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102. Microenvironment involved in FPR1 expression by human glioblastomas

Author

MMB Research line 1, Infection & Immunity, Boer, J. C., van Marion, D. M S, Joseph, J. V., Kliphuis, N. M., Timmer-Bosscha, H., van Strijp, J. A G, de Vries, E. G E, den Dunnen, W. F A, Kruyt, F. A E, Walenkamp, A. M E, MMB Research line 1, Infection & Immunity, Boer, J. C., van Marion, D. M S, Joseph, J. V., Kliphuis, N. M., Timmer-Bosscha, H., van Strijp, J. A G, de Vries, E. G E, den Dunnen, W. F A, Kruyt, F. A E, and Walenkamp, A. M E

Published
2015

103. Other Radiopharmaceuticals for Imaging GEP‐NET

Author

Hubalewska‐Dydejczyk, Alicja, Signore, Alberto, de Jong, Marion, Dierckx, Rudi A., Buscombe, John, Van de Wiele, Christophe, Koopmans, K P, Dierckx, Rudi, Elsinga, Philip H., Links, Thera, Kema, Ido, Fiebrich, Helle Brit, Walekamp, A M E, de Vries, E. G. E., Brouwers, Adrienne, Hubalewska‐Dydejczyk, Alicja, Signore, Alberto, de Jong, Marion, Dierckx, Rudi A., Buscombe, John, Van de Wiele, Christophe, Koopmans, K P, Dierckx, Rudi, Elsinga, Philip H., Links, Thera, Kema, Ido, Fiebrich, Helle Brit, Walekamp, A M E, de Vries, E. G. E., and Brouwers, Adrienne

Abstract

In GEP‐NETs, especially the catecholamine and serotonin biosynthetic pathways are upregulated. Therefore, increased biosynthesis of these specific amines in GEP‐NETs enables imaging with specific amine precursors. For the catecholamine pathway, 6‐18F ‐l‐3,4‐dihydroxyphenylalanine (18F‐DOPA) is available, while for the serotonin pathway, carbon‐11‐labeled 5‐hydroxy‐l‐tryptophan ([11C]‐5‐HTP) is available as tracer. 11C‐5‐HTP PET and 18F‐DOPA PET are excellent functional imaging techniques for evaluating patients with proven pancreatic islet cell tumors and carcinoids. For both tracers, the combination with CT further improves the detection rate of NET, which shows that performing PET scans with these tracers in PET/CT scanners is beneficial for patients. Since well‐differentiated GEP‐NETs generally have a low glucose metabolism, 18F‐fluorodexyglucose (18F‐FDG) PET scanning has limited value for the primary staging of patients with well‐differentiated GEP‐NETs. However, in patients with rapidly progressive disease, dedifferentiation of GEP‐NET tumors can lead to a higher glucose metabolism in tumor cells. In these patients, 18F‐FDG PET can be of benefit for tumor staging. Also, 18F‐FDG PET can be of value when other malignancies are suspected in patients with GEP‐NETs, since these patients experience a higher incidence of these malignancies compared to the general population. Nowadays, (GEP)‐NETs can also be imaged with 68Ga‐labeled analogues of somatostatin, which are also PET tracers. Advantages of 68Ga‐labeled somatostatin analogues are the relatively easy generator‐based synthesis and the possibility to evaluate whether peptide (somatostatin) receptor radionuclide therapy (PRRT) for NETs can be considered.

Published
2015

106. Abstracts of papers clinical pharmacological meeting

Author

Merkus, F. W. H. M., Gribnau, F. W. J., Thien, Th., Louwerenburg, Hans W., Kingma, J. Herre, van Gilst, Wiek H., Six, A. Jacob, de Graeff, Pieter, Wesseling, Harry, BoeLaert, J. R., Schurgers, M. L., Matthys, E. G., Belpaire, F., Daneels, R. F., de Cre, M. J., Boqaert, M. G., D'Haese, P. C., Verpooten, G. A., Lamberts, L. V., Liang, L., de Broe, M. E., de Meijer, P. H. E. M., Russel, F. G. M., Russel, A. J. M., van Ginneken, C. A. M., van Liedekerke, B. M., Lambert, W. E., Yousouf, M. A., de Roose, J. E., de Leenheer, A. P., Lambert, W., de Bersaques, J., Vanneste, L., de Leenheer, A., de Marie, S., Slaghuis, G., Rozing, P. M., Mattie, H., Poelma, F. G. J., Hilbers, H. W., Jansen, A. C. A., Tukker, J. J., Augusti, Jr, P., Verbeke, N., van Peer, A., Snoeck, E., Heykants, J., Bruynseels, J., Peeters, J., Amery, W., Rogiers, V., Vandenberghe, Y., Comet, M., Callaerts, A., Sonck, W., Guillouzo, A., Vercruysse, A., van Rooy, P., Rombaut, N., vanden Bussche, G., Tan, A. C. I. T. L., Jansen, T. L. Th. A., Termond, E. F. S., Kloppenborg, P. W. C., Thien, Th., Benraad, Th. J., van de Velde, V., Woestenbprghs, R., Hermens, W. A. J. J., Romeijn, S. G., Deurloo, M. J. M., Merkus, F. W. H. M., Musch, G., Massart, D. L., van Hengstum, M., Festen, J., van den Broek, W., Corstens, F., Beurskens, C., Hankel, M., de Smet, M., van Belle, S. J. P., de May, J., Storme, G. A., Kuppen, P. J. K., Schuitemaker, H., Veer, L. J. van't, van Oosterom, A. T., Schrier, P. I., de Bruijn, E. A., de Pooter, C. H., Tjaden, U. R., van Slooten, H., Roelevink, H. P., Smit, E., de Vries, E. G. E., Ijmker, J., Uges, D. R. A., Moors, M., Mertens, K., van Hecken, A., de Lepeleire, I., Verbesselt, R., Tjandra-Maga, T. B., de Schepper, P. J., Guelen, P. J. M., Jansen, T. J., Vrijhof, W. P., de Vos, D., Scharpé, S., Verkerk, R., Lsmeire, N., Zijlstra, I. F., Gribnau, F. W. J., Haaijer-Ruskamp, F. M., Post, D., Reddingius, P. F., Wesseling, H., Wollersheim, H. C. H., van den Meiracker, A. H., Veld, A. J. Man in 't, Admiraal, P., Boomsma, F., Derkx, F., Schalekamp, M. A. D. H., Schoors, D. F., Dupont, A. G., Claessen, F., Reljenga, J., Lenders, J. W. M., Thlen, Th., Laekeman, G., Muylle, L., van Hoydonck, A., Herman, A. G., and Peetermans, M. E.

Published
1988
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110. Abstracts of papers clinical pharmacological meeting

Author

van den Ouweland, F. A., Eenhoorn, P. C., Tan, Y., Gribnau, F. W. J., van Brupgen, A., de Graeff, P. A., van den Toren, E. W., van Gilst, W. H., Wesseling, H., Lie, K. I., Postula, C. T., Hoefnagels, W. B. L., de Boo, Th., Thien, Th., Boon E. S., Goyskes, C. G., Boor, P., van Schalk, B. A. M., Abma, C., Frijns, T. R. J. A., Wamer, J., Elving, L. D., de Nobel, E., Mattie, H., van Gulpen, C., Lammers, J-W. J., Minette, P., Barnes, P. J., Jongejan, R. C., de Jongste, J. C., Raatgeep, H. C., Bonta, I. L., Kerrebijn, K. F., Mol, M. J., Stalenhoef, A. F., Stuyt, P. M., van 't Laar, A., Ermens, A. A. M., Schoester, M., Lindemans, J., Abels, J., van Baak, M. A., Mooij, J. M. V., Schiffers, P. M. H., Wetzels, J. F. M., v. Berqeyk, J. D., v. Heusden, F. H. J. A., Huysmans, F. Th. M., Hoitsma, A. J., Koene, R. A. P., Jansen, H. M. L., Russel, F. G. M., Wouterse, A. C., van Ginneken, C. A. M., Pol, Y. W. A. v. d., de Vries, E. G. E., Greidanus, J., Mulder, N. H., Sleijfer, D. Th., Willemse, P. H. B., Uges, D. R. A., Smits, P. A. B. M., Louwerenburg, J. W., Kingma, J. H., IJdenberg, F. N., Poelma, F. G. J., Breŝ, R., Tukker, J. J., Remmert, H. P., Olling, M., Slob, W., van der Giesen, W., Rauws, A. G., Runhaar, E. A., Neijt, J. P., Holthuis, J. J. M., de Vos, D., Tukker, J J, Poelma, F G J, Thijssen, H. H. W., Hamulyák, K., Franssen, C., Wollersheim, H., Jansen, R. W. M. M., van Lier, H. J. J., Hoefnagels, W. H. L., Grgen, C., Horan, M-A., Oomerjee, Z. A. R., Breimer, D. D., van Bezooijen, C. F. A., Keizer, H. J., Cleton, F. J., de Bruijn, E. A., Tiaden, U. R., de Boer, A., Stiekema, J. C. J., and Danhof, M.

Published
1988
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111. Development of a radioiodinated apoptosis-inducing ligand, rhTRAIL, and a radiolabelled agonist TRAIL receptor antibody for clinical imaging studies

Author

Duiker, E. W., Dijkers, E. C. F., Heerspink, H. Lambers, de Jong, S., van der Zee, A. G. J., Jager, P. L., Kosterink, J. G. W., de Vries, E. G. E., Lub-de Hooge, M. N., Faculteit Medische Wetenschappen/UMCG, Guided Treatment in Optimal Selected Cancer Patients (GUTS), Groningen Kidney Center (GKC), Methods in Medicines evaluation & Outcomes research (M2O), Biopharmaceuticals, Discovery, Design and Delivery (BDDD), and Targeted Gynaecologic Oncology (TARGON)

Subjects
PHARMACOKINETICS, MONOCLONAL-ANTIBODY, CARCINOMA, IDENTIFICATION, COLORECTAL TUMORS, TRAIL-R1, molecular imaging, CANCER, NUDE-MICE, rhTRAIL, DEATH RECEPTORS, TRAIL receptor monoclonal antibody, radiopharmaceuticals, IN-VIVO, TISSUE DISTRIBUTION
Abstract

BACKGROUND AND PURPOSE The TNF-related apoptosis inducing ligand (TRAIL) induces apoptosis through activation of the death receptors, TRAIL-R1 and TRAIL-R2. Recombinant human (rh) TRAIL and the TRAIL-R1 directed monoclonal antibody mapatumumab are currently clinically evaluated as anticancer agents. The objective of this study was to develop radiopharmaceuticals targeting the TRAIL-R1, suitable for clinical use to help understand and predict clinical efficacy in patients. EXPERIMENTAL APPROACH rhTRAIL was radioiodinated with 125I, and conjugated mapatumumab was radiolabelled with 111In. The radiopharmaceuticals were characterized, their in vitro stability and death receptor targeting capacities were determined and in vivo biodistribution was studied in nude mice bearing human tumour xenografts with different expression of TRAIL- R1. KEY RESULTS Labelling efficiencies, radiochemical purity, stability and binding properties were optimized for the radioimmunoconjugates. In vivo biodistribution showed rapid renal clearance of [125I] rhTRAIL, with highest kidney activity at 15 min and almost no detectable activity after 4 h. Activity rapidly decreased in almost all organs, except for the xenografts. Radiolabelled mapatumumab showed blood clearance between 24 and 168 h and a reduced decrease in radioactivity in the high receptor expression xenograft. CONCLUSIONS AND IMPLICATIONS rhTRAIL and mapatumumab can be efficiently radiolabelled. The new radiopharmaceuticals can be used clinically to study pharmacokinetics, biodistribution and tumour targeting, which could support evaluation of the native targeted agents in phase I/II trials.

Published
2012

113. Oncologie

Author

de Vries, E. G. E., Reyners, An K.L., Schroder, Carolina, Walenkamp, Anna, Gietema, Jourik A., Stehouwer, CDA, Koopmans, RP, van der Meer, J, Guided Treatment in Optimal Selected Cancer Patients (GUTS), Targeted Gynaecologic Oncology (TARGON), and Damage and Repair in Cancer Development and Cancer Treatment (DARE)

Published
2010

114. Molecular imaging of breast cancer

Author

Munnink, T. H. Oude, Nagengast, W. B., Brouwers, A. H., Schroder, C. P., Hospers, G. A., Lub-de Hooge, M. N., van der Wall, E., van Diest, P. J., de Vries, E. G. E., Faculteit Medische Wetenschappen/UMCG, and Guided Treatment in Optimal Selected Cancer Patients (GUTS)

Subjects
Positron emission tomography, Breast cancer, Staging, Single photon emission computed tomography, Molecular imaging
Abstract

Molecular imaging of breast cancer can potentially be used for breast cancer screening, staging, restaging, response evaluation and guiding therapies. Techniques for molecular breast cancer imaging include magnetic resonance imaging (MRI), optical imaging, and radionuclide imaging with positron emission tomography (PET) or single photon emission computed tomography (SPECT). This review focuses on PET and SPECT imaging which can provide sensitive serial non invasive information of tumor characteristics. Most clinical data are gathered on the visualization of general processes such as glucose metabolism with the PET-tracer [F-18]fluorodeoxyglucose (FDG) and DNA synthesis with [18F]fluoro-L-thymidine (FLT). Increasingly more breast cancer specific targets are imaged such as the estrogen receptor (ER), growth factors and growth factor receptors. Imaging of the ER with the PET tracer 16-alpha-[F-18]fluoro-17-beta-estradiol (FES) has shown a good correlation between FES tumor uptake and ER density. In-111-trastuzumab SPECT to image the human epidermal growth factor receptor 2 (HER2) showed that in most patients with metastatic HER2 overexpressing disease more lesions were detected than with conventional staging procedures. The PET tracer Zr-89-trastuzumab showed excellent, quantifiable, and specific tumor uptake. In-111-bevacizumab for SPECT and Zr-89-bevacizumab for PET-imaging have been developed for vascular endothelial growth factor (VEGF) imaging as an angiogenic marker. Lastly, tracers for the receptors EGFR, IGF-1R, PDGF-beta R and the ligand TGF beta are under development. Although molecular imaging of breast cancer is still not commonly used in daily clinical practice, its application portfolio is expanding rapidly. (c) 2009 Elsevier Ltd. All rights reserved.

Published
2009

115. Indomethacin induces apoptosis via a MRPI-dependent mechanism in doxorubicin-resistant small-cell lung cancer cells overexpressing MRPI

Author

de Groot, D. J. A., van der Deen, M., Le, T. K. P., Regeling, A., de Jong, S., de Vries, E. G. E., Guided Treatment in Optimal Selected Cancer Patients (GUTS), and Targeted Gynaecologic Oncology (TARGON)

Subjects
DRUG-RESISTANCE, EXPRESSION, EFFLUX, PROTEINS, COX-1, TRANSPORTER, apoptosis, SCLC, LINE, NSAID, doxorubicin resistance, MRPI, indomethacin, CYTOTOXICITY, MULTIDRUG-RESISTANCE
Abstract

Small-cell lung cancers (SCLCs) initially respond to chemotherapy, but are often resistant at recurrence. The non-steroidal anti-inflammatory drug indomethacin is an inhibitor of multidrug resistance protein 1 (MRPI) function. The doxorubicin-resistant MRPI-overexpressing human SCLC cell line GLC(4)-Adr was highly sensitive for indomethacin compared with the parental doxorubicin-sensitive line GLC(4). The purpose of this study was to analyse the relationship between hypersensitivity to indomethacin and MRPI overexpression. The experimental design involved analysis of the effect of MRPI downregulation on indomethacin-induced cell survival and apoptosis in GLC(4)-Adr and GLC(4), using siRNA. In addition the effect of indomethacin on glutathione levels and mitochondrial membrane potential was investigated. Small interfering RNAs directed against MRPI reduced MRPI mRNA levels twofold and reduced efflux pump function of MRPI, which was reflected by a 1.8-fold higher accumulation of MRPI substrate carboxyfluorescein, in si-MRPI versus si-Luciferase-transfected GLC(4)-Adr cells. Multidrug resistance protein 1 downregulation decreased initial high apoptosis levels 2-fold in GLC(4)-Adr after indomethacin treatment for 24 h, and increased cell survival (IC50) from 22.8 +/- 2.6 to 30.4 +/- 5.1 mM following continuous indomethacin exposure. Multidrug resistance protein 1 downregulation had no effect on apoptosis in GLC4 or on glutathione levels in both lines. Although indomethacin (20 mM) for 2 h decreased glutathione levels by 31.5% in GLC(4)-Adr, complete depletion of cellular glutathione by L-buthionine (S, R)-sulphoximine only resulted in a small increase in indomethacin-induced apoptosis in GLC(4)-Adr, demonstrating that a reduced cellular glutathione level is not the primary cause of indomethacin-induced apoptosis. Indomethacin exposure decreased mitochondrial membrane potential in GLC(4)-Adr cells, suggesting activation of the mitochondrial apoptosis pathway. Indomethacin induces apoptosis in a doxorubicin-resistant SCLC cell line through an MRPI-dependent mechanism. This may have implications for the treatment of patients with MRPI-overexpressing tumours.

Published
2007

116. [Letter to the editor]

Author

Stokman, M. A., Spijkervet, F. K. L., Boezen, H. M., Schouten, J. P., Roodenburg, J. L. N., de Vries, E. G. E., Guided Treatment in Optimal Selected Cancer Patients (GUTS), Translational Immunology Groningen (TRIGR), Life Course Epidemiology (LCE), Groningen Research Institute for Asthma and COPD (GRIAC), and Damage and Repair in Cancer Development and Cancer Treatment (DARE)

Subjects
ORAL MUCOSITIS
Published
2006

117. Oncologie

Author

de Vries, E. G. E., Reyners, An K.L., Rodenburg, CJ, Willemse, Pax, Gietema, Jourik A., van der Meer, J, Stehouwer, CDA, Guided Treatment in Optimal Selected Cancer Patients (GUTS), Targeted Gynaecologic Oncology (TARGON), and Damage and Repair in Cancer Development and Cancer Treatment (DARE)

Published
2005

123. Options for modulation of drug resistance in ovarian cancer

Author

Arts, H. J. G., Van Der Zee, A. G. J., De Jong, S., De Vries, E. G. E., and Targeted Gynaecologic Oncology (TARGON)

Subjects
EXPRESSION, CMOAT MRP2, drug resistance, endocrine system diseases, CARCINOMA, review, P-GLYCOPROTEIN, PROTEIN, CELL-LINES, CHEMOTHERAPY, TOPOISOMERASE-I, GLUTATHIONE-S-TRANSFERASE, ovarian cancer, MULTIDRUG RESISTANCE
Abstract

The objective of this paper is to present an update of mechanisms responsible for drug resistance in ovarian cancer and the possible therapeutic options to modulate this resistance using literature review with emphasis on data acquired in studies comprising ovarian tumor samples. The classic concepts on resistance in ovarian cancer, namely platinum and multidrug resistance, are briefly discussed, followed by a description of more recent insights concerning the role of apoptosis in the development of chemoresistance. A wide variety of mechanisms may be responsible for drug resistance in ovarian cancer. However, a growing body of evidence indicates that defects in the intra- and extracellular apoptotic pathways are an important cause of resistance to cytotoxic agents which opens several new treatment strategies.

Published
2000

128. Phase I study of saracatinib (AZD0530) in combination with paclitaxel and/or carboplatin in patients with solid tumours

Author

Kaye, S, primary, Aamdal, S, additional, Jones, R, additional, Freyer, G, additional, Pujade-Lauraine, E, additional, de Vries, E G E, additional, Barriuso, J, additional, Sandhu, S, additional, Tan, D S-W, additional, Hartog, V, additional, Kuenen, B, additional, Ruijter, R, additional, Kristensen, G B, additional, Nyakas, M, additional, Barrett, S, additional, Burke, W, additional, Pietersma, D, additional, Stuart, M, additional, Emeribe, U, additional, and Boven, E, additional

Published
2012
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130. Carboplatin- and cisplatin-induced potentiation of moderate-dose radiation cytotoxicity in human lung cancer cell lines

Author

Groen, H. J., Sleijfer, S., Meijer, C., Kampinga, H. H., Konings, A. W. T., de Vries, E. G. E., and Mulder, N. H.

Subjects
PLATINUM, CHEF ELECTROPHORESIS, CARCINOMA, LUNG CANCER, DNA, female genital diseases and pregnancy complications, HYPOXIC CELLS, HUMAN TUMOR-CELLS, IONIZING-RADIATION, DNA DOUBLE-STRAND BREAKS, SEMIAUTOMATED COLORIMETRIC ASSAY, RESISTANCE, RADIOSENSITIZATION, RADIOTHERAPY
Abstract

The interaction between moderate-dose radiation and cisplatin or carboplatin was studied in a cisplatin-sensitive (GLC(4)) and -resistant (GLC(4)-CDDP) human small-cell lung cancer cell line. Cellular toxicity was analysed under oxic conditions with the microculture tetrazolium assay. For the platinum and radiation toxicity with the clinically relevant dose ranges applied, this assay was used to obtain information on cell survival after the treatments. Apart from effects on cell survival effects on DNA were also investigated. Configurational DNA changes could be induced by platinum drugs and thereby these drugs might change the frequency of DNA double-strand breaks (dsbs). DNA fragmentation assayed with the clamped homogeneous electric field (CHEF) technique was used as a measure for dsbs in DNA. The radiosensitising effect of the platinum drugs was expressed as enhancement ratio (ER) calculated directly from survival levels of the initial slope of the curve. The highest ER for cisplatin in GLC(4) was 1.39 and in GLC(4)-CDDP 1.38. These were all at 75% cell survival. Carboplatin showed increased enhancement with prolonged incubation up to 1.21 in GLC(4) and was equally effective as cisplatin in GLC(4)-CDDP. According to isobologram analysis, prolonged incubation with both platinum drugs showed at least additivity with radiation for both cell lines at clinically achievable doses. GLC(4)-CDDP showed cross-resistance to radiation. The radiosensitising capacity of both lung cancer cell lines was not dependent on their platinum sensitivity. The formation of dsbs in DNA directly after radiation was not influenced by pretreatment of either drug in the sensitive or in the resistant cell line. Drug treatment resulted in decreased DNA extractability in control as well as in irradiated cells. Modest enhancement ratio for radiosensitisation by platinum drugs cannot be explained on the level of dsb formation in DNA in both cell lines. Interaction of radiation with the clinically less toxic carboplatin can be improved by prolonged low-dose carboplatin exposure before irradiation and is as potent as cisplatin in the resistant lung cancer cell line. This suggests an advantage in combining radiation and carboplatin in lung cancer patients.

Published
1995

131. High-dose methotrexate, vincristine and cisplatin as salvage treatment for relapsed non-seminomatous germ-cell cancer

Author

Sleijfer, S., van der Graaf, W. T. A., Willemse, P. H. B., de Vries, E. G. E., Schraffordt Koops, H., and Mulder, N. H.

Subjects
TESTIS, SALVAGE CHEMOTHERAPY, CHEMOTHERAPY, BLEOMYCIN, TUMORS, THERAPY, METHOTREXATE, TESTICULAR CANCER, CISPLATIN, IFOSFAMIDE, ETOPOSIDE, MANAGEMENT, VINCRISTINE, VINBLASTINE
Abstract

Eight patients with non-seminomatous testicular cancel relapsing after primary chemotherapy were treated with salvage chemotherapy consisting of high-dose methotrexate (12 g/m(2)), vincristine (1.2 mg/m(2) weekly for four weeks, followed after an interval of four weeks by 3 times 100 mg/m(2) cisplatin (50 mg/m(2) on day 1 and 2) every 10 days. This regimen resulted in 2 partial (PR) and 2 complete responses (CR). The two patients achieving CR remain disease-free for 43+ and 53+ months. Toxicity was mainly methotrexate-related and could be ameliorated to a large extent by leucovorin rescue. This small study shows that methotrexate, vincristine, followed by cisplatin is effective in the treatment of relapsed non-seminomatous testicular cancer at the cost of manageable toxicity.

Published
1995

135. A phase I dose escalation study of BIBW 2992, an irreversible dual inhibitor of epidermal growth factor receptor 1 (EGFR) and 2 (HER2) tyrosine kinase in a 2-week on, 2-week off schedule in patients with advanced solid tumours

Author

Eskens, F A L M, primary, Mom, C H, additional, Planting, A S T, additional, Gietema, J A, additional, Amelsberg, A, additional, Huisman, H, additional, van Doorn, L, additional, Burger, H, additional, Stopfer, P, additional, Verweij, J, additional, and de Vries, E G E, additional

Published
2007
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137. Molecular subtypes of breast cancer and amplification of topoisomerase IIα: predictive role in dose intensive adjuvant chemotherapy

Author

Hannemann, J, primary, Kristel, P, additional, van Tinteren, H, additional, Bontenbal, M, additional, van Hoesel, Q G C M, additional, Smit, W M, additional, Nooij, M A, additional, Voest, E E, additional, van der Wall, E, additional, Hupperets, P, additional, de Vries, E G E, additional, Rodenhuis, S, additional, and van de Vijver, M J, additional

Published
2006
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142. Efficacy of high-dose alkylating chemotherapy in the adjuvant treatment of HER2/neu-negative primary breast cancer: Update of the Dutch Randomized Trial

Author

Rodenhuis, S., primary, Bontenbal, M., additional, Beex, L. V. A. M., additional, Richel, D. J., additional, Nooij, M. A., additional, Voest, E. E., additional, van der Wall, E., additional, Hupperets, P., additional, van Tinteren, H., additional, van de Vijver, M., additional, and de Vries, E. G. E., additional

Published
2005
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