg. 2005 Feb;200(2):203-7 [15664095.001]
  • [Cites] Arch Pathol Lab Med. 1998 Jan;122(1):37-41 [9448014.001]
  • [Cites] Clin Endocrinol (Oxf). 2005 Feb;62(2):236-41 [15670202.001]
  • (PMID = 18157914.001).
  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2246133
  •  go-up   go-down


97. 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

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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


98. 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
antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).

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


99. 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
The Lens. Cited by Patents in .

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

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


100. Gerber DE, Minna JD: ALK inhibition for non-small cell lung cancer: from discovery to therapy in record time. Cancer Cell; 2010 Dec 14;18(6):548-51
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] ALK inhibition for non-small cell lung cancer: from discovery to therapy in record time.
  • It was only 3 years ago that an acquired translocation of EML4 with ALK leading to the expression of an EML4-ALK oncoprotein in non-small cell lung cancer (NSCLC) was reported.
  • Tumor cells expressing EML4-ALK are "addicted" to its continued function.






Advertisement