Search Results - (Author, Cooperation:J. A. Foekens)
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1S. Nik-Zainal ; H. Davies ; J. Staaf ; M. Ramakrishna ; D. Glodzik ; X. Zou ; I. Martincorena ; L. B. Alexandrov ; S. Martin ; D. C. Wedge ; P. Van Loo ; Y. S. Ju ; M. Smid ; A. B. Brinkman ; S. Morganella ; M. R. Aure ; O. C. Lingjaerde ; A. Langerod ; M. Ringner ; S. M. Ahn ; S. Boyault ; J. E. Brock ; A. Broeks ; A. Butler ; C. Desmedt ; L. Dirix ; S. Dronov ; A. Fatima ; J. A. Foekens ; M. Gerstung ; G. K. Hooijer ; S. J. Jang ; D. R. Jones ; H. Y. Kim ; T. A. King ; S. Krishnamurthy ; H. J. Lee ; J. Y. Lee ; Y. Li ; S. McLaren ; A. Menzies ; V. Mustonen ; S. O'Meara ; I. Pauporte ; X. Pivot ; C. A. Purdie ; K. Raine ; K. Ramakrishnan ; F. G. Rodriguez-Gonzalez ; G. Romieu ; A. M. Sieuwerts ; P. T. Simpson ; R. Shepherd ; L. Stebbings ; O. A. Stefansson ; J. Teague ; S. Tommasi ; I. Treilleux ; G. G. Van den Eynden ; P. Vermeulen ; A. Vincent-Salomon ; L. Yates ; C. Caldas ; L. V. Veer ; A. Tutt ; S. Knappskog ; B. K. Tan ; J. Jonkers ; A. Borg ; N. T. Ueno ; C. Sotiriou ; A. Viari ; P. A. Futreal ; P. J. Campbell ; P. N. Span ; S. Van Laere ; S. R. Lakhani ; J. E. Eyfjord ; A. M. Thompson ; E. Birney ; H. G. Stunnenberg ; M. J. van de Vijver ; J. W. Martens ; A. L. Borresen-Dale ; A. L. Richardson ; G. Kong ; G. Thomas ; M. R. Stratton
Nature Publishing Group (NPG)
Published 2016Staff ViewPublication Date: 2016-05-03Publisher: Nature Publishing Group (NPG)Print ISSN: 0028-0836Electronic ISSN: 1476-4687Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsPublished by: -
2L. B. Alexandrov ; S. Nik-Zainal ; D. C. Wedge ; S. A. Aparicio ; S. Behjati ; A. V. Biankin ; G. R. Bignell ; N. Bolli ; A. Borg ; A. L. Borresen-Dale ; S. Boyault ; B. Burkhardt ; A. P. Butler ; C. Caldas ; H. R. Davies ; C. Desmedt ; R. Eils ; J. E. Eyfjord ; J. A. Foekens ; M. Greaves ; F. Hosoda ; B. Hutter ; T. Ilicic ; S. Imbeaud ; M. Imielinski ; N. Jager ; D. T. Jones ; D. Jones ; S. Knappskog ; M. Kool ; S. R. Lakhani ; C. Lopez-Otin ; S. Martin ; N. C. Munshi ; H. Nakamura ; P. A. Northcott ; M. Pajic ; E. Papaemmanuil ; A. Paradiso ; J. V. Pearson ; X. S. Puente ; K. Raine ; M. Ramakrishna ; A. L. Richardson ; J. Richter ; P. Rosenstiel ; M. Schlesner ; T. N. Schumacher ; P. N. Span ; J. W. Teague ; Y. Totoki ; A. N. Tutt ; R. Valdes-Mas ; M. M. van Buuren ; L. van 't Veer ; A. Vincent-Salomon ; N. Waddell ; L. R. Yates ; J. Zucman-Rossi ; P. A. Futreal ; U. McDermott ; P. Lichter ; M. Meyerson ; S. M. Grimmond ; R. Siebert ; E. Campo ; T. Shibata ; S. M. Pfister ; P. J. Campbell ; M. R. Stratton
Nature Publishing Group (NPG)
Published 2013Staff ViewPublication Date: 2013-08-16Publisher: Nature Publishing Group (NPG)Print ISSN: 0028-0836Electronic ISSN: 1476-4687Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsKeywords: Aging/genetics ; Algorithms ; Cell Transformation, Neoplastic/*genetics/pathology ; Cytidine Deaminase/genetics ; DNA/genetics/metabolism ; DNA Mutational Analysis ; Humans ; Models, Genetic ; Mutagenesis/*genetics ; Mutagenesis, Insertional/genetics ; Mutagens/pharmacology ; Mutation/*genetics ; Neoplasms/enzymology/*genetics/pathology ; Organ Specificity ; Reproducibility of Results ; Sequence Deletion/genetics ; Transcription, Genetic/geneticsPublished by: -
3J. M. Tubio ; Y. Li ; Y. S. Ju ; I. Martincorena ; S. L. Cooke ; M. Tojo ; G. Gundem ; C. P. Pipinikas ; J. Zamora ; K. Raine ; A. Menzies ; P. Roman-Garcia ; A. Fullam ; M. Gerstung ; A. Shlien ; P. S. Tarpey ; E. Papaemmanuil ; S. Knappskog ; P. Van Loo ; M. Ramakrishna ; H. R. Davies ; J. Marshall ; D. C. Wedge ; J. W. Teague ; A. P. Butler ; S. Nik-Zainal ; L. Alexandrov ; S. Behjati ; L. R. Yates ; N. Bolli ; L. Mudie ; C. Hardy ; S. Martin ; S. McLaren ; S. O'Meara ; E. Anderson ; M. Maddison ; S. Gamble ; C. Foster ; A. Y. Warren ; H. Whitaker ; D. Brewer ; R. Eeles ; C. Cooper ; D. Neal ; A. G. Lynch ; T. Visakorpi ; W. B. Isaacs ; L. van't Veer ; C. Caldas ; C. Desmedt ; C. Sotiriou ; S. Aparicio ; J. A. Foekens ; J. E. Eyfjord ; S. R. Lakhani ; G. Thomas ; O. Myklebost ; P. N. Span ; A. L. Borresen-Dale ; A. L. Richardson ; M. Van de Vijver ; A. Vincent-Salomon ; G. G. Van den Eynden ; A. M. Flanagan ; P. A. Futreal ; S. M. Janes ; G. S. Bova ; M. R. Stratton ; U. McDermott ; P. J. Campbell
American Association for the Advancement of Science (AAAS)
Published 2014Staff ViewPublication Date: 2014-08-02Publisher: American Association for the Advancement of Science (AAAS)Print ISSN: 0036-8075Electronic ISSN: 1095-9203Topics: BiologyChemistry and PharmacologyComputer ScienceMedicineNatural Sciences in GeneralPhysicsKeywords: Carcinogenesis/genetics ; Chromatin/chemistry ; *DNA Transposable Elements ; Exons ; Genome, Human ; Humans ; *Long Interspersed Nucleotide Elements ; Mutagenesis, Insertional ; Neoplasms/*genetics ; *Transduction, Genetic ; Translocation, GeneticPublished by: -
4KLIJN, J. G. M. ; BERNS, P. M. J. J. ; BONTENBAL, M. ; FOEKENS, J. A.
Oxford, UK : Blackwell Publishing Ltd
Published 1993Staff ViewISSN: 1749-6632Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: Natural Sciences in GeneralType of Medium: Electronic ResourceURL: -
5Salden, M. ; Splinter, T. A. W. ; Peters, H. A. ; Look, M. P. ; Timmermans, M. ; van Meerbeeck, J. P. A. M. ; Foekens, J. A.
Springer
Published 2000Staff ViewISSN: 1569-8041Keywords: non-small-cell lung cancer ; PAI-1 ; PAI-2 ; uPA ; uPARSource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Abstract Background:Urokinase-type plasminogen activator (uPA), itsreceptor (uPAR) and plasminogen activator inhibitors (PAI-1 and PAI-2), allplay important roles in tumour invasion and metastasis. The tumour levels ofthe components of the urokinase-type plasminogen activator system (uPA-system)may help to identify individuals with a poor prognosis in postoperativenon-small-cell lung cancer (NSCLC) patients. Patients and methods:The levels of uPA, uPAR PAI-1 and PAI-2 weremeasured by enzyme-linked immunosorbent assay (ELISA) in triton-extracts,prepared from 88 NSCLC tissues (stage I–IIIa) and 74 normal lung tissuesfrom the same patients. Results:The expression levels of uPA, uPAR, PAI-1 and PAI-2 weresignificantly higher in tumour tissues as compared to their normal equivalents(all, P 〈 0.0001). Significant relations were found between genderand uPA (P = 0.04) or uPAR (P 〈 0.001), and between PAI-2and pathological stage (P = 0.03). For none of the studied factorsof the uPA-system a significant relation with survival was found, neither inall patients, nor in the subgroups of patients with squamous-cell lungcarcinoma or adenocarcinoma. Conclusions:The expression levels of the components of theuPA-system were higher in NSCLC tissue as compared to normal lung tissue, butthere were no significant relationships between their levels and survival.Type of Medium: Electronic ResourceURL: -
6Henzen-Logmans, S. C. ; Burg, M. E. L. ; Foekens, J. A. ; Berns, P. M. J. J. ; Brussée, R. ; Fieret, J. H. ; Klijn, J. G. M. ; Chadha, S. ; Rodenburg, C. J.
Springer
Published 1992Staff ViewISSN: 1432-1335Keywords: EGF receptors ; Immunohistochemistry ; Ovarian carcinomasSource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Summary Epidermal growth factor receptor (EGF-R) was studied with monoclonal antibody 2E9 on 50 ovarian tumors of various histological types and 10 non-tumorous ovarian tissues by immunohistochemistry. Enhanced expression was observed in 26/50 (52%) of the tumors. Only 25 out of 46 epithelial tumors (54%) showed positivity in epithelial tumor cells. Staining was cytoplasmic in all cases. No correlation was established between EGF-R expression and the histological type of the epithelial tumor. Apart from EGF-R expression in tumor cells, low immunoreactivity was also observed in stromal and endothelial cells in both normal and tumorous ovarian tissues. Furthermore in 8/9 specimens containing necrotic areas, EGF-R was noticed in these areas as well. Both of the latter observations may have impact on the evaluation of the prognostic value of EGF-R activity in tumors, when based on EGF-R measurements using biochemical binding studies. We therefore recommend that EGF-R is measured with both methods in studies regarding its clinical value.Type of Medium: Electronic ResourceURL: -
7Bakker, G. H. ; Setyono-Han, B. ; Foekens, J. A. ; Portengen, H. ; Putten, W. L. J. ; Jong, F. H. ; Lamberts, S. W. J. ; Reubi, J. C. ; Klijn, J. G. M.
Springer
Published 1990Staff ViewISSN: 1573-7217Keywords: buserelin ; LHRH-agonists ; rat mammary tumor ; sandostatin ; somatostatin analogsSource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Summary The effects of treatment with a somatostatin analog (Sandostatin, SMS201-995) were investigated in female rats with dimethylbenzanthracene(DMBA)-induced rat mammary tumors. A 3-week treatment was performed using sandostatin, the LHRH-agonist buserelin alone, or buserelin in combination with sandostatin. Twice daily sandostatin treatment was performed with dosages of 0.05 µg, 0.2 µg, 1 µg, 5 µg, and 20 µg. Buserelin was used in a 2 × 5 µg/day dosage. The combined results from six different experiments show that the various dosages of sandostatin caused no tumor growth inhibition. Somatostatin receptors could not be demonstrated in these mammary tumors. Sandostatin treatment by daily injections did not suppress levels of growth hormone, prolactin, or epidermal growth factor-like activities. Estrogen (ER) and progesterone (PgR) receptor contents of the mammary tumors were not changed. In contrast, buserelin treatment caused highly significant tumor remission. The combined treatment with sandostatin and buserelin did not alter the treatment results obtained after treatment with buserelin alone. In conclusion, sandostatin treatment in this tumor model had no direct growth inhibitory effect and did not cause an endocrine inhibition of mammary tumor growth. However, these results do not exclude antitumor effects in human breast cancer in view of the presence of somatostatin receptors in approximately 20–45% of human tumors, besides possible different endocrine effects.Type of Medium: Electronic ResourceURL: -
8Rutteman, G. R. ; Foekens, J. A. ; Portengen, H. ; Vos, J. H. ; Blankenstein, M. A. ; Teske, E. ; Cornelisse, C. J. ; Misdorp, W.
Springer
Published 1994Staff ViewISSN: 1573-7217Keywords: dog ; epidermal growth factor receptor ; mammary gland ; mammary tumour ; steroid receptorSource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Summary Epidermal growth factor (EGFR), oestrogen (ER), and progestin (PR) receptor concentrations were determined by radioligand binding assay in non-affected mammary tissues (n = 13) and benign (n = 11) and primary/locally recurrent malignant proliferative mammary lesions (n = 45) and metastases (n = 19) in 65 female dogs. The number of specimens expressing EGFR was not significantly different among these tissues, but EGFR concentration was lower in metastases (P = 0.02) than in benign or primary/locally recurrent malignant lesions not mixed with non-affected mammary tissue. The presence of non-affected mammary tissue in primary cancer specimens was noticed as a factor that may influence results of receptor measurements. No relation was found between the expression of EGFR and that of ER or PR in non-affected or in tumorous mammary tissues. It was concluded that in the dog mammary gland EGFR expression is not associated with conditions of steroid receptor absence or biological agressiveness of neoplastic growth.Type of Medium: Electronic ResourceURL: