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Article ; Online: Tyrosine kinase inhibitors of VEGF receptors: clinical issues and remaining questions.

van Cruijsen, Hester / van der Veldt, Astrid / Hoekman, Klaas

Frontiers in bioscience (Landmark edition)

2009 Volume 14, Issue 6, Page(s) 2248–2268

Abstract: The number of VEGFR tyrosine kinase inhibitors (TKIs) used as an anti-cancer agent is rapidly increasing, but several issues in clinical practice remain to be elucidated. VEGFR TKIs are multikinase inhibitors that have additional targets such platelet- ... ...

Abstract	The number of VEGFR tyrosine kinase inhibitors (TKIs) used as an anti-cancer agent is rapidly increasing, but several issues in clinical practice remain to be elucidated. VEGFR TKIs are multikinase inhibitors that have additional targets such platelet-derived growth factor receptors, which may result in an increased efficacy as well as an increased toxicity. Efficacy in several cancers has been shown, but acquired resistance also occurs during treatment with this new class of drugs. Tumor response evaluation can be a challenge, because VEGFR TKIs can cause extensive tumor necrosis without a marked decrease in tumor size. Therefore, new response criteria and functional imaging techniques are required. In this review we will also focus on the specific toxicities and their management: hypertension, proteinuria, cardiac toxicity, fatigue, hypothyroidism, voice changes, gastrointestinal toxicity, cutaneous reactions, wound healing, hemorrhage and thromboembolic events, hematological toxicity and cerebral toxicity. Furthermore we will discuss some issues regarding the pharmacology and dosing of these drugs. This review may provide important information to clinicians who prescribe VEGFR TKIs to their patients.
MeSH term(s)	Angiogenesis Inhibitors/pharmacology ; Angiogenesis Inhibitors/toxicity ; Humans ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/toxicity ; Receptors, Vascular Endothelial Growth Factor/antagonists & inhibitors
Chemical Substances	Angiogenesis Inhibitors ; Protein Kinase Inhibitors ; Receptors, Vascular Endothelial Growth Factor (EC 2.7.10.1)
Language	English
Publishing date	2009-01-01
Publishing country	Singapore
Document type	Journal Article ; Review
ZDB-ID	2704569-9
ISSN	2768-6698 ; 1093-9946
ISSN (online)	2768-6698
ISSN	1093-9946
DOI	10.2741/3377
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Article ; Online: Direct activation of caspases by RGD-peptides may increase drug sensitivity of tumour cells.

Broxterman, Henk J. / Hoekman, Klaas

Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy

1999 Volume 2, Issue 3, Page(s) 139–141

Abstract: The realization that cellular homeostasis is dependent on the continuous integration of survival and death signals picked up from the environment and the recent advances in identifying the molecular players involved in these networks may increase our ... ...

Abstract	The realization that cellular homeostasis is dependent on the continuous integration of survival and death signals picked up from the environment and the recent advances in identifying the molecular players involved in these networks may increase our ability to manipulate apoptosis for therapeutic purposes. A recent paper by Buckley et al. in Nature(1)brings this goal one step closer by identifying peptides, containing the motif arginine-glycine-aspartate (RGD), that induce apoptosis by direct activation of caspase-3. We put this finding in the context of what is known about the RGD motif in the light of cancer treatment and suggest the possibility of a synergistic action with anticancer drugs. Copyright 1999 Harcourt Publishers Ltd.
Language	English
Publishing date	1999-06
Publishing country	Scotland
Document type	Journal Article
ZDB-ID	1474513-6
ISSN	1532-2084 ; 1368-7646
ISSN (online)	1532-2084
ISSN	1368-7646
DOI	10.1054/drup.1999.0081
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Zs.A 5099: Show issues

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Article: Epidermal growth factor receptor and angiogenesis: Opportunities for combined anticancer strategies.

van Cruijsen, Hester / Giaccone, Giuseppe / Hoekman, Klaas

International journal of cancer

2005 Volume 117, Issue 6, Page(s) 883–888

Abstract: Tumor-induced angiogenesis is essential for malignant growth. This mini review focuses on the role of vascular endothelial growth factor (VEGF) and epidermal growth factor (EGF) and their receptors in this process, and the rationale to combine inhibitors ...

Abstract	Tumor-induced angiogenesis is essential for malignant growth. This mini review focuses on the role of vascular endothelial growth factor (VEGF) and epidermal growth factor (EGF) and their receptors in this process, and the rationale to combine inhibitors of these growth factors as anticancer therapy. Concomitantly, targeting the VEGF(R) and the EGF(R) signaling pathway may circumvent the problem of acquired resistance to EGFR inhibitors. By targeting both pathways, the antiangiogenic effect may be more pronounced, which may lead to greater antitumor activity. Preliminary efficacy data from clinical trials encourage further exploration of this combined anticancer strategy.
MeSH term(s)	Cells, Cultured ; Endothelial Cells ; Humans ; Microcirculation ; Neoplasms/blood supply ; Neoplasms/therapy ; Neovascularization, Pathologic ; Receptor, Epidermal Growth Factor/antagonists & inhibitors ; Receptor, Epidermal Growth Factor/physiology ; Receptors, Vascular Endothelial Growth Factor/antagonists & inhibitors ; Receptors, Vascular Endothelial Growth Factor/physiology ; Signal Transduction ; Umbilical Veins
Chemical Substances	Receptor, Epidermal Growth Factor (EC 2.7.10.1) ; Receptors, Vascular Endothelial Growth Factor (EC 2.7.10.1)
Language	English
Publishing date	2005-12-20
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	218257-9
ISSN	1097-0215 ; 0020-7136
ISSN (online)	1097-0215
ISSN	0020-7136
DOI	10.1002/ijc.21479
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Zs.A 478: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article: The hemostatic system in angiogenesis.

van Hinsbergh, Victor W M / Koolwijk, Pieter / Hoekman, Klaas

EXS

2004 , Issue 94, Page(s) 247–266

MeSH term(s)	Animals ; Blood Platelets/physiology ; Hemostasis/physiology ; Humans ; Neoplasms/blood supply ; Neovascularization, Pathologic/physiopathology ; Neovascularization, Physiologic/physiology ; Signal Transduction/physiology ; Vascular Endothelial Growth Factor A/physiology
Chemical Substances	Vascular Endothelial Growth Factor A
Language	English
Publishing date	2004-12-15
Publishing country	Switzerland
Document type	Journal Article ; Review
ISSN	1023-294X
ISSN	1023-294X
DOI	10.1007/3-7643-7311-3_17
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Article: Resistance to cytotoxic and anti-angiogenic anticancer agents: similarities and differences.

Broxterman, Henk J / Lankelma, Jan / Hoekman, Klaas

Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy

2003 Volume 6, Issue 3, Page(s) 111–127

Abstract: Intrinsic resistance to anticancer drugs, or resistance developed during chemotherapy, remains a major obstacle to successful treatment. This is the case both for resistance to cytotoxic agents, directed at malignant cells, and for resistance to anti- ... ...

Abstract	Intrinsic resistance to anticancer drugs, or resistance developed during chemotherapy, remains a major obstacle to successful treatment. This is the case both for resistance to cytotoxic agents, directed at malignant cells, and for resistance to anti-angiogenic agents, directed at non-malignant endothelial cells. In this review, we will discuss mechanisms of resistance which have a bearing on both these conceptually different classes of drugs. The complexity of drug resistance, involving drug transporters, such as P-glycoprotein, as well as resistance related to the tissue structure of solid tumors and its consequences for drug delivery is discussed. Possible mechanisms of resistance to endothelial cell-targeted drugs, including inhibitors of the VEGF receptor and EGF receptor family, are reviewed. The resistance of cancer cells as well as endothelial cells related to anti-apoptotic signaling events initiated by cell integrin-matrix interactions is discussed. Current strategies to overcome resistance mechanisms are summarized; they include high-dose chemotherapy, tumor targeting of cytotoxics to improve tumor uptake, low-dose protracted (metronomic) chemotherapy and combinations of classical agents with anti-angiogenic agents. This review discusses primarily literature published in 2001 and 2002.
MeSH term(s)	Angiogenesis Inhibitors/pharmacology ; Animals ; Antineoplastic Agents/pharmacology ; Cell Survival/drug effects ; Drug Resistance, Neoplasm ; Humans ; Neoplasms/blood supply ; Neoplasms/drug therapy ; Neoplasms/pathology ; Tumor Cells, Cultured
Chemical Substances	Angiogenesis Inhibitors ; Antineoplastic Agents
Language	English
Publishing date	2003-07-14
Publishing country	Scotland
Document type	Journal Article ; Review
ZDB-ID	1474513-6
ISSN	1532-2084 ; 1368-7646
ISSN (online)	1532-2084
ISSN	1368-7646
DOI	10.1016/s1368-7646(03)00026-8
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Zs.A 5099: Show issues

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Article: Neurotoxic complications of chemotherapy in patients with cancer: clinical signs and optimal management.

Verstappen, Carla C P / Heimans, Jan J / Hoekman, Klaas / Postma, Tjeerd J

Drugs

2003 Volume 63, Issue 15, Page(s) 1549–1563

Abstract: Neurotoxic side effects of chemotherapy occur frequently and are often a reason to limit the dose of chemotherapy. Since bone marrow toxicity, as the major limiting factor in most chemotherapeutic regimens, can be overcome with growth factors or bone ... ...

Abstract	Neurotoxic side effects of chemotherapy occur frequently and are often a reason to limit the dose of chemotherapy. Since bone marrow toxicity, as the major limiting factor in most chemotherapeutic regimens, can be overcome with growth factors or bone marrow transplantation, the use of higher doses of chemotherapy is possible, which increases the risk of neurotoxicity. Chemotherapy may cause both peripheral neurotoxicity, consisting mainly of a peripheral neuropathy, and central neurotoxicity, ranging from minor cognitive deficits to encephalopathy with dementia or even coma. In this article we describe the neurological adverse effects of the most commonly used chemotherapeutic agents. The vinca-alkaloids, cisplatin and the taxanes are amongst the most important drugs inducing peripheral neurotoxicity. These drugs are widely used for various malignancies such as ovarian and breast cancer, and haematological cancers. Chemotherapy-induced neuropathy is clearly related to cumulative dose or dose-intensities. Patients who already have neuropathic symptoms due to diabetes mellitus, hereditary neuropathies or earlier treatment with neurotoxic chemotherapy are thought to be more vulnerable for the development of chemotherapy-induced peripheral neuropathy. Methotrexate, cytarabine (cytosine arabinoside) and ifosfamide are primarily known for their central neurotoxic side effects. Central neurotoxicity ranges from acute toxicity such as aseptic meningitis, to delayed toxicities comprising cognitive deficits, hemiparesis, aphasia and progressive dementia. Risk factors are high doses, frequent administration and radiotherapy preceding methotrexate chemotherapy, which appears to be more neurotoxic than methotrexate as single modality. Data on management and neuroprotective agents are discussed. Management mainly consists of cumulative dose-reduction or lower dose-intensities, especially in patients who are at higher risk to develop neurotoxic side effects. None of the neuroprotective agents described in this article can be recommended for standard use in daily practise at this moment, and further studies are needed to confirm some of the beneficial effects described.
MeSH term(s)	Antineoplastic Agents/administration & dosage ; Antineoplastic Agents/adverse effects ; Central Nervous System Diseases/chemically induced ; Dose-Response Relationship, Drug ; Drug Administration Schedule ; Humans ; Peripheral Nervous System Diseases/chemically induced
Chemical Substances	Antineoplastic Agents
Language	English
Publishing date	2003-07-10
Publishing country	New Zealand
Document type	Journal Article ; Review
ZDB-ID	120316-2
ISSN	1179-1950 ; 0012-6667
ISSN (online)	1179-1950
ISSN	0012-6667
DOI	10.2165/00003495-200363150-00003
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Zs.A 762: Show issues

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Article: Proteomics of the TRAP-induced platelet releasate.

Piersma, Sander R / Broxterman, Henk J / Kapci, Muhammed / de Haas, Richard R / Hoekman, Klaas / Verheul, Henk M W / Jiménez, Connie R

Journal of proteomics

2009 Volume 72, Issue 1, Page(s) 91–109

Abstract: Upon stimulation, platelets release the soluble content of their cytoplasmic granules along with microparticles. This sub-proteome is of interest since many of its constituents are associated with coagulation, (tumor) angiogenesis, cell growth and ... ...

Abstract	Upon stimulation, platelets release the soluble content of their cytoplasmic granules along with microparticles. This sub-proteome is of interest since many of its constituents are associated with coagulation, (tumor) angiogenesis, cell growth and adhesion. Previously, differential - antibody-based - serum analysis has yielded information on the proteins released from platelets upon stimulation. A promising alternative strategy is formed by identifying the proteins released by freshly isolated platelets from blood using proteomics. Here we report on the analysis of the thrombin receptor activating peptide (TRAP)-induced releasate from 3 different volunteers using high resolution, high mass accuracy hybrid LTQ-FT mass spectrometry in a GeLC-MS/MS workflow. We obtained an activated platelet releasate proteome comprising a total of 716 identified proteins with 225 proteins present in the releasate of 3/3 volunteers. This core dataset is characterized by gene ontology mining and signal peptide analysis. Meta-analysis of our dataset and two published datasets of platelet a-granules and microparticles reveals that 55% of our platelet releasate proteins can be annotated using these previous platelet subproteome data, of the remaining releasate proteome 5% overlaps with a published platelet secretome while 40% of our data consists of novel releasate proteins. This high-accuracy activated platelet releasate proteome represents the largest and most comprehensive analysis to date. This approach offers unique possibilities to analyse the role of platelet-secreted proteins in physiology and in diseases such as atherosclerosis and cancer.
MeSH term(s)	Blood Platelets/metabolism ; Exocytosis ; Humans ; Proteome/metabolism ; Receptors, Thrombin/metabolism ; Secretory Vesicles/metabolism ; Tandem Mass Spectrometry
Chemical Substances	Proteome ; Receptors, Thrombin
Language	English
Publishing date	2009-02-15
Publishing country	Netherlands
Document type	Journal Article ; Meta-Analysis ; Research Support, Non-U.S. Gov't
ZDB-ID	2400835-7
ISSN	1876-7737 ; 1874-3919
ISSN (online)	1876-7737
ISSN	1874-3919
DOI	10.1016/j.jprot.2008.10.009
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Article: Advanced glycation end products in human cancer tissues: detection of Nepsilon-(carboxymethyl)lysine and argpyrimidine.

van Heijst, Jeroen W J / Niessen, Hans W M / Hoekman, Klaas / Schalkwijk, Casper G

Annals of the New York Academy of Sciences

2005 Volume 1043, Page(s) 725–733

Abstract: Tumors are generally characterized by an increased glucose uptake and a high rate of glycolysis. Since one consequence of an elevated glycolysis is the nonenzymatic glycation of proteins, we studied the presence of advanced glycation end products (AGEs) ... ...

Abstract	Tumors are generally characterized by an increased glucose uptake and a high rate of glycolysis. Since one consequence of an elevated glycolysis is the nonenzymatic glycation of proteins, we studied the presence of advanced glycation end products (AGEs) in human cancer tissues. We detected the presence of the AGEs N(epsilon)-(carboxymethyl)lysine (CML) and argpyrimidine in several human tumors using specific antibodies. Because AGEs have been associated with the etiology of a variety of different diseases, these results suggest that CML and argpyrimidine could be implicated in the biology of human cancer.
MeSH term(s)	Enzyme-Linked Immunosorbent Assay ; Glycation End Products, Advanced/analysis ; Glycolysis ; Humans ; Lysine/analogs & derivatives ; Lysine/analysis ; Neoplasm Proteins/chemistry ; Neoplasm Proteins/metabolism ; Neoplasms/chemistry ; Neoplasms/pathology ; Pyruvaldehyde/analysis
Chemical Substances	Glycation End Products, Advanced ; Neoplasm Proteins ; N(6)-carboxymethyllysine (70YDX3Z2O7) ; Pyruvaldehyde (722KLD7415) ; Lysine (K3Z4F929H6)
Language	English
Publishing date	2005-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	211003-9
ISSN	1749-6632 ; 0077-8923
ISSN (online)	1749-6632
ISSN	0077-8923
DOI	10.1196/annals.1333.084
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Article: Automated serum peptide profiling using novel magnetic C18 beads off-line coupled to MALDI-TOF-MS.

Jimenez, Connie R / El Filali, Zineb / Knol, Jaco C / Hoekman, Klaas / Kruyt, Frank A E / Giaccone, Giuseppe / Smit, August B / Li, Ka Wan

Proteomics. Clinical applications

2007 Volume 1, Issue 6, Page(s) 598–604

Abstract: Serum peptide profiling by MS is an emerging approach for disease diagnosis and biomarker discovery. A magnetic bead-based method for off-line serum peptide capture coupled to MALDI-TOF-MS has been recently introduced. However, the reagents are not ... ...

Abstract	Serum peptide profiling by MS is an emerging approach for disease diagnosis and biomarker discovery. A magnetic bead-based method for off-line serum peptide capture coupled to MALDI-TOF-MS has been recently introduced. However, the reagents are not available to the general scientific community. Here, we developed a protocol for serum peptide capture using novel magnetic C18 beads, and automated the procedure on a high-throughput magnetic particle processor. We investigated bead equilibration, peptide binding and peptide elution conditions. The method is evaluated in terms of peaks counts and reproducibility of ion intensities in control serum. Overall, the DynaBead-RPC18-based serum sample processing protocol reported here is reproducible, robust and allows for the detection of ˜200 peptides at m/z 800-4000 of serum that was allowed to clot for 1 h. The average intra-experiment %CV of normalized ion intensities for crude serum and 0.5% TFA/0.15% n-octyl glucoside-treated serum, respectively, were 12% (range 2-38%) and 10% (3-21%) and the inter-experiment %CVs were 24% (10-53%) and 31% (10-59%). Importantly, this method can be used for serum peptide profiling by anyone in possession of a MALDI-TOF instrument. In conjunction with the KingFisher® 96, the whole serum peptide capture procedure is high-throughput (˜20 min per isolation of 96 samples in parallel), thereby facilitating large-scale disease profiling studies.
Language	English
Publishing date	2007-06
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2261788-7
ISSN	1862-8354 ; 1862-8346
ISSN (online)	1862-8354
ISSN	1862-8346
DOI	10.1002/prca.200600483
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Zs.A 6575: Show issues

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Article ; Online: Glioblastoma-induced inhibition of Langerhans cell differentiation from CD34(+) precursors is mediated by IL-6 but unaffected by JAK2/STAT3 inhibition.

van Cruijsen, Hester / Oosterhoff, Dinja / Lindenberg, Jelle J / Lougheed, Sinéad M / Fehres, Cynthia / Weijers, Karin / van Boerdonk, Robert / Giaccone, Giuseppe / Scheper, Rik J / Hoekman, Klaas / de Gruijl, Tanja D

Immunotherapy

2011 Volume 3, Issue 9, Page(s) 1051–1061

Abstract: Aims: Langerhans cell (LC) infiltration has been observed in glioblastoma, but the glioblastoma microenvironment may be conditioned to resist antitumor immune responses. As little is known about how glioblastoma may affect dendritic cell differentiation, ...

Abstract	Aims: Langerhans cell (LC) infiltration has been observed in glioblastoma, but the glioblastoma microenvironment may be conditioned to resist antitumor immune responses. As little is known about how glioblastoma may affect dendritic cell differentiation, here we set out to delineate the effects of glioblastoma-derived soluble factors on LC differentiation. Methods: CD34(+) precursor cells of the human myeloid cell line MUTZ-3 were differentiated into LC in the presence of conditioned media of the human glioblastoma cell lines U251 or U373 and phenotypically and functionally characterized. Results: Glioblastoma-conditioned media inhibited LC differentiation, resulting in functional impairment, as determined by allogeneic mixed leukocyte reactivity, and induction of STAT3 activation. IL-6 blockade completely abrogated these glioblastoma-induced immunosuppressive effects and reduced STAT3 phosphorylation. However, neither addition of JSI-124 (cucurbitacin-I; a JAK2/STAT3 inhibitor), nor of GW5074 (a Raf-1 inhibitor), both of which interfere with signaling pathways reported to act downstream of the IL-6 receptor, prevented the observed inhibitory effects on LC differentiation. Conclusion: Glioblastoma-derived IL-6 is responsible for the observed suppression of LC differentiation from CD34(+) precursors but appears to exert this effect in a STAT3 and Raf-1 independent fashion.
MeSH term(s)	Antigens, CD34/analysis ; Brain Neoplasms/pathology ; Cell Differentiation ; Cell Line, Tumor ; Glioblastoma/pathology ; Hematopoietic Stem Cells/cytology ; Humans ; Interleukin-6/physiology ; Janus Kinase 2/antagonists & inhibitors ; Janus Kinase 2/physiology ; Langerhans Cells/cytology ; STAT3 Transcription Factor/antagonists & inhibitors ; STAT3 Transcription Factor/physiology ; Transforming Growth Factor beta/physiology
Chemical Substances	Antigens, CD34 ; Interleukin-6 ; STAT3 Transcription Factor ; STAT3 protein, human ; Transforming Growth Factor beta ; JAK2 protein, human (EC 2.7.10.2) ; Janus Kinase 2 (EC 2.7.10.2)
Language	English
Publishing date	2011-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1750-7448
ISSN (online)	1750-7448
DOI	10.2217/imt.11.107
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