Publications by authors named "Annemieke De Wilde"

9 Publications

  • Page 1 of 1

The Experts Speak on Biobank Education.

Biopreserv Biobank 2020 Feb;18(1):14-17

Vanderbilt University Medical Center, Nashville, Tennessee.

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http://dx.doi.org/10.1089/bio.2020.29064.sodDOI Listing
February 2020

Cardiogeneticsbank@UZA: A Collection of DNA, Tissues, and Cell Lines as a Translational Tool.

Front Med (Lausanne) 2019 6;6:198. Epub 2019 Sep 6.

Center of Medical Genetics, Antwerp University Hospital, University of Antwerp, Antwerp, Belgium.

Cardiogeneticsbank@UZA is an academic hospital integrated biobank that collects aortic tissue, blood, cell lines (fibroblasts, vascular smooth muscle cells, peripheral blood mononuclear cells, and induced pluripotent stem cells), and DNA from patients with cardiogenetic disorders, for both diagnostic and research purposes. We adhere to a quality management system and have established standard protocols for the sampling and processing of all cardiogenetic patient related materials. Cardiogeneticsbank@UZA is embedded in the Biobanking and Biomolecular Resources Research Infrastructure Belgium (BBMRI.be) and samples from this biobank are available for commercial and academic researchers, through an established access procedure. Currently, the extremely valuable cardiogenetics collection consists of more than 8,700 DNA samples, 380 tissue samples, and 500 cell lines of 7,578 patients, and is linked with extensive clinical data. Some interesting potential research applications are discussed.
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http://dx.doi.org/10.3389/fmed.2019.00198DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6742711PMC
September 2019

Cachexia in cancer: what is in the definition?

BMJ Open Gastroenterol 2016 18;3(1):e000097. Epub 2016 Oct 18.

Department of Oncology (MOCA) , University Hospital Antwerp (UZA) , Edegem , Belgium.

Objective: This study aimed to provide evidence-based results on differences in overall survival (OS) rate to guide the diagnosis of cancer cachexia.

Design: Data collection and clinical assessment was performed every 3 months (5 visits): baseline data, muscle strength, nutritional and psychosocial status. 2 definitions on cachexia using different diagnostic criteria were applied for the same patient population. Fearon 's definition is based on weight loss, body mass index (BMI) and sarcopenia. Evans nuances the contribution of sarcopenia and attaches additional attention to abnormal biochemistry parameters, fatigue and anorexia. The mean OS rates were compared between patients with and without cachexia for both definitions.

Results: Based on the population of 167 patients who enrolled, 70% developed cachexia according to Fearon 's definition and 40% according to Evans 's definition. The OS in the cachectic population is 0.97 and 0.55 years, respectively. The difference in OS between patients with and without cachexia is more significant using the diagnostic criteria of Evans . The focus of Fearon on weight loss and sarcopenia over-rates the assignment of patients to the cachectic group and OS rates have less prognostic value.

Conclusion: This study presents a correlation with prognosis in favour of Evans ' definition as a tool for cachexia diagnosis. This means that weight loss and BMI decline are both key factors in patients with cancer leading to cachexia but less decisive as stated by Fearon . Instead, extra factors gain importance in order to predict survival, such as chronic inflammation, anaemia, protein depletion, reduced food intake, fatigue, decreased muscle strength and lean tissue depletion.

Trial Registration Number: B300201112334.
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http://dx.doi.org/10.1136/bmjgast-2016-000097DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5093365PMC
October 2016

A Biospecimen Proficiency Testing Program for Biobank Accreditation: Four Years of Experience.

Biopreserv Biobank 2016 Oct 19;14(5):429-439. Epub 2016 May 19.

1 Integrated Biobank of Luxembourg , Luxembourg, Luxembourg .

Biobanks produce and distribute biospecimens, ensuring their fitness for purpose and accurately qualifying them before distribution. In their efforts toward professionalization, biobanks can nowadays seek certification or accreditation. One of the requirements of these standards is regular participation in Proficiency Testing (PT) programs. An international PT program has been developed and provided to biobanks and other laboratories that perform specific tests to qualify different types of biospecimens. This PT program includes biospecimen testing schemes, as well as biospecimen processing interlaboratory exercises. This PT program supports the development of biobank quality assurance by providing the possibility to assess biobank laboratory performance and useful insights into biobank laboratory method performance characteristics and thus fulfill the demands from accreditation authorities.
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http://dx.doi.org/10.1089/bio.2015.0108DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6445200PMC
October 2016

Assays for Qualification and Quality Stratification of Clinical Biospecimens Used in Research: A Technical Report from the ISBER Biospecimen Science Working Group.

Biopreserv Biobank 2016 Oct 5;14(5):398-409. Epub 2016 Apr 5.

27 Baylor College of Medicine , Houston, Texas.

This technical report presents quality control (QC) assays that can be performed in order to qualify clinical biospecimens that have been biobanked for use in research. Some QC assays are specific to a disease area. Some QC assays are specific to a particular downstream analytical platform. When such a qualification is not possible, QC assays are presented that can be performed to stratify clinical biospecimens according to their biomolecular quality.
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http://dx.doi.org/10.1089/bio.2016.0018DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5896556PMC
October 2016

ALK and crizotinib: after the honeymoon…what else? Resistance mechanisms and new therapies to overcome it.

Transl Lung Cancer Res 2014 Aug;3(4):250-61

1 Phase I-Early Clinical Trials Unit, Oncology Department and Multidisciplinary Oncology Center Antwerp (MOCA), Antwerp University Hospital, Edegem, Belgium ; 2 Department of Surgical, Oncological and Oral Sciences, Section of Medical Oncology, University of Palermo, Palermo, Italy ; 3 Molecular Pathology Unit, Pathology Department, Antwerp University Hospital, Edegem, Belgium ; 4 Memorial Cancer Institute, Memorial Health Care System, Florida International University, Miami, FL, USA ; 5 Thoracic Oncology Unit, Integrated Cancer Centre, AZ Maria Middelares, Gent, Belgium ; 6 Lung Cancer Unit, Department of Oncology, Clinica Universidad de Navarra, Pamplona, Spain ; 7 Thoracic Oncology, Multidisciplinary Oncology Center Antwerp (MOCA), Antwerp University Hospital, Edegem, Belgium ; 8 Thoracic Surgery Department, Antwerp University Hospital, Edegem, Belgium.

The last few decades have witnessed a silent revolution in the war against NSCLC, thanks to the discovery of "oncogenic drivers" and the subsequent development of targeted therapies. The discovery of the EML4-ALK fusion gene in a subgroup of patients with NSCLC and the subsequent clinical development of crizotinib has been an amazing success story in lung cancer translational-research, and its accelerated approval [only 4 years from the discovery of ALK rearrangement in NSCLC to the approval by the Food and Drug Administration (FDA)] marked the beginning of the new decade of targeted therapy. However, common to all targeted therapies, despite an initial benefit, patients inevitably experience tumor progression, due to the development of resistance. Several molecular mechanisms are responsible for acquired resistance, such as secondary mutations of ALK kinase domain or amplification of ALK fusion gene, or the activation of other oncogenic drivers, which may cause resistance independently of ALK genetic alterations. Pre-clinical data and early clinical trials showed the promising efficacy of a new class of ALK-inhibitors in overcoming acquired resistance. The inhibition of the molecular chaperone, HSP90, represents another promising strategy to overcome crizotinib resistance in ALK-rearranged NSCLC. Several molecules are currently under investigation in order to establish their specific role in the treatment of ALK-rearranged NSCLC.
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http://dx.doi.org/10.3978/j.issn.2218-6751.2014.03.01DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4367701PMC
August 2014

Expression profiling of migrated and invaded breast cancer cells predicts early metastatic relapse and reveals Krüppel-like factor 9 as a potential suppressor of invasive growth in breast cancer.

Oncoscience 2014 18;1(1):69-81. Epub 2013 Jan 18.

Center for Oncological Research (CORE), University of Antwerp, Universiteitsplein 1, B-2610 Antwerp, Belgium ; Laboratory of Pathology, Antwerp University Hospital, Wilrijkstraat 10, B-2650 Edegem (Antwerp), Belgium.

Cell motility and invasion initiate metastasis. However, only a subpopulation of cancer cells within a tumor will ultimately become invasive. Due to this stochastic and transient nature, in an experimental setting, migrating and invading cells need to be isolated from the general population in order to study the gene expression profiles linked to these processes. This report describes microarray analysis on RNA derived from migrated or invaded subpopulations of triple negative breast cancer cells in a Transwell set-up, at two different time points during motility and invasion, pre-determined as "early" and "late" in real-time kinetic assessments. Invasion- and migration-related gene expression signatures were generated through comparison with non-invasive cells, remaining at the upper side of the Transwell membranes. Late-phase signatures of both invasion and migration indicated poor prognosis in a series of breast cancer data sets. Furthermore, evaluation of the genes constituting the prognostic invasion-related gene signature revealed Krüppel-like factor 9 (KLF9) as a putative suppressor of invasive growth in breast cancer. Next to loss in invasive vs non-invasive cell lines, KLF9 also showed significantly lower expression levels in the "early" invasive cell population, in several public expression data sets and in clinical breast cancer samples when compared to normal tissue. Overexpression of EGFP-KLF9 fusion protein significantly altered morphology and blocked invasion and growth of MDA-MB-231 cells in vitro. In addition, KLF9 expression correlated inversely with mitotic activity in clinical samples, indicating anti-proliferative effects.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4295756PMC
http://dx.doi.org/10.18632/oncoscience.10DOI Listing
January 2015

Standard preanalytical coding for biospecimens: review and implementation of the Sample PREanalytical Code (SPREC).

Biopreserv Biobank 2012 Aug;10(4):366-74

1 Integrated Biobank of Luxembourg , Luxembourg .

The first version of the Standard PREanalytical Code (SPREC) was developed in 2009 by the International Society for Biological and Environmental Repositories (ISBER) Biospecimen Science Working Group to facilitate documentation and communication of the most important preanalytical quality parameters of different types of biospecimens used for research. This same Working Group has now updated the SPREC to version 2.0, presented here, so that it contains more options to allow for recent technological developments. Existing elements have been fine tuned. An interface to the Biospecimen Reporting for Improved Study Quality (BRISQ) has been defined, and informatics solutions for SPREC implementation have been developed. A glossary with SPREC-related definitions has also been added.
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http://dx.doi.org/10.1089/bio.2012.0012DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6463986PMC
August 2012