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13 results on '"Doodeman, V."'

5. Germline Tyms Genotype is Highly Predictive in Patients with Advanced Colorectal and Gastroesophageal Cancer Independent of Fluoropyrimidine Pharmacology: Results from Two Prospective Translational Studies

Author

Joerger, M., primary, Huitema, A.D.R., additional, Boot, H., additional, Cats, A., additional, Doodeman, V., additional, Smits, P., additional, Vainchtein, L., additional, Rosing, H., additional, Meijerman, I., additional, Zueger, M., additional, Cerny, T.T., additional, Beijnen, J.H.M., additional, and Schellens, J., additional

Published
2014
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6. FUS pathology defines the majority of tau-and TDP-43-negative frontotemporal lobar degeneration

Author

Urwin, H. (Hazel), Josephs, K.A. (Keith), Rohrer, J.D. (Jonathan), Mackenzie, I.R.A. (Ian), Neumann, H.A.M. (Martino), Authier, A. (Astrid), Seelaar, H. (Harro), Swieten, J.C. (John) van, Brown, J.M. (Jeremy), Johannsen, P. (Peter), Nielsen, J.E. (Jorgen), Holm, I.E. (Ida), Dickson, D. (Dennis), Rademakers, R. (Rosa), Graff-Radford, N.R. (Neill), Parisi, J.E. (Joseph), Petersen, R.C. (Ronald), Hatanpaa, K.J. (Kimmo), White III, C.L. (Charles), Geser, F. (Felix), Deerlin, V.M. (Vivianna), Weiner, M.F. (Myron), Trojanowski, J.Q. (John), Miller, B.L. (Bruce Lars), Seeley, W. (William), Zee, J. (Jill) van der, Kumar-Singh, S. (Samir), Engelborghs, S. (Sebastiaan), Deyn, P.P. (Peter) de, Broeckhoven, C. (Christine) van, Bigio, E.H. (Eileen), Deng, H-X. (Han-Xiang), Halliday, G.M. (Glenda Margaret), Kril, J.J. (Jillian), Munoz, D.G. (David), Mann, D. (David), Pickering-Brown, S. (Stuart), Doodeman, V. (Valerie), Adamson, G. (Gary), Ghazi-Noori, S. (Shabnam), Fisher, E.M.C. (Elizabeth), Holton, J.L. (Janice), Revesz, T. (Tamas), Rossor, M.N. (Martin), Collinge, J. (John), Mead, S. (Simon), Isaacs, A.M. (Adrian), Urwin, H. (Hazel), Josephs, K.A. (Keith), Rohrer, J.D. (Jonathan), Mackenzie, I.R.A. (Ian), Neumann, H.A.M. (Martino), Authier, A. (Astrid), Seelaar, H. (Harro), Swieten, J.C. (John) van, Brown, J.M. (Jeremy), Johannsen, P. (Peter), Nielsen, J.E. (Jorgen), Holm, I.E. (Ida), Dickson, D. (Dennis), Rademakers, R. (Rosa), Graff-Radford, N.R. (Neill), Parisi, J.E. (Joseph), Petersen, R.C. (Ronald), Hatanpaa, K.J. (Kimmo), White III, C.L. (Charles), Geser, F. (Felix), Deerlin, V.M. (Vivianna), Weiner, M.F. (Myron), Trojanowski, J.Q. (John), Miller, B.L. (Bruce Lars), Seeley, W. (William), Zee, J. (Jill) van der, Kumar-Singh, S. (Samir), Engelborghs, S. (Sebastiaan), Deyn, P.P. (Peter) de, Broeckhoven, C. (Christine) van, Bigio, E.H. (Eileen), Deng, H-X. (Han-Xiang), Halliday, G.M. (Glenda Margaret), Kril, J.J. (Jillian), Munoz, D.G. (David), Mann, D. (David), Pickering-Brown, S. (Stuart), Doodeman, V. (Valerie), Adamson, G. (Gary), Ghazi-Noori, S. (Shabnam), Fisher, E.M.C. (Elizabeth), Holton, J.L. (Janice), Revesz, T. (Tamas), Rossor, M.N. (Martin), Collinge, J. (John), Mead, S. (Simon), and Isaacs, A.M. (Adrian)

Abstract

Through an international consortium, we have collected 37 tau-and TAR DNA-binding protein 43 (TDP-43)-negative frontotemporal lobar degeneration (FTLD) cases, and present here the first comprehensive analysis of these cases in terms of neuropathology, genetics, demographics and clinical data. 92% (34/37) had fused in sarcoma (FUS) protein pathology, indicating that FTLD-FUS is an important FTLD subtype. This FTLD-FUS

Published
2010
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7. FUS pathology defines the majority of tau- and TDP-43-negative frontotemporal lobar degeneration

Author

Urwin, H, Josephs, KA, Rohrer, JD, Mackenzie, IR, Neumann, M (Manuela), Authier, A, Seelaar, Harro, van Swieten, J.C., Brown, JM, Johannsen, P, Nielsen, JE, Holm, IE, Dickson, DW, Rademakers, R, Graff-Radford, NR, Parisi, JE, Petersen, RC, Hatanpaa, KJ, White, CL, Weiner, MF, Geser, F, Van Deerlin, VM, Trojanowski, JQ, Miller, BL, Seeley, WW, Zee, JA, Kumar-Singh, S, Engelborghs, S, de Deyn, PP, van Broeckhoven, C, Bigio, EH, Deng, HX, Halliday, GM, Kril, JJ, Munoz, DG, Mann, DM, Pickering-Brown, SM, Doodeman, V, Adamson, G, Ghazi-Noori, S, Fisher, EMC, Holton, JL, Revesz, T, Rossor, MN, Collinge, J, Mead, S, Isaacs, AM, Urwin, H, Josephs, KA, Rohrer, JD, Mackenzie, IR, Neumann, M (Manuela), Authier, A, Seelaar, Harro, van Swieten, J.C., Brown, JM, Johannsen, P, Nielsen, JE, Holm, IE, Dickson, DW, Rademakers, R, Graff-Radford, NR, Parisi, JE, Petersen, RC, Hatanpaa, KJ, White, CL, Weiner, MF, Geser, F, Van Deerlin, VM, Trojanowski, JQ, Miller, BL, Seeley, WW, Zee, JA, Kumar-Singh, S, Engelborghs, S, de Deyn, PP, van Broeckhoven, C, Bigio, EH, Deng, HX, Halliday, GM, Kril, JJ, Munoz, DG, Mann, DM, Pickering-Brown, SM, Doodeman, V, Adamson, G, Ghazi-Noori, S, Fisher, EMC, Holton, JL, Revesz, T, Rossor, MN, Collinge, J, Mead, S, and Isaacs, AM

Abstract

Through an international consortium, we have collected 37 tau- and TAR DNA-binding protein 43 (TDP-43)-negative frontotemporal lobar degeneration (FTLD) cases, and present here the first comprehensive analysis of these cases in terms of neuropathology, genetics, demographics and clinical data. 92% (34/37) had fused in sarcoma (FUS) protein pathology, indicating that FTLD-FUS is an important FTLD subtype. This FTLD-FUS collection specifically focussed on aFTLD-U cases, one of three recently defined subtypes of FTLD-FUS. The aFTLD-U subtype of FTLD-FUS is characterised clinically by behavioural variant frontotemporal dementia (bvFTD) and has a particularly young age of onset with a mean of 41 years. Further, this subtype had a high prevalence of psychotic symptoms (36% of cases) and low prevalence of motor symptoms (3% of cases). We did not find FUS mutations in any aFTLD-U case. To date, the only subtype of cases reported to have ubiquitin-positive but tau-, TDP-43- and FUS-negative pathology, termed FTLD-UPS, is the result of charged multivesicular body protein 2B gene (CHMP2B) mutation. We identified three FTLD-UPS cases, which are negative for CHMP2B mutation, suggesting that the full complement of FTLD pathologies is yet to be elucidated.

Published
2010

9. Drug pathway–associated gene polymorphisms in patients with advanced non-small cell lung cancer receiving first-line platinum-gemcitabine combination chemotherapy: A prospective multicenter observational study.

Author

Joerger, M., primary, Burgers, S. A., additional, Baas, P., additional, Smit, E. F., additional, Haitjema, T. J., additional, Bard, M. P. L., additional, Doodeman, V. D., additional, Smits, P. H. M., additional, Vincent, A., additional, Huitema, A., additional, Beijnen, J. H., additional, and Schellens, J. H. M., additional

Published
2011
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10. Gene polymorphisms, pharmacokinetics, and hematological toxicity in advanced non-small-cell lung cancer patients receiving cisplatin/gemcitabine

Author

Joerger, M., primary, Burgers, J. A., additional, Baas, P., additional, Doodeman, V. D., additional, Smits, P. H. M., additional, Jansen, R. S., additional, Vainchtein, L. D., additional, Rosing, H., additional, Huitema, A. D. R., additional, Beijnen, J. H., additional, and Schellens, J. H. M., additional

Published
2011
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12. FUS pathology defines the majority of tau- and TDP-43-negative frontotemporal lobar degeneration.

Author

Urwin H, Josephs KA, Rohrer JD, Mackenzie IR, Neumann M, Authier A, Seelaar H, Van Swieten JC, Brown JM, Johannsen P, Nielsen JE, Holm IE, Dickson DW, Rademakers R, Graff-Radford NR, Parisi JE, Petersen RC, Hatanpaa KJ, White CL 3rd, Weiner MF, Geser F, Van Deerlin VM, Trojanowski JQ, Miller BL, Seeley WW, van der Zee J, Kumar-Singh S, Engelborghs S, De Deyn PP, Van Broeckhoven C, Bigio EH, Deng HX, Halliday GM, Kril JJ, Munoz DG, Mann DM, Pickering-Brown SM, Doodeman V, Adamson G, Ghazi-Noori S, Fisher EM, Holton JL, Revesz T, Rossor MN, Collinge J, Mead S, and Isaacs AM

Subjects
Adult, Age of Onset, DNA-Binding Proteins metabolism, Dyskinesias epidemiology, Female, Frontal Lobe metabolism, Frontotemporal Lobar Degeneration genetics, Hippocampus metabolism, Humans, Male, Mental Disorders epidemiology, Middle Aged, Mutation, Prevalence, RNA-Binding Protein FUS genetics, Sequence Analysis, DNA, tau Proteins metabolism, Frontotemporal Lobar Degeneration epidemiology, Frontotemporal Lobar Degeneration metabolism, RNA-Binding Protein FUS metabolism
Abstract

Through an international consortium, we have collected 37 tau- and TAR DNA-binding protein 43 (TDP-43)-negative frontotemporal lobar degeneration (FTLD) cases, and present here the first comprehensive analysis of these cases in terms of neuropathology, genetics, demographics and clinical data. 92% (34/37) had fused in sarcoma (FUS) protein pathology, indicating that FTLD-FUS is an important FTLD subtype. This FTLD-FUS collection specifically focussed on aFTLD-U cases, one of three recently defined subtypes of FTLD-FUS. The aFTLD-U subtype of FTLD-FUS is characterised clinically by behavioural variant frontotemporal dementia (bvFTD) and has a particularly young age of onset with a mean of 41 years. Further, this subtype had a high prevalence of psychotic symptoms (36% of cases) and low prevalence of motor symptoms (3% of cases). We did not find FUS mutations in any aFTLD-U case. To date, the only subtype of cases reported to have ubiquitin-positive but tau-, TDP-43- and FUS-negative pathology, termed FTLD-UPS, is the result of charged multivesicular body protein 2B gene (CHMP2B) mutation. We identified three FTLD-UPS cases, which are negative for CHMP2B mutation, suggesting that the full complement of FTLD pathologies is yet to be elucidated.

Published
2010
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13. Mitogen requirement for cell cycle progression in the absence of pocket protein activity.

Author

Foijer F, Wolthuis RM, Doodeman V, Medema RH, and te Riele H

Subjects
Animals, Apoptosis physiology, CDC2 Protein Kinase antagonists & inhibitors, CDC2 Protein Kinase drug effects, CDC2 Protein Kinase metabolism, Cell Cycle genetics, Cyclin A antagonists & inhibitors, Cyclin A metabolism, Cyclin B drug effects, Cyclin B metabolism, Cyclin B1, Cyclin-Dependent Kinase Inhibitor p21 pharmacology, Cyclin-Dependent Kinase Inhibitor p27 pharmacology, DNA Damage, Fibroblasts cytology, Fibroblasts metabolism, G1 Phase drug effects, G1 Phase physiology, G2 Phase drug effects, G2 Phase physiology, Mice, Mice, Knockout, Mitogens pharmacology, Neurons drug effects, Neurons physiology, Retinoblastoma Protein genetics, Retinoblastoma-Like Protein p107 genetics, Retinoblastoma-Like Protein p130 genetics, Tumor Suppressor Protein p53 metabolism, Cell Cycle drug effects, Cell Cycle physiology, Mitogens physiology, Retinoblastoma Protein physiology, Retinoblastoma-Like Protein p107 physiology, Retinoblastoma-Like Protein p130 physiology
Abstract

Primary mouse embryonic fibroblasts lacking expression of all three retinoblastoma protein family members (TKO MEFs) have lost the G1 restriction point. However, in the absence of mitogens these cells become highly sensitive to apoptosis. Here, we show that TKO MEFs that survive serum depletion pass G1 but completely arrest in G2. p21CIP1 and p27KIP1 inhibit Cyclin A-Cdk2 activity and sequester Cyclin B1-Cdk1 in inactive complexes in the nucleus. This response is alleviated by mitogen restimulation or inactivation of p53. Thus, our results disclose a cell cycle arrest mechanism in G2 that restricts the proliferative capacity of mitogen-deprived cells that have lost the G1 restriction point. The involvement of p53 provides a rationale for the synergism between loss of Rb and p53 in tumorigenesis.

Published
2005
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