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Search Results: 1 - 10 of 572 matches for " Wouter Bossuyt "
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The Atonal Proneural Transcription Factor Links Differentiation and Tumor Formation in Drosophila
Wouter Bossuyt,Natalie De Geest,Stein Aerts,Iris Leenaerts,Peter Marynen,Bassem A. Hassan
PLOS Biology , 2012, DOI: 10.1371/journal.pbio.1000040
Abstract: The acquisition of terminal cell fate and onset of differentiation are instructed by cell type–specific master control genes. Loss of differentiation is frequently observed during cancer progression, but the underlying causes and mechanisms remain poorly understood. We tested the hypothesis that master regulators of differentiation may be key regulators of tumor formation. Using loss- and gain-of-function analyses in Drosophila, we describe a critical anti-oncogenic function for the atonal transcription factor in the fly retina, where atonal instructs tissue differentiation. In the tumor context, atonal acts by regulating cell proliferation and death via the JNK stress response pathway. Combined with evidence that atonal's mammalian homolog, ATOH1, is a tumor suppressor gene, our data support a critical, evolutionarily conserved, function for ato in oncogenesis.
The Atonal Proneural Transcription Factor Links Differentiation and Tumor Formation in Drosophila
Wouter Bossuyt,Natalie De Geest,Stein Aerts,Iris Leenaerts,Peter Marynen,Bassem A Hassan
PLOS Biology , 2009, DOI: 10.1371/journal.pbio.1000040
Abstract: The acquisition of terminal cell fate and onset of differentiation are instructed by cell type–specific master control genes. Loss of differentiation is frequently observed during cancer progression, but the underlying causes and mechanisms remain poorly understood. We tested the hypothesis that master regulators of differentiation may be key regulators of tumor formation. Using loss- and gain-of-function analyses in Drosophila, we describe a critical anti-oncogenic function for the atonal transcription factor in the fly retina, where atonal instructs tissue differentiation. In the tumor context, atonal acts by regulating cell proliferation and death via the JNK stress response pathway. Combined with evidence that atonal's mammalian homolog, ATOH1, is a tumor suppressor gene, our data support a critical, evolutionarily conserved, function for ato in oncogenesis.
Abortive Autophagy Induces Endoplasmic Reticulum Stress and Cell Death in Cancer Cells
Sofie Claerhout, Bhaskar Dutta, Wouter Bossuyt, Fan Zhang, Catherine Nguyen-Charles, Jennifer B. Dennison, Qinghua Yu, Shuangxing Yu, Gábor Balázsi, Yiling Lu, Gordon B. Mills
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0039400
Abstract: Autophagic cell death or abortive autophagy has been proposed to eliminate damaged as well as cancer cells, but there remains a critical gap in our knowledge in how this process is regulated. The goal of this study was to identify modulators of the autophagic cell death pathway and elucidate their effects on cellular signaling and function. The result of our siRNA library screenings show that an intact coatomer complex I (COPI) is obligatory for productive autophagy. Depletion of COPI complex members decreased cell survival and impaired productive autophagy which preceded endoplasmic reticulum stress. Further, abortive autophagy provoked by COPI depletion significantly altered growth factor signaling in multiple cancer cell lines. Finally, we show that COPI complex members are overexpressed in an array of cancer cell lines and several types of cancer tissues as compared to normal cell lines or tissues. In cancer tissues, overexpression of COPI members is associated with poor prognosis. Our results demonstrate that the coatomer complex is essential for productive autophagy and cellular survival, and thus inhibition of COPI members may promote cell death of cancer cells when apoptosis is compromised.
Exposé introductif : composition et compétences de la Cour constitutionnelle de la RDC
Marc Bossuyt
Fédéralisme-Régionalisme , 2007,
Abstract:
Atonal homolog 1 Is a Tumor Suppressor Gene
Wouter Bossuyt,Avedis Kazanjian,Natalie De Geest,Sofie Van Kelst,Gert De Hertogh,Karel Geboes,Greg P. Boivin,Judith Luciani,Francois Fuks,Marinee Chuah,Thierry VandenDriessche,Peter Marynen,Jan Cools,Noah F. Shroyer,Bassem A. Hassan
PLOS Biology , 2012, DOI: 10.1371/journal.pbio.1000039
Abstract: Colon cancer accounts for more than 10% of all cancer deaths annually. Our genetic evidence from Drosophila and previous in vitro studies of mammalian Atonal homolog 1 (Atoh1, also called Math1 or Hath1) suggest an anti-oncogenic function for the Atonal group of proneural basic helix-loop-helix transcription factors. We asked whether mouse Atoh1 and human ATOH1 act as tumor suppressor genes in vivo. Genetic knockouts in mouse and molecular analyses in the mouse and in human cancer cell lines support a tumor suppressor function for ATOH1. ATOH1 antagonizes tumor formation and growth by regulating proliferation and apoptosis, likely via activation of the Jun N-terminal kinase signaling pathway. Furthermore, colorectal cancer and Merkel cell carcinoma patients show genetic and epigenetic ATOH1 loss-of-function mutations. Our data indicate that ATOH1 may be an early target for oncogenic mutations in tissues where it instructs cellular differentiation.
Atonal homolog 1 Is a Tumor Suppressor Gene
Wouter Bossuyt equal contributor,Avedis Kazanjian equal contributor,Natalie De Geest,Sofie Van Kelst,Gert De Hertogh,Karel Geboes,Greg P Boivin,Judith Luciani,Francois Fuks,Marinee Chuah,Thierry VandenDriessche,Peter Marynen,Jan Cools,Noah F Shroyer ,Bassem A Hassan
PLOS Biology , 2009, DOI: 10.1371/journal.pbio.1000039
Abstract: Colon cancer accounts for more than 10% of all cancer deaths annually. Our genetic evidence from Drosophila and previous in vitro studies of mammalian Atonal homolog 1 (Atoh1, also called Math1 or Hath1) suggest an anti-oncogenic function for the Atonal group of proneural basic helix-loop-helix transcription factors. We asked whether mouse Atoh1 and human ATOH1 act as tumor suppressor genes in vivo. Genetic knockouts in mouse and molecular analyses in the mouse and in human cancer cell lines support a tumor suppressor function for ATOH1. ATOH1 antagonizes tumor formation and growth by regulating proliferation and apoptosis, likely via activation of the Jun N-terminal kinase signaling pathway. Furthermore, colorectal cancer and Merkel cell carcinoma patients show genetic and epigenetic ATOH1 loss-of-function mutations. Our data indicate that ATOH1 may be an early target for oncogenic mutations in tissues where it instructs cellular differentiation.
Defining Biomarker Performance and Clinical Validity
Patrick M. M. Bossuyt
Journal of Medical Biochemistry , 2011, DOI: 10.2478/v10011-011-0028-0
Abstract: In the evaluation of biomarkers three questions can be answered: what is the analytical validity of the marker, what is its clinical validity, and does the marker have clinical utility? In most cases, clinical validity will be expressed in terms of the marker's accuracy: the degree to which it can be used to correctly identify diseased patients or, more generally, patients with the target condition. Diagnostic accuracy is evaluated in studies in which the biomarker values are compared to the outcome of the clinical reference standard in the same patients. There are several ways in which the results of diagnostic accuracy studies can be summarized, reported, and interpreted. In this paper we summarize and present the available measures. We classify these as error-based measures, information-based measures, and measures of the strength of the association. Clinical validity is linked to clinical utility. If the target condition is well defined and associated with unequivocal downstream management decisions, clinical validity, when defined in comparative terms, may sometimes act as a surrogate outcome measure for clinical utility.
Fit for Purpose or Faulty Design? Analysis of the Jurisprudence of the European Court of Human Rights and the European Court of Justice on the Legal Protection of Minorities
Anneleen Van Bossuyt
Journal on Ethnopolitics and Minority Issues in Europe , 2007,
Abstract: This paper examines whether the European Court of Justice (ECJ), even in the absence of explicit competencies, could play a role in the creation of a European Union policy promoting the protection of minorities and thus preventing their social exclusion. Comparison is made with the jurisprudence of the European Court of Human Rights (ECtHR) because of the cross-fertilisation between the two Courts. The author argues that there is a conspicuous absence in ECJ jurisprudence on the rights of minorities to their culture and identity, whereas the jurisprudence of the ECtHR in this regard is progressive. In contrast, the ECJ takes the fore when it comes to the protection of the linguistic rights of minorities. In conclusion, the author argues that the ECJ is not fit for purpose, but that to speak of a faulty design is taking a step too far.
Ontogenetic pattern change in amphibians: the case of Salamandra corsica
Wouter Beukema
Acta Herpetologica , 2011,
Abstract: Ontogenetic, post-metamorphic pattern development is a rarely studied topic in amphibian science. As there are indications that the pattern of Salamandra corsica might expand over time, digital image analyses were applied in order to measure several phenotypical variables which were related to the snout vent length. Results show a significant increase of patches which change to irregular shapes while SVL increases. Digital image analysis is identified as a suitable tool to explore pattern shape and change in general, while the documented pattern development in S. corsica might be one of the first quantified cases of post-metamorphic ontogenetic pattern change in amphibians.
Rereading: Theory of the Partisan
Wouter Werner
Amsterdam Law Forum , 2009,
Abstract:
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