Zobrazeno 1 - 10
of 15
pro vyhledávání: '"Sanne Huijberts"'
Autor:
Frans L. Opdam, Robin M. J. M. van Geel, Neeltje Steeghs, Emilie M.J. van Brummelen, Alwin D. R. Huitema, Serena Marchetti, Jos H. Beijnen, Jan H.M. Schellens, Sanne Huijberts, Hilde Rosing, Kim Monkhorst, Saskia M. Pulleman, Bas Thijssen, René Bernards
Publikováno v:
Cancer Chemotherapy and Pharmacology, 85(5), 917-930. Springer Verlag
Purpose KRAS oncogene mutations cause sustained signaling through the MAPK pathway. Concurrent inhibition of MEK, EGFR, and HER2 resulted in complete inhibition of tumor growth in KRAS-mutant (KRASm) and PIK3CA wild-type tumors, in vitro and in vivo.
Autor:
Hilde Rosing, Jan H.M. Schellens, Jos H. Beijnen, Sofie Wilgenhof, Sanne Huijberts, Bastiaan Nuijen, Rodrigo Leite de Oliveira, René Bernards, Liqin Wang
Publikováno v:
Future Oncology. 16:619-629
The clinical benefit of treatment with BRAF- and MEK-inhibitors in melanoma is limited due to resistance associated with emerging secondary mutations. Preclinical and clinical studies have shown that short-term treatment with the HDAC inhibitor vorin
Publikováno v:
Future Oncology, 16(6), 161-174. Future Medicine Ltd.
Approximately 10–15% of colorectal cancers (CRCs) harbor an activating BRAF mutation, leading to tumor growth promotion by activation of the mitogen-activated protein kinases pathway. BRAFV600E mutations are prognostic for treatment failure after f
Autor:
Filip De Vos, Ferry A.L.M. Eskens, Martijn P. Lolkema, Bas Thijssen, Robin van Geel, Neeltje Steeghs, Emilie M.J. van Brummelen, Serena Marchetti, Lot A. Devriese, René Bernards, Frans L. Opdam, Alwin D. R. Huitema, Hilde Rosing, Jan H.M. Schellens, Kim Monkhorst, Jos H. Beijnen, Sanne Huijberts
Publikováno v:
British Journal of Cancer, 122(8), 1166. Nature Publishing Group
British Journal of Cancer
British Journal of Cancer, 122(8), 1166-1174. Nature Publishing Group
British Journal of Cancer
British Journal of Cancer, 122(8), 1166-1174. Nature Publishing Group
Background Mutations in KRAS result in a constitutively activated MAPK pathway. In KRAS-mutant tumours existing treatment options, e.g. MEK inhibition, have limited efficacy due to resistance through feedback activation of epidermal growth factor rec
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::93b187e3733cbb74ac196b6f9e85915e
https://dspace.library.uu.nl/handle/1874/411157
https://dspace.library.uu.nl/handle/1874/411157
Autor:
Sanne, Huijberts, Liqin, Wang, Rodrigo Leite, de Oliveira, Hilde, Rosing, Bastiaan, Nuijen, Jos, Beijnen, Rene, Bernards, Jan, Schellens, Sofie, Wilgenhof
Publikováno v:
Future oncology (London, England). 16(11)
The clinical benefit of treatment with BRAF- and MEK-inhibitors in melanoma is limited due to resistance associated with emerging secondary mutations. Preclinical and clinical studies have shown that short-term treatment with the HDAC inhibitor vorin
Autor:
Sanne Huijberts, R.M.J.M. van Geel, J.H.M. Schellens, Frans L. Opdam, Hilde Rosing, Kim Monkhorst, René Bernards, A. D. R. Huitema, E. van Brummelen, Serena Marchetti, J. H. Beijnen, Neeltje Steeghs, Saskia M. Pulleman, Bas Thijssen
Publikováno v:
Annals of Oncology. 30:v178-v179
Background KRAS oncogene mutations are causing sustained signaling through the mitogen-activated protein kinase (MAPK) pathway resulting in uncontrolled cell growth. Efforts to target KRAS directly or to inhibit downstream effectors have been unsucce
Autor:
J.H.M. Schellens, Sofie Wilgenhof, René Bernards, Sanne Huijberts, Hilde Rosing, J. H. Beijnen, Bastiaan Nuijen, R Leite de Oliveira, Liqin Wang
Publikováno v:
Annals of Oncology. 30:v561-v562
Background The clinical benefit of combined treatment with BRAF- and MEK-inhibitors (BRAFi; MEKi) in BRAFV600 mutant (BRAFm) melanoma is limited due to resistance after 6-14 months, associated with emerging secondary mutations. Withholding of treatme
Autor:
Neeltje Steeghs, Jan H.M. Schellens, Kim Monkhorst, Emilie M.J. van Brummelen, Bas Thijssen, René Bernards, Jos H. Beijnen, Robin van Geel, Hilde Rosing, Sanne Huijberts, Ingrid M.E. Desar, Alwin D. R. Huitema, Serena Marchetti, Carla M.L. van Herpen, Frans L. Opdam
Publikováno v:
Oncologist, 26, 4, pp. 290-e545
Oncologist, 26, 290-e545
Oncologist
Oncologist, 26(4), 290-e545. AlphaMed Press
Oncologist, 26, 290-e545
Oncologist
Oncologist, 26(4), 290-e545. AlphaMed Press
Lessons Learned Afatinib and selumetinib can be combined in continuous and intermittent dosing schedules, albeit at lower doses than approved for monotherapy. Maximum tolerated dose for continuous and intermittent schedules is afatinib 20 mg once dai
Publikováno v:
Palliative Medicine, 30(1), 75-82. SAGE Publications Inc.
Palliative medicine, 30(1), 75-82. SAGE Publications Ltd
Palliative medicine, 30(1), 75-82. SAGE Publications Ltd
Background: Many patients show deterioration in functioning and increased care needs in the last year of life. End-of-life care needs and health care utilization might differ between groups of acutely hospitalized older patients. Aim: To investigate
Autor:
Bas Thijssen, Alwin D. R. Huitema, Neeltje Steeghs, Emilie M.J. van Brummelen, Jan H.M. Schellens, Carla M.L. van Herpen, Serena Marchetti, Jos H. Beijnen, Robin van Geel, Kim Monkhorst, Sanne Huijberts, Ingrid M.E. Desar, René Bernards, Hilde Rosing, Frans L. Opdam
Publikováno v:
Journal of Clinical Oncology. 38:3613-3613
3613 Background: Mutations in the KRAS gene result in a constitutively activated RAS-RAF-MEK-ERK (MAPK) pathway. In KRAS mutant tumors, the anti-tumor activity of MEK inhibitors is limited due to intrinsic resistance caused by feedback activation of