Scientific Annual Report 2015 Scientific Annual Report 2015

281 Pages·2016·6.26 MB·English

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Scientific Annual Report 2015
Netherlands Cancer Institute
Plesmanlaan 121
1066 CX Amsterdam
The Netherlands
www.nki.nl
Contents
2 Introduction 10 Institutional 22 Board members
Director of Research site visit report
26 Group leaders
26 Neil Aaronson 64 Jacqueline Jacobs 102 Jan-Jakob Sonke
28 R euven Agami 66 Kees Jalink 104 Arnoud Sonnenberg
30 Roderick Beijersbergen 68 Jos Jonkers 106 Hein te Riele
32 Jos Beijnen 70 Sabine Linn 108 Uulke van der Heide
36 André Bergman 72 Rene Medema 110 Michiel van der Heijden
38 René Bernards 74 Gerrit Meijer 112 Wim van Harten
40 Anton Berns 76 Wouter Moolenaar 114 Flora van Leeuwen
42 Christian Blank 78 Jacques Neefjes en Matti Rookus
44 Eveline Bleiker 80 Huib Ovaa 118 Fred van Leeuwen
46 Jannie Borst 82 Daniel Peeper 120 Maarten van Lohuizen
48 Piet Borst 84 Anastassis Perrakis 122 Bas van Steensel
50 Thijn Brummelkamp 86 Sven Rottenberg 124 Marcel Verheij
52 Karin de Visser 88 Sanne Schagen 126 Emile Voest
54 John Haanen 90 Jan Schellens 128 Jelle Wesseling
56 Michael Hauptmann 94 Alfred Schinkel 130 Lodewyk Wessels
58 John Hilkens 96 Marjanka Schmidt 132 Lotje Zuur
60 Metello Innocenti 98 Ton Schumacher 134 Wilbert Zwart
62 Heinz Jacobs 100 Titia Sixma
138 Division of 158 Division of 174 Division of
Diagnostic Oncology Medical Oncology Radiation Oncology
194 Division of 210 Biometrics 218 Research
Surgical Oncology Department facilities
220 Education in 224 Clinical 248 Invited
oncology trials speakers
250 Research 270 Personnel
projects index
Scientific Annual Report 2015
Introduction
I am pleased to present our Scientific Annual Report that contains an overview of the
Director of Research
scientific achievements of the Netherlands Cancer Institute in 2015. More background
René Medema
information on our research programs and principle investigators can be found on our
website (www.nki.nl) or in our Scientific Brochure that is available for download on our
website.
The Netherlands Cancer Institute is a Comprehensive Cancer Center, combining a dedicated
cancer hospital and cancer research institute in a single organization. Our hospital
underwent a significant expansion in 2015. These new facilities are complemented by a
large radiotherapy department and an extensive infrastructure for clinical research that
includes clinical data management and a large array of diagnostic facilities. Over the years
the hospital has built a large repository of patient data and a large collection of tumor and
normal tissues. Clinical research spans across medical, surgical and diagnostic oncology,
radiotherapy, pharmacology, epidemiology and psychosocial oncology and research into
cost effectiveness of health care and efficiency of planning and organization. Our hospital
has seen steady growth in patient numbers over the last years, with an average annual
growth of 5%. As a result of this growth, we have registered ~10.000 new unique patients
at our hospital in 2015. To continue to accommodate this growth, we will need to plan
additional expansions of our clinical capacity, and foresee that new building activities (in
addition to the ones that are currently ongoing) will be required from 2018 onwards. We
are currently nearing completion of our new unit for rehabilitation and the expansion of
our pathology department, which will become operational during the course of 2016. Also,
we have established joint clinical programs for urology, neuro-endocrine and head-and-
neck tumors together with the UMC Utrecht, and aim to expand this alliance to encompass
pathology during the course of 2016. At the end of 2015 Wim van Harten stepped down
from our Board of Directors, to become the chairman of the Board of Directors at Rijnstate
hospital in Arnhem. Wim was our financial director for almost 15 years. We are very
thankful for everything Wim has achieved in those years, and very pleased that as of March
1st, 2016, Marien van der Meer joined our board as the new Financial Director.
At the end of 2015 we closed down our former laboratory animal facility and at the same
time, our mouse cancer clinic became fully operational. This new facility incorporates a
transgenic unit, an intervention unit and an imaging unit equipped with Bioluminescence,
SPECT, MRI and a linear beam irradiation set-up for the treatment of small laboratory
animals. The mouse cancer clinic is equipped with most of the clinical modalities that we
use in our regular clinic, so that we can use all of these for preclinical testing of new
treatment strategies that are identified in our preclinical research program. Our former
animal facility will be broken down in 2016 to make space for the construction of our new
hospital pharmacy to create our own production units for experimental drugs and clinical
grade biologicals preparations.
We managed to end 2015 with a profit for the hospital and finalized the much needed
expansion of our clinical facilities. But the sustained growth in numbers of patients that
come to our hospital continues to put a strain on our system. Our excellent reputation is
attracting more patients than we can possibly treat due to limitations in physical space
and personnel. This, combined with tighter budgets from health insurance companies, are
putting an increasing strain on all of our activities. Our progress is severely hampered
by limitations in the time that clinicians can dedicate to research during their training.
An important challenge for our institute is to accommodate sufficient growth to be able
to provide the required clinical care for the growing numbers of cancer patients and at
the same time be able to continue to develop better treatments. We strive to improve
treatment options for all types of cancer, and given the development of personalized
medicine this requires higher number of patients to provide the evidence that is necessary
2
to make these new treatment options available to patients throughout the Netherlands.
The financial challenges that we face at the national level to be able to achieve the desired
innovations to improve the outlook for our patients are daunting, and we currently lack
the resources to take benefit from all of the new opportunities that have presented
themselves in the most recent years. We see this as a serious and nationwide shortcoming.
Despite the consistent growth of our research budget over the last years (table 1), the
growth does not parallel the rate of growth of the financial demands that our research
program brings forward. We need to invest in large programs such as immunotherapy
and image-guided interventions, but maintaining an international competitive program
requires continuous investments in infrastructure which remains a challenge. Also, we run
many projects that produce very large datasets, but the long-term maintenance of these
valuable resources requires extensive management and storage costs. These challenges
are not unique to the Netherlands Cancer Institute, but they are more difficult for us to
overcome due to the fact that our research program is in the largest part financed from
project (short-term) funding. That ratio has steadily shifted towards external grants,
donations and short-term research agreements with third parties. Currently ~65% of
our total research budget comes from such sources, making it challenging to maintain
sufficient manpower in the underlying infrastructure. On top of that, the complexity of
current day cancer research also requires that we adopt a team-science approach.
We are very excited that in 2015, the Dutch Cancer Society (KWF) and the NKI have
renewed their collaboration, adding a 5-year extension to our collaboration that has been
active for over 65 years. The goal of this collaboration is to decrease the incidence of
cancer, to improve treatment and the improve quality of life for cancer patients. Under
this new 5-year agreement, KWF has committed 14% of its annual revenues (in 2015; 16
million euros), as an institutional subsidy to the NKI. This is in line with the vision of KWF to
support a national institute for cancer research that takes a leading role in dedicated and
most promising areas of cancer research. As part of this new contract, KWF will monitor
and evaluate the planning, results and impact of the research program with respect to the
mission of KWF. With this new mode of interaction, we aim to better visualize the impact
on our research on the knowledge of cancer and the development of new treatment
strategies. In addition, it will help KWF to improve its role as the facilitator of cancer
research. In addition to this core funding, our Antoni van Leeuwenhoek Foundation, that we
have established together with the Dutch Cancer Society, totaled over 1.5 million euro’s in
2015. We are very grateful for these generous donations, as they make it possible for us to
quickly seize new opportunities in cancer research.
TABLE 1
CORE RESEARCH FUNDING THE NETHERLANDS CANCER INSTITUTE - ANTONI VAN LEEUWENHOEK HOSPITAL
BY THE DUTCH CANCER SOCIETY AND THE MINISTRY OF HEALTH, WELFARE AND SPORT IN THE PERIOD
2004 – 2015 IN MILLION EUROS.
30 2004 2005 2006 2007 2008 2009 2010 2011 2012 2013 2014 2015
25
20
15
10
5
0
DUTCH CANCER SOCIETY
MINISTRY OF HEALTH, WELFARE & SPORT*
TOTAL
* EXCLUDED ARE THE REIMBURSEMENT FOR INTEREST
AND DEPRECIATION OF BUILDINGS
3
HIGHLIGHTS
It is impossible to provide a complete overview of the total impact generated by our
Institute in 2015 in this introduction. Many of the highlights can be found in the reports
of the individual group leaders further on in this annual report or on our website. I have
chosen to mention just a few highlights here.
The Agami lab devised a novel genetic approach to screen for cancerous enhancers
using the genome-editing CRISPR-Cas9 tool. This approach yielded novel insights in
enhancers with potential tumor suppressor and oncogenic roles. Following the initial
functional annotation of the identified enhancers, the group setup experiments to
investigate local mutations that cause resistance to cancer therapy. This information
will be used for cancer diagnosis and treatment. The lab of Thijn Brummelkamp identified
all of the essential genes in the human genome, and characterized novel synthetic lethal
interactions, providing very useful information for the development of novel combination
therapies. The lab of Emile Voest unraveled a fatty acid signaling pathway that confers
chemoresistance and started personalized medicine trials based on genomics and tumor
organoids.
In collaboration with his clinical colleagues John Haanen and Christian Blank, Daniel
Peeper’s group showed that in melanoma, distinct mechanisms of drug-resistance are
operational in different metastatic lesions from a single patient. Several of the genetic
alterations responsible for the resistance could already be identified in the pre-treatment
melanoma. This indicates that drug-resistant tumor clones may be pre-existing, causing
heterogeneous treatment responses and thereby limiting durable clinical benefit.
The group of René Bernards identified a vulnerability that BRAF mutant melanomas
acquire when they become resistant to MAP kinase pathway inhibitors. His group found
that treatment of these drug resistant cells with histone deacetylases (HDAC) inhibitors
results in persistently increased MEK-ERK signaling and a more lasting proliferation
arrest. Their data indicate that sequential treatment of BRAF inhibitor resistant
melanomas with HDACi leads to a prolonged state of proliferation arrest and cell death,
which ultimately leads to regression of the BRAF-inhibitor resistant tumor in vivo. A
clinical study with HDAC inhibitors in drug-resistant melanoma will start in 2016.
Nienke de Vries and colleagues in the Van Lohuizen lab showed that in high grade
Glioma, long term exposure to Ezh2 inhibition resulted in a tumor identity switch to a
more aggressive stem cell like subtype. This finding is highly relevant to the application
of Ezh2 inhibitors in Glioma, a concept based on the observation that short term
Polycomb inhibition can be beneficial. This shows that dosing and exposure time to Ezh2
inhibitors matters and that long term Ezh2 inhibition can unleash an unsuspected tumor
suppressive role in Glioma. In collaboration with the the groups of Wim Vermeulen and
Jurgen Marteijn at the Erasmus MC in Rotterdam, the Medema group identified the core
spliceosome as a target of the DNA damage-activated kinase ATM, thus demonstrating
that transcription-blocking lesions play an important role in the DNA damage response of
non-replicating cells.
Bas van Steensel and colleagues developed a method to map the contacts of the genome
with the nuclear lamina in single human cells.  This enabled them to obtain a detailed view
of the spatial organization of DNA inside the cell nucleus, and how this varies from cell
to cell. Hundreds of genomic regions were identified that are anchored to the lamina in
nearly every cell; these regions may help to package the genome inside the nucleus. It
will be interesting to investigate how genome rearrangements, which frequently occur in
cancer, affect this spatial organization.
Hanna van Waart in the group of Neil Aaronson showed that various physical exercise
interventions resulted in significantly less decline in cardiorespiratory fitness and better
physical functioning, compared to usual care. A high intensity, supervised exercise
program also resulted in significantly less necessity for reduction in chemotherapy
doses. This is the first clinical trial to demonstrate that women who exercise during their
breast cancer treatment are significantly more likely to complete their chemotherapy
regimen without dose adjustments.
Michael Schaapveld in Flora van Leeuwen’s group reported that the risk of second solid
cancers had not changed appreciably among patients with Hodgkin lymphoma who were
treated during the 1990s, as compared with those who were treated during earlier
decades. The results suggest that reduction of the incidence of second cancers can best
be achieved by more substantial reductions in the radiation exposure of healthy organs
4
and tissues and by avoidance of high-dose procarbazine. In addition, the Van Leeuwen
group also reported on substantially increased risk of several cardiovascular diseases
after treatment for Hodgkin lymphoma and identified a linear radiation dose response
curve for the association between mean heart dose and risk of coronary heart disease. 
These results provide a solid basis for future research that can help us to develop
novel anti-cancer therapies. In recent years, our research program has become very
successful in clinical translation of the therapeutic concepts that stem from our basic
and translational research program. Several clinical trials were already ongoing at the
Netherlands Cancer Institute at the start of 2015 that are the direct result of basic and
translational research that was performed in our Institute (table 2). During the course
of 2015, a number of new trials that are based on our own (pre-)clinical research were
added to this list (table 3). We are very pleased with the fact that we have managed to
significantly shorten the time between discovery and clinical application in the last few
years, with examples of clinical studies that were opened before the original discovery
was published.
TABLE 2
THERAPEUTIC CONCEPTS THAT ARE THE PRODUCT OF FUNDAMENTAL AND TRANSLATIONAL RESEARCH
PERFORMED AT THE NETHERLANDS CANCER INSTITUTE, AND CURRENTLY IN CLINICAL DEVELOPMENT IN
OUR INSTITUTE
REFERENCE CLINICALTRIALS. AVL CODE NOVEL TREATMENT TUMOR TYPE
NUMBER** GOV
1 NCT01719380 M12LGX EGFRi + BRAFi ± PI3Ki Mutant BRaf Colorectal Cancer
1 NCT01750918 M13DPT EGFRi + BRAFi ± MEKi Mutant BRaf Colorectal Cancer
2 NCT02039336 M13DAP Pan-HERi + MEKi Mutant KRas Colorectal Cancer
2 NCT02230553 M14LTK Pan-HERi + MEKi Mutant KRas Colorectal Cancer
3-5 Registration M14REV Carboplatin + PARPi Advanced Breast Cancer with
pending BRCA mutation
6,7 NCT02285179 M14POS Tamoxifen + PI3Ki ER/PR+ and HER2- Breast Cancer
8-10 NCT01057069 M09TNM Neo-adjuvant Chemo Triple-Negative Breast Cancer
8-15 NCT01898117 M13TNB Paclitaxel ± VEGFi BRCA1-like Breast Cancer
16,17 NTC02278887 M14TIL TIL vs. Ipilimumab Metastatic Melanoma
18-20 NCT00407186 M06CRI Chemoradiotherapy + surgery Resectable Gastric Cancer
21 NCT02229656 N13ORH Radiotherapy + PARPi Laryngeal and HPV-Negative
Oropharyngeal SCC
21 NCT01562210 N11ORL Radiotherapy ± Cisplatin + Locally Advanced NSCLC
PARPi
21 NCT02227082 N13ORB Radiotherapy + PARPi Locally Advanced Triple-Negative
Breast Cancer
22 NCT01504815 M11ART Cisplatin + Adaptive High Dose Locally Advanced Oropharynx, Oral
Radiotherapy Cavity or Hypopharynx SCC
23 *NCT01024829 M09PBO FDG-PET-based Boosting RT Inoperable NSCLC
24 NCT01780675 M12PHA Hippocampus Avoidance PCI SCLC
25 NCT01933568 N12HYB Combined Stereotactic and Stage II-III NSCLC
Conventional Fractionated RT
26 *NCT01543672 M11VOL MLD-based SBRT Inoperable + Peripheral NSCLC
27 NCT01024582 M08PBI Partial Accelerated Early Stage Operable Breast
Preoperative Irradiation Cancer
28,29 NCT00582244 P07CB Cognitive Behavioral Therapy & Breast Cancer
Physical exercise
30 NCT00783822 P08TIM Rapid Genetics BRCA mutant Breast Cancer
31,32 NCT015622431 P11SIG Problem checklist Breast & Colon Cancer
REFERENCE NTR CODE AVL CODE NOVEL TREATMENT TUMOR TYPE
NUMBER
33 *NTR4607 N14HPV DNA vaccination HPV16+ Vulvar Neoplasia
34 NTR3539 M11TCR MART-1 TCR gene therapy Metastatic Melanoma
35 NTR2159 P09PHY Physical Exercise Breast & Colon Cancer
* THERAPEUTIC CONCEPT NOT SOLELY, BUT PRIMARILY DEVELOPED AT THE NETHERLANDS CANCER INSTITUTE
** SEE REFERENCE ON THE NEXT PAGE
5
1. Prahallad A et al. Unresponsiveness 12. Wessels LF et al. Molecular 23. Van Kesteren Z et al. A practical 33. Bins AD et al. A rapid and potent
of colon cancer to BRAF(V600E) classification of breast carcinomas by technique to avoid the hippocampus in DNA vaccination strategy defined by in
inhibition through feedback activation comparative genomic hybridization: prophylactic cranial irradiation for lung vivo monitoring of antigen expression.
of EGFR. Nature 2012;483:100-3 a specific somatic genetic profile cancer. Radiother Oncol. 2012;102:225- Nat Med. 2005;11:899-904
for BRCA1 tumors. Cancer Res 7
2. Sun C et al. Intrinsic resistance to 2002;62:7110-7117 34. Gomez-Eerland R et al. Manufacture
MEK inhibition in KRAS mutant lung and 24. Grills IS et al. A collaborative of gene-modified human T-cells with
colon cancer through transcriptional 13. van Beers EH et al. Comparative analysis of stereotactic lung a memory stem/central memory
induction of ERBB3. Cell Rep. genomic hybridization profiles in human radiotherapy outcomes for early-stage phenotype. Hum GeneTher Methods.
2014;7:86-93 BRCA1 and BRCA2 breast tumors non-small-cell lung cancer using 2014;25:277-87
highlight differential sets of genomic daily online cone-beam computed
3. Rottenbwerg S et al. High sensitivity aberrations. Cancer Res 2005;65:822- tomography image-guided radiotherapy. 35. de Vos van Steenwijk PJ et al.
of BRCA1-deficient mammary tumors to 827 J Thorac Oncol. 2012;7:1382-93 The long-term immune response
the PARP inhibitor AZD2281 alone and in after HPV16 peptide vaccination
combination with platinum drugs. Proc. 14. Joosse SA et al. Prediction of 25. Peulen H et al. Mid-ventilation in women with low-grade pre-
Natl. Acad. Sci. USA 2008;105:17079-84 BRCA1-association in hereditary based PTV margins in Stereotactic malignant disorders of the uterine
non-BRCA1/2 breast carcinomas with Body radiotherapy (SBRT): a cervix: a placebo-controlled phase II
4. Fong PC et al. Inhibition of poly(ADP- array-CGH. Breast Cancer Res Treat clinical evaluation. Radiother Oncol. study. Cancer Immunol Immunother.
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number analysis by Multiplex Ligation- delineation in external beam partial intensity physical activity and high
5. Oonk AM et al. Clinical correlates dependent Probe Amplification (MLPA) breast irradiation: less inter-observer intensity physical exercise during
of 'BRCAness' in triple-negative of BRCA1-associated breast cancer variation with preoperative- compared adjuvant chemotherapy on physical
breast cancer of patients receiving regions identifies BRCAness. Breast to postoperative delineation. Radiother fitness, fatigue and chemotherapy
adjuvant chemotherapy. Ann Oncol. Cancer Res 2011;13:R107 Oncol. 2014;110:467-70 completion rates: Results of the PACES
2012;23:2301-5 randomized clinical trial. J Clin Oncol
16. Kvistborg P et al. TIL therapy 27. Kenter GG et al. Vaccination 2015;33:1918-27
6. Beelen K et al. PIK3CA mutations, broadens the tumor-reactive CD8(+) T against HPV-16 oncoproteinsfor vulvar
phosphatase and tensin homolog, cell compartment in melanoma patients. intraepithelial neoplasia. N Engl J Med.
human epidermal growth factor Oncoimmunology 1:409-418 2009;361:1838-47
receptor 2, and insulin-like
growth factor 1 receptor and 17. Dikken JL et al. Neo-adjuvant 28. Duijts SFA et al. Efficacy of
adjuvant tamoxifen resistance in chemotherapy followed by surgery cognitive behavioral therapy and
postmenopausal breast cancer and chemotherapy or by surgery and physical exercise in alleviating
patients. Breast Cancer Res. chemoradiotherapy for patients with treatment-induced menopausal
2014;16:R13 resectable gastric cancer (CRITICS). symptoms in patients with breast
BMC Cancer 2011;11:329 cancer: Results of a randomized
7. Beelen K et al. Phosphorylated controlled multicenter trial. J Clin Oncol
p-70S6K predicts tamoxifen resistance 18. Trip AK et al. Preoperative 2012;30:4124-33
in postmenopausal breast cancer chemoradiotherapy in locally advanced
patients randomized between adjuvant gastric cancer, a phase I/II feasibility 29. Mewes JC et al. Cost-effectiveness
tamoxifen versus no systemic and efficacy study. Radiother Oncol. of cognitive behavioral therapy and
treatment. Breast Cancer Res. 2014;112: 284-8 physical exercise for alleviating
2014;16:R6 treatment-induced menopausal
19. Trip AK et al. IMRT limits symptoms in breast cancer patients. J
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21. Heukelom J et al. Adaptive and 31. Eijzenga W et al. Effect of
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patterns resembling BRCA1- and improving Cancer treatment outcomE psychosocial problems on personalized
BRCA2-mutated breast cancers predict (ARTFORCE); a randomized controlled communication, referrals and distress
benefit of intensified carboplatin-based phase II trial for individualized levels in cancer genetic counseling
chemotherapy. Breast Cancer Res. treatment of head and neck cancer. practice: A randomized controlled trial.
2014;16:R47 BMC Cancer 2013;13:84 J Clin Oncol. 2014;32:2998-3004
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6
TABLE 3
STUDIES STARTED IN 2015, BASED ON (PRE-)CLINICAL RESEARCH PERFORMED
AT THE NETHERLANDS CANCER INSTITUTE
CLINICALTRIALS.GOV AVL CODE NOVEL TREATMENT TUMOR TYPE
NCT02575066 M15PAS Panopanib + RT Non-metastatic Sarcoma
NCT02450656 M14AFS Afatinib + Selumetinib Advanced Mutant KRas and PIK3CA
wildtype Colorectal, NSCLC or
Pancreatic Cancer
NCT02278133 M14WLC WNT974 + LGX818 + Cetuximab Colorectal Cancer with Mutant
BRAF and Wnt Pathway mutations
NCT02418624 M14REV Carboplatin + PARPi Advanced Breast Cancer with
BRCA mutation
NCT02437279 N14OPC Ipilumimab + Nivolumab Melanoma
NCT02316197 M15MSR DNA-PKi + Radiotherapy Advanced Solid Tumors
NCT02324452 M14PDP Genotype-directed dosing of Various Neoplasms
Fluoropyrimidines
NCT02572661 N14SUS Sentinel node mapping using SPECT Head and Neck Cancer
NTR CODE AVL CODE NOVEL TREATMENT TUMOR TYPE
NTR5219 N14LMN Lymphatic mapping of the neck with Oral Cavity Malignancies
ICG-nanocolloid
NTR5220 M14HSN Sentinel node mapping with ICG- Bladder Cancer
99mTc-nanocolloid
pilot N14IMR Immunological effects of (chemo) HPV positive Squamous Cell
radiotherapy Carcinoma
pilot N15MML Magnetic Marker Localization Non-palpable Breast Cancer
- M14SEA Strengthening exercises using the Head and Neck Cancer
Swallowing Exercise Aid
QUALITY OF RESEARCH
The quality of our research can be monitored in several ways. First of all, objective
bibliometric parameters (citations and impact of scientific articles published by NKI staff)
demonstrate that our scientific productivity, as measured in numbers of citations, is
significantly increasing over time (table 4). Our position at the international forefront of
cancer research was confirmed by the institutional site visit that took place in 2015, the
full report of this site visit can be found on pages 10-20. Every five years this institutional
site visit is executed under supervision of the Royal Netherlands Academy of Science and
Arts (KNAW), the Dutch Cancer Society (KWF) and the Ministry of Health, Welfare and Sport
(VWS). In consultation with the KNAW, KWF and VWS, we select a site visit committee that
comprises world-leading experts in cancer research. In addition, reflecting our strong
interest in performing translational research we include a patient advocate. For this
edition of the institutional site visit we were very honored that Prof. Dr. Harold Varmus
(Nobel Prize winner and former director of the National Institutes of Health and the
National Cancer Institute was willing to chair this committee. In addition, the committee
consisted of: Dr. Margaret Frame (Director of Research of the Edinburgh Cancer Research
Centre), Prof. Dr. David Livingston (Emil Frei Professor, Harvard Medical School and chair
of the research committee of the Dana-Farber Cancer Institute), Prof. Dr. Simon Powell
(Enid A. Haupt Professor and chair of the department of Radiotherapy, Memorial Sloan-
Kettering Cancer Center), Prof. Dr. Charles Sawyers (HHMI Investigator and chair of the
department of Medical Oncology, Memorial Sloan-Kettering Cancer Center), Dr. Daniel
Speiser (Chair of the Clinical Immunotherapy Development and Trial Program at the Ludwig
Cancer Research Center, Lausanne), Dr. Thomas Würdinger (representative for KWF and
staff researcher at the department of Neuro-Oncology, VUMC, Amsterdam), Prof. Dr.
Rick Grobbee (representative from the Royal Dutch Academy of Sciences (KNAW) and
University Professor Clinical Epidemiology at the UMC Utrecht) and Dr. Jurgen Seppen
(Patient advocate, Chair of the Stichting Lynch Polyposis and staff researcher at the AMC).
We were very proud to receive excellent marks from this committee of international top-
class scientists. The general conclusion of the committee was that the NKI manages “to
perform at an exceptionally high level and remains one of the world’s leading institutions
7