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2. Isatuximab plus atezolizumab in patients with advanced solid tumors: results from a phase I/II, open-label, multicenter study

Author

Simonelli, M., Garralda, E., Eskens, F., Gil-Martin, M., Yen, C.-J., Obermannova, R., Chao, Y., Lonardi, S., Melichar, B., Moreno, V., Yu, M.-L., Bongiovanni, A., Calvo, E., Rottey, S., Machiels, J.-P., Gonzalez-Martin, A., Paz-Ares, L., Chang, C.-L., Mason, W., Lin, C.-C., Reardon, D.A., Vieito, M., Santoro, A., Meng, R., Abbadessa, G., Menas, F., Lee, H., Liu, Q., Combeau, C., Ternes, N., Ziti-Ljajic, S., and Massard, C.

Published
2022
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4. A phase I dose-escalation study of LRP5/6 antagonist BI 905677 in patients with advanced solid tumors

Author

Lenz, H. J., Argilés, G., de Jonge, M. J.A., Yaeger, R., Doi, T., El-Khoueiry, A., Eskens, F., Kuboki, Y., Bertulis, J., Nazabadioko, S., Pronk, L., Tabernero, J., Lenz, H. J., Argilés, G., de Jonge, M. J.A., Yaeger, R., Doi, T., El-Khoueiry, A., Eskens, F., Kuboki, Y., Bertulis, J., Nazabadioko, S., Pronk, L., and Tabernero, J.

Abstract

Background: Aberrant Wnt pathway signaling has been implicated in the development of many cancers. Targeting of low-density lipoprotein receptor-related protein 5/6 (LRP5/6) co-receptors inhibits Wnt signaling and may be a novel therapy. BI 905677 is an LRP5/6 antagonist that has demonstrated preclinical antitumor activity. Patients and methods: This (NCT03604445) was a phase I, dose-escalation study evaluating BI 905677 for patients with advanced solid tumors over two dosing schedules (A: i.v. infusion every 3 weeks, 3-week cycles; B: i.v. infusion every 2 weeks, 4-week cycles). Adult patients were eligible if they had exhausted treatment options and had an Eastern Cooperative Oncology Group performance status of 0-1. The primary endpoints were the maximum tolerated dose (MTD) and safety. Other endpoints were pharmacokinetics, pharmacodynamics, and efficacy. Results:In total, 37 patients received BI 905677 over nine dose cohorts (0.05-3.6 mg/kg/every 3 weeks). Dose-limiting toxicities were only reported during cycle 1 in the 3.6 mg/kg cohort and the MTD was established at 2.8 mg/kg every 3 weeks. Enrollment for schedule B was not pursued. The most frequently reported adverse events were diarrhea (35.1%), vomiting (21.6%), and C-telopeptide increase (18.9%). All patients in the 3.6 mg/kg cohort experienced a dose-limiting toxicity, suggesting a narrow therapeutic index. Paired pre-treatment and on-treatment biopsies, where available, showed decreased Axin2 expression by reverse transcriptase polymerase chain reaction with treatment, suggesting target inhibition. Best response observed was stable disease in 14 (38%) patients. Conclusion: The MTD of BI 905677 was set at 2.8 mg/kg every 3 weeks. BI 905677 was well tolerated but a narrow therapeutic range and minimal efficacy led to early termination of the trial.

Published
2024

8. Harmonising patient-access programmes: the Dutch DRUG Access Protocol platform

Author

Zeverijn, L.J., Waalwijk van Doorn-Khosrovani, S.B., Roy, A., Timmers, L., Tran, Thai, Boer, J.E. de, Wit, G.F. de, Geurts, B.S., Gelderblom, H., Verheul, H.M.W., Blijlevens, N.M., Wymenga, A.N., Eskens, F., Smit, E.F., Bloemendal, H.J., Voest, E.E., Zeverijn, L.J., Waalwijk van Doorn-Khosrovani, S.B., Roy, A., Timmers, L., Tran, Thai, Boer, J.E. de, Wit, G.F. de, Geurts, B.S., Gelderblom, H., Verheul, H.M.W., Blijlevens, N.M., Wymenga, A.N., Eskens, F., Smit, E.F., Bloemendal, H.J., and Voest, E.E.

Abstract

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Published
2022

9. Feasibility of therapeutic drug monitoring of sorafenib in patients with liver or thyroid cancer

Author

Guchelaar, N.A.D., Eerden, R.A.G. van, Groenland, S.L., Doorn, L.V., Desar, I.M.E., Eskens, F., Steeghs, N., Erp, N.P. van, Huitema, A.D., Mathijssen, R.H., Koolen, S.L., Guchelaar, N.A.D., Eerden, R.A.G. van, Groenland, S.L., Doorn, L.V., Desar, I.M.E., Eskens, F., Steeghs, N., Erp, N.P. van, Huitema, A.D., Mathijssen, R.H., and Koolen, S.L.

Abstract

Contains fulltext : 283013.pdf (Publisher’s version ) (Open Access), INTRODUCTION: Sorafenib is a tyrosine-kinase inhibitor approved for the treatment of renal cell carcinoma, hepatocellular carcinoma, thyroid carcinoma, and desmoid fibromatosis. As high inter-individual variability exists in exposure, there is a scientific rationale to pursue therapeutic drug monitoring (TDM). We investigated the feasibility of TDM in patients on sorafenib and tried to identify sub-groups in whom pharmacokinetically (PK) guided-dosing might be of added value. METHODS: We included patients who started on sorafenib (between October 2017 and June 2020) at the recommended dose of 400 mg BID or with a step-up dosing schedule. Plasma trough levels (C(trough)) were measured at pre-specified time-points. Increasing the dose was advised if C(trough) was below the target of 3750 ng/mL and toxicity was manageable. RESULTS: A total of 150 samples from 36 patients were collected. Thirty patients (83 %) had a C(trough) below the prespecified target concentration at a certain time point during treatment. Toxicity from sorafenib hampered dosing according to target C(trough) in almost half of the patients. In 11 patients, dosing was adjusted based on C(trough). In three patients, this resulted in an adequate C(trough) without additional toxicity four weeks after the dose increase. In the remaining eight patients, dose adjustment based on C(trough) did not result in a C(trough) above the target or caused excessive toxicity. CONCLUSIONS: TDM for sorafenib is not of added value in daily clinical practice. In most cases, toxicity restricts the possibility of dose escalations.

Published
2022

10. Isatuximab plus atezolizumab in patients with advanced solid tumors:results from a phase I/II, open-label, multicenter study

Author

Simonelli, M., Garralda, E., Eskens, F., Gil-Martin, M., Yen, C. J., Obermannova, R., Chao, Y., Lonardi, S., Melichar, B., Moreno, V., Yu, M. L., Bongiovanni, A., Calvo, E., Rottey, S., Machiels, J. P., Gonzalez-Martin, A., Paz-Ares, L., Chang, C. L., Mason, W., Lin, C. C., Reardon, D. A., Vieito, M., Santoro, A., Meng, R., Abbadessa, G., Menas, F., Lee, H., Liu, Q., Combeau, C., Ternes, N., Ziti-Ljajic, S., Massard, C., Simonelli, M., Garralda, E., Eskens, F., Gil-Martin, M., Yen, C. J., Obermannova, R., Chao, Y., Lonardi, S., Melichar, B., Moreno, V., Yu, M. L., Bongiovanni, A., Calvo, E., Rottey, S., Machiels, J. P., Gonzalez-Martin, A., Paz-Ares, L., Chang, C. L., Mason, W., Lin, C. C., Reardon, D. A., Vieito, M., Santoro, A., Meng, R., Abbadessa, G., Menas, F., Lee, H., Liu, Q., Combeau, C., Ternes, N., Ziti-Ljajic, S., and Massard, C.

Abstract

Background: The anti-CD38 antibody isatuximab is approved for the treatment of relapsed/refractory multiple myeloma, but there are no data on its efficacy in solid tumors. This phase I/II study (NCT03637764) assessed the safety and activity of isatuximab plus atezolizumab (Isa + Atezo), an anti-programmed death-ligand 1 (PD-L1) antibody, in patients with immunotherapy-naive solid tumors: epithelial ovarian cancer (EOC), glioblastoma (GBM), hepatocellular carcinoma (HCC), and squamous cell carcinoma of the head and neck (SCCHN). Patients and methods: Phase I assessed safety, tolerability, pharmacokinetics, pharmacodynamics, and the recommended phase II dose (RP2D) of isatuximab 10 mg/kg intravenously (i.v.) every week for 3 weeks followed by once every 3 weeks + atezolizumab 1200 mg i.v. every 3 weeks. Phase II used a Simon's two-stage design to assess the overall response rate or progression-free survival rate at 6 months (GBM cohort). Interim analysis was carried out at 6 months following first dose of the last enrolled patient in each cohort. Pharmacodynamic biomarkers were tested for CD38, PD-L1, tumor-infiltrating immune cells, and FOXP3+ regulatory T cells (Tregs) in the tumor microenvironment (TME). Results: Overall, 107 patients were treated (EOC, n = 18; GBM, n = 33; HCC, n = 27; SCCHN, n = 29). In phase I, Isa + Atezo showed an acceptable safety profile, no dose-limiting toxicities were observed, and RP2D was confirmed. Most patients experienced ≥1 treatment-emergent adverse event (TEAE), with ≤48.5% being grade ≥3. The most frequent TEAE was infusion reactions. The study did not continue to stage 2 based on prespecified targets. Tumor-infiltrating CD38+ immune cells were reduced and almost cleared after treatment. Isa + Atezo did not significantly modulate Tregs or PD-L1 expression in the TME. Conclusions: Isa + Atezo had acceptable safety and tolerability. Clinical pharmacodynamic evaluation revealed efficient target engagement of isatuximab via treatm

Published
2022

13. In-depth analysis of the genomic landscape of 86 metastatic neuroendocrine neoplasms reveals subtype-heterogeneity and potential therapeutic targets

Author

Veenendaal L, Valk G, Klümpen H, Lolkema M, Dercksen M, Cuppen E, Werken Hvd, Mostert B, Sleijfer S, Riet Jv, Eskens F, and Tesselaar M

Subjects
Text mining, business.industry, Computational biology, Biology, business
Abstract

Metastatic neuroendocrine neoplasms (mNEN) form clinically and genetically heterogeneous malignancies, characterized by distinct prognoses based upon primary tumor localization, functionality, grade, proliferation index and diverse outcomes to treatment. Here, we report the mutational landscape of 86 whole-genome sequenced mNEN. This landscape revealed distinct genomic subpopulations of mNEN based on primary localization and differentiation grade; we observed relatively high tumor mutational burdens (TMB) in neuroendocrine carcinoma (5.45 somatic mutations per megabase) with TP53, KRAS, RB1, MYC and APC as major drivers versus an overall low TMB in neuroendocrine tumors (1.08). Furthermore, we observed distinct drivers which were enriched with somatic aberrations in pancreatic (MEN1, ATRX, DAXX, PCNT and SETD2) and midgut-derived neuroendocrine tumors (CDKN1B). Finally, 49% of mNEN patients revealed extensions of their treatment-repertoire based upon actionable (and responsive) somatic aberrations; potentially directing improvements in mNEN treatment strategies.

Published
2020
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15. 115MO Long-term efficacy, tolerability and overall survival in patients (pts) with unresectable or metastatic (U/M) PDGFRA D842V-mutant gastrointestinal stromal tumour (GIST) treated with avapritinib: NAVIGATOR phase I trial update

Author

Kang, Y-K., primary, Jones, R.L., additional, von Mehren, M., additional, Serrano, C., additional, George, S., additional, Heinrich, M.C., additional, Schöffski, P., additional, Mir, O., additional, Cassier, P.A., additional, Eskens, F., additional, Rutkowski, P., additional, Tap, W.D., additional, Chawla, S.P., additional, Shi, H., additional, Roche, M., additional, and Bauer, S., additional

Published
2020
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16. Long-term efficacy, tolerability, and overall survival in patients with unresectable or metastatic platelet-derived growth factor receptor A (PDGFRA) D842V-mutant gastrointestinal stromal tumors (GIST) treated with avapritinib : NAVIGATOR phase 1 trial update

Author

Bauer, Sebastian, Serrano, C., Mehren, M. von, George, S., Heinrich, M. C., Kang, Y.-K., Schöffski, P., Cassier, P. A., Mir, O., Eskens, F., Rutkowski, P., Tap, W., Roche, M., and Jones, R. L.

Subjects
Medizin
Abstract

weitere Verfasser ausserhalb der UDE

Published
2020

19. A phase 1 dose-escalation with expansion study of the antibody-drug conjugate trastuzumab duocarmazine (SYD985) in locally advanced and metastatic solid tumours and HER2-expressing breast cancer

Author

Banerji, U, Van Herpen, CML, Saura, C, Thistlethwaite, F, Lord, S, Moreno, V, Macpherson, IR, Boni, V, Rolfo, C, De Vries, E, Rottey, S, Geenen, J, Eskens, F, Gil-Martin, M, Mommers, EC, Koper, NP, Aftimos, P, and Cox, AJ

Abstract

Background: Trastuzumab duocarmazine is a novel HER2-targeting antibody-drug conjugate comprised of trastuzumab covalently bound to a linker-drug containing duocarmycin. Preclinical studies showed impressive antitumour activity in various models. In this first-in-human study we evaluated the safety and activity in patients with solid tumours. Methods: In the dose-escalation part, patients aged 18 years or older with locally advanced or metastatic solid tumours with variable HER2 status and refractory to standard therapy were enrolled. The expansion cohorts included patients with breast, gastric, urothelial, or endometrial cancer with at least HER2 immunohistochemistry 1+ expression and measurable disease according to RECIST. Trastuzumab duocarmazine was administered intravenously on day 1 of each 3-week cycle at doses of 0·3 to 2·4 mg/kg until disease progression or unacceptable toxicity. A 3+3 design was used in the dose-escalation part and the primary endpoint was to evaluate safety and determine the recommended phase 2 dose. The primary endpoint of the expansion part was the proportion of patients who achieved an objective response. This ongoing study is registered with ClinicalTrials.gov, number NCT02277717, and is fully recruited. Findings: Between October 30, 2014 and April 2, 2018, 39 patients were enrolled and treated in the dose-escalation part and 146 patients in the expansion part of the study. One dose-limiting toxicity (fatal pneumonitis) occurred at the highest administered dose. Grade ≥ 3 treatment-related adverse events reported more than once were keratitis (three patients) and fatigue (two patients). Based on all available data, the recommended phase 2 dose was set at 1·2 mg/kg. In de expansion part of the study, treatment-related serious adverse events were reported in 16 (11%) of 146 patients. The most common treatment-related adverse events were fatigue (48 [33%] of 146 patients), conjunctivitis (45 [31%]), and dry eye (45 [31%]). The majority of patients had one or more ocular adverse events, with grade 3 events in 10 (7%) of 146 patients. In the breast cancer expansion cohorts, 16 (33%, 95% CI 20·4-48·4) of 48 evaluable patients with HER2-positive breast cancer achieved an objective response. The proportion of patients with HER2-low, HR-positive breast cancer who achieved an objective response was 28% (95% CI 13·8-46·8; nine of 32 patients) and for patients with HER2-low, HR-negative breast cancer 40% (95% CI 16·3-67·6; six of 15 patients). Responses were also observed in one (6%; 95% CI 0·2-30·2) of 16 gastric cancer, four (25%; 95% CI 7·3-52·4) of 16 urothelial cancer, and five (39%; 95% CI 13·9-68·4) of 13 endometrial cancer patients. Interpretation: Trastuzumab duocarmazine has shown important clinical activity in heavily pretreated patients with HER2-expressing metastatic cancer, including HER2-positive trastuzumab emtansine-resistant and HER2-low breast cancer, with a manageable safety profile.

Published
2019

27. Differentiation and Definition of Vascular-Targeted Therapies

Author

Siemann, D. W., Bibby, M. C., Dark, G. G., Dicker, A. P., Eskens, F. A. L. M., Michael Horsman, Marmé, D., Lorusso, P. M., Medical Oncology, and Virology

Subjects
Cancer Research, Oncology
Abstract

The therapeutic potential of targeting the tumor vascular supply is now widely recognized. Intense research and development activity has resulted in a variety of investigational agents, a number of which are currently in clinical development. As these novel agents are quite distinct from the cytotoxic drugs conventionally used in the treatment of solid tumors, it will be particularly important to ensure early differentiation of these vascular-targeted therapies in order to encourage widespread understanding of their potential benefits and application in the clinic. Two distinct groups of vascular-targeted therapies have evolved: antiangiogenic agents and vascular-disrupting approaches. These differ in three key respects: their physiologic target, the type or extent of disease that is likely to be susceptible, and the treatment scheduling. Inhibitors of angiogenesis interfere with new vessel formation and therefore have a preventative action, require chronic administration, and are likely to be of particular benefit in early-stage or asymptomatic metastatic disease. Vascular-disrupting agents target the established tumor blood vessels, resulting in tumor ischemia and necrosis. These agents are therefore given acutely, show more immediate effects, and may have particular efficacy against advanced disease. It is essential that these agents can be readily distinguished from conventional therapies and that an understanding of key differences between the two types of vascular-targeted therapies is fostered. Here, a simple taxonomy and nomenclature is proposed in anticipation that the therapeutic potential of this novel class can be realized as these approaches advance in clinical settings and a new anticancer strategy becomes available in the clinic.

Published
2005
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28. A phase I study of the MDM2 inhibitor AMG 232 in patients with advanced p53 wild type (p53WT) solid tumors or multiple myeloma

Author

Langenberg, M. H., Gluck, L., Weger, V., Frank, R., Eskens, F., Blay, J. Y., Soria, J. C., Chawla, S., Gounder, M., Wagner, A., Zhang, Y., Kambuj, P., Loberg, R., Henary, H., Langenberg, M. H., Gluck, L., Weger, V., Frank, R., Eskens, F., Blay, J. Y., Soria, J. C., Chawla, S., Gounder, M., Wagner, A., Zhang, Y., Kambuj, P., Loberg, R., and Henary, H.

Published
2016

29. A phase I study of the MDM2 inhibitor AMG 232 in patients with advanced p53 wild type (p53WT) solid tumors or multiple myeloma

Author

MS Medische Oncologie, Cancer, Langenberg, M. H., Gluck, L., Weger, V., Frank, R., Eskens, F., Blay, J. Y., Soria, J. C., Chawla, S., Gounder, M., Wagner, A., Zhang, Y., Kambuj, P., Loberg, R., Henary, H., MS Medische Oncologie, Cancer, Langenberg, M. H., Gluck, L., Weger, V., Frank, R., Eskens, F., Blay, J. Y., Soria, J. C., Chawla, S., Gounder, M., Wagner, A., Zhang, Y., Kambuj, P., Loberg, R., and Henary, H.

Published
2016

30. A phase I study of the MDM2 inhibitor AMG 232 in patients with advanced p53 wild type (p53WT) solid tumors or multiple myeloma

Author

Langenberg, M.H., primary, Gluck, L., additional, Weger, V., additional, Frank, R., additional, Eskens, F., additional, Blay, J.Y., additional, Soria, J.C., additional, Chawla, S., additional, Gounder, M., additional, Wagner, A., additional, Zhang, Y., additional, Kambuj, P., additional, Loberg, R., additional, and Henary, H., additional

Published
2016
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31. Preliminary safety and activity in a first-in-human phase 1 study of BLU-285, a potent, highly-selective inhibitor of KIT and PDGFRα activation loop mutants in advanced gastrointestinal stromal tumor (GIST)

Author

Heinrich, M., primary, Jones, R., additional, Schoffski, P., additional, Bauer, S., additional, von Mehren, M., additional, Eskens, F., additional, Cassier, P., additional, Mir, O., additional, Shi, H., additional, Alvarez-Diez, T., additional, Healy, M.E., additional, Wolf, B., additional, and George, S., additional

Published
2016
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34. Abstracts of papers Rational use of drugs: 18th European Symposium on Clinical Pharmacy

Author

Dukes, M. N. G., Elenbaas, Robert M., Tognoni, G., Smith, Dorothy L., Lunde, Inga, Leufkens, H. G. M., Hekster, Y. A., Bakker, A., Ostino, G., Petri, H., Sturmans, F., Banta, H. D., Rutten, F. F. H., Martens, L. L., Noyce, P. R., Merkus, F. W. H. M., de Jong-v.d.Berg, Lolkje, Haaijer-Ruskamp, Flora, Dukes, Graham, Vidgren, B. -M., Vidgren, S., Martini, N., Sala, M. L., Scroccaro, G., Olivencia, P., McLcod, D. C., Coln, W. G., Hartzcma, A. G., Thaver, C. F., Rodriguez-Sasiain, J. M., Sangroniz, B., Mauleon, M. D., Wood, M. A., Martinez, M. J., Leinebø, O., Saugen, J. N., Marini, P., Olivato, R., Alberola, C., Cruz-Martos, E., Cruz, T., Marfagon, N., de Tejada, A. Herreros, Denig, P., Haaijer-Ruskamp, F. M., Wesseling, H., Versluis, A., Gascón, M. P., Horne, Robert, Hough, Jane, Klazinga, N. S., van Everdingen, J. J. -E., van den Broek, P. J., Roberts, D. K., Veitch, G. B. A., Tan K. K. C., Holland D. A., Allwood M. C., Nicholls, A., Astobieta, A., Calvo, R., Rodriquez-Sasiain, J. M., Barriquand, D., Pochon, C., Aulagner, G., Vial, A., Dumarest, C., Maire, P. H., Jelliffe, R. W., Brouwers, J. R. B. J., Cramer, K., Gulyas, J., vd Kam, H. J., Sijtsma, J., Donadio, C., Tramonti, G., Garcea, G., Costagli, M., Lucchetti, A., Giordani, R., Paizis, G., Pierotti, R., Falcone, G., Bianchi, C., Gallastegui C., Farré R., Jiménez I., Mangues M. A., Guasch E., Ginovart G., Sagrera X., Raspall F., Queralto J. M., Kovarik, J. M., Rademaker, C. M. A., Verhoef, J., Silvestri, L., Caputo, M., Andrew, M., Toverud, E. -L., Jimenez I., Castro I., Alvarez E., Altimiras J., van de Leur, J. J. J. P. M., Muller, N. F., Van Turnhout, J. M., Mendizabal, L., Sasiain, J. M. Rodriguez, Morana, G., Ofstad, K. Moss, Timenes, A. -M., Vroom, J. K. F., de Jong-van den Berg, L. T. W., van den Berg, P. B., de Gier, J. J., Ferres J., Recoder O., Sanchez Rio T., Garcia M. P., Julia A., Balet A., Farre R., Manques M. A., Berod, T., Dufay, E., Naveau, C., Combe, M., Sauvageon, A., Hansen, Erik Wind, Christensen, Jens Dencker, Lie-A-Huen, L., Kinqma, J. H., Meijer, D. K. P., Le Meur, F., Isoard, P., Salek, M. S., Finlay, A. Y., Khan, G. K., Luscombe, D. K., Stuurman, A., Boidin, M. P., Wallenius, K., Ojala, R., Kariluoto, A., Ikonen, M., Paes, A. H. P., Blom, A. Th. G., Bakker, A., Wallenius, S., Enlund, H., Vainio, K., Codina, C., Roca, M., Sardà, P., Corominas, N., Massó, J., Ribas, J., Kentra, K., Myllyntausta, M., Saarenpää, M., Airaksinen, M. S. A., Mendarte, L., Rimola, A., Meisters, R., Hekster, Y., Janssen, W., Cox, A., Kempen, R., Aerdts, S. J. A., van Dalen, R., Clasener, H. A. L., Festen, J., Schjphorst, PP, Benraad, HB, van Asten, P., de Wit, R., Muller, N. F., Limbeek, R. J. G., Nagel, H. G. M., Mgyboom, R. H. B., Stricker, B. H. C., van den Berg, B. A. M., Nelen, T. H. A., Tijssen, T. A. G., Wassink, P., Wassink-L'Ortije, M. J. E., Gascón, P., Selva, C., Bassons, T., Pardo, C., Mas, M. P., Saqalés, M., Sánchez, F., Mercade, V., Pujol, R., Agustí, C., Cano, M., Gurrera, T., Gorchs, M., Fabregas, X., Murgui, L. L., Verdaguer, A., Witjes, W. P. J., Vollaard, E. J., Crul, B. J. P., Limpens, C., Ahonen, K., Klaukka, T., Vohlonen, I., Martikainen, J., Goldenberg, Daniel, Brodsky, Andres, Aparici, Ines, Argeri, Cecilia, Goldenberg D., Saidman C., Sevinski L., Allevato N., Mujico B., Ubogui J., Dorfman P., Rodriguez Lupo L., Varela M., Higa J., Fourrier, Annie, Larrouturou, Philippe, Samarran, Claire, Huchet, Jacqueline, Barber, N. D., Party, N., Wilson, P., Eide, Grethe, Horvei, Kari, Kruse-Jensen, Angelika, Wold, Ingrid, Møark, Turid, Barrett, C. W., Tugwell, A. C., Søndergaard, B., Rasmussen, M., Davidsen, F., Hey, H., Kierkeby, L., Riis, L., Korhonen, M., Vidgren, P., Ojanen, T., Vidqren, M., Ferrés J., Sanchez T., Gallastequi C., Julià A., Herings, R. M. C., Stricker, B. H. Ch., Janssen, A. J. H. H., Dinter, Heike, Janssen, A. J. H. M., Barbaut, X., Proust, S., Amlagner, G., Eskens, F. A. L. M., Clasener, H. A. L., Vollaard, E. J., Arnoldussen, E., Sieradzki, E., Wanat-Słupska, E., Zlółkowska, M., Pankowska, I., Mazur, R., Ksiazkiewicz, B., Jankowski, A., Marzec, A., Marzec, C., Marzec, M. O., Marzec, J. P., Marzec, A., Mungall, D. R., Portnoy, Lynne, Lucas, F., Kadir, F., Pijpers, A., Vulto, A., Zuidema, J., Tan, K. K. C., Sutton, P., Samu, Antal, Murphy, John E., Chapman, Ronnie, Wieringa, Nicolien, de Gier, J. J., Rolloos, J., Voesten, M. T. P. J., de Meijer, P. J. J., de Koning, G. H. P., Salek, S., Reerink, E., Mungall, D. R., Farrow, L., Raskob G., Rosenbloom D., Hull R., Ferres J., Torras A., Farre R., Recorder O., Garcia M. P., Torras C., Cubellsl J., Font, M., Madridejos, R., Catalán, A., Huguet, M., Franquesa, N., Gratacós, J., Martinez, M., Saltó, A., van der Kleijn, E., ter Wee, R. J. M., Holmberg, N., and Brenninkmeijer, R. F.

Published
1989
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38. LBA-08 Results of a phase 1b study of the selective BRAF V600 inhibitor encorafenib in combination with cetuximab alone or cetuximab + alpelisib for treatment of patients with advanced BRAF-mutant metastatic colorectal cancer

Author

Elez, E., primary, Schellens, J., additional, van Geel, R., additional, Bendell, J., additional, Spreafico, A., additional, Schuler, M., additional, Yoshino, T., additional, Delord, J-P., additional, Yamada, Y., additional, Lolkema, M., additional, Faris, J.E., additional, Eskens, F., additional, Sharma, S., additional, Yaeger, R., additional, Lenz, H-J., additional, Wainberg, Z., additional, Avsar, E., additional, Chatterjee, A., additional, Jaeger, S., additional, Demuth, T., additional, and Tabernero, J., additional

Published
2015
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48. A phase I safety and pharmacokinetic (PK) study of navitoclax (N) in combination with docetaxel (D) in patients (pts) with solid tumors.

Author

Puglisi, M., primary, van Doorn, L., additional, Blanco-Codesido, M., additional, De Jonge, M. J., additional, Moran, K., additional, Yang, J., additional, Busman, T., additional, Franklin, C., additional, Mabry, M., additional, Krivoshik, A., additional, Humerickhouse, R., additional, Molife, L. R., additional, and Eskens, F., additional

Published
2011
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49. Oral PI3 kinase inhibitor BKM120 monotherapy in patients (pts) with advanced solid tumors: An update on safety and efficacy.

Author

Grana, B., primary, Burris, H. A., additional, Rodon Ahnert, J., additional, Abdul Razak, A. R., additional, De Jonge, M. J., additional, Eskens, F., additional, Siu, L. L., additional, Ru, Q. C., additional, Homji, N. F., additional, Demanse, D., additional, Di Tomaso, E., additional, Cosaert, J. G. C. E., additional, Quadt, C., additional, Baselga, J., additional, and Bendell, J. C., additional

Published
2011
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