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    <title>Houben, M.P.W.A.</title>
    <link>http://repub.eur.nl/res/aut/552/</link>
    <description>List of Publications</description>
    <language>en</language>
    <image>
      <url>http://repub.eur.nl/static-eur/img/logo.png</url>
      <title>RePub, Erasmus University Rotterdam</title>
      <link>http://repub.eur.nl</link>
    </image>
    <item>
      <title>The first case of variant Creutzfeldt-Jakob disease in the Netherlands [6] (Article)</title>
      <link>http://repub.eur.nl/res/pub/36075/</link>
      <pubDate>2007-07-01T00:00:00Z</pubDate>
      <description></description>
    </item> <item>
      <title>IGF-1 CA repeat variant and breast cancer risk in postmenopausal women (Article)</title>
      <link>http://repub.eur.nl/res/pub/36446/</link>
      <pubDate>2007-07-01T00:00:00Z</pubDate>
      <description>IGF-I is an important growth factor for the mammary gland. We evaluated the relationship of the IGF-I CAnpolymorphism with breast cancer risk in Caucasian postmenopausal women and performed a meta-analysis of published data. The IGF-I CAnpolymorphism was genotyped in 4091 from the Rotterdam Study. A disease-free survival analysis was performed along with a meta-analysis of all available data on IGF-I CAnpolymorphism and breast cancer risk. During follow-up 159 women were diagnosed with breast cancer. The disease-free survival analysis adjusted for age at entry, age at menopause, body mass index and waist hip ratio yielded a HR = 0.97 (95% CI=0.59-1.58) for CA19non-carriers against carriers. The meta-analysis using the random-effects model gave a pooled OR of 1.26 (95% CI = 0.95-1.82) for IGF-I CA19non-carriers versus CA19homozygous carriers. According to these results, the IGF-I CA19promoter polymorphism is not likely to predict the risk of breast cancer. </description>
    </item> <item>
      <title>Cerebrovascular risk factors do not contribute to genetic variance of cognitive function. The ERF study (Article)</title>
      <link>http://repub.eur.nl/res/pub/35801/</link>
      <pubDate>2007-05-01T00:00:00Z</pubDate>
      <description>Impaired cognition in later life may result from Alzheimer's disease-related pathology, but also from vascular pathology. We studied to what extent vascular risk explained heritability of cognition in 780 individuals, related in one extended pedigree in a genetically isolated population, in the ERF study. Heritability was estimated using variance components modelling (SOLAR). Univariate analyses included models with and without vascular disease; bivariate analyses included both cognitive and vascular traits, such as blood pressure, serum glucose or lipids. Heritability for immediate and delayed recall, recognition, semantic fluency, Trail making B and Stroop tests was significant, with estimates from 0.16 to 0.36. Vascular factors did not affect cognitive functions, except immediate recall and the Stroop test. Heritability estimates did not change significantly when adjusted for vascular disease. We found no genetic correlation between cognition and vascular traits. Therefore, in this population vascular disease is mildly associated with cognitive dysfunction, and in those with vascular disease, the underlying genetic risk factors are not likely to account for the genetic variation in cognition at adult age. </description>
    </item> <item>
      <title>Determinants of Glioma: An epidemiological and genetic study (Doctoral Thesis)</title>
      <link>http://repub.eur.nl/res/pub/7401/</link>
      <pubDate>2006-02-15T00:00:00Z</pubDate>
      <description>Gliomas are malignant brain tumours of neuroepithelial origin.
Less than one thousand patients are diagnosed with glioma each year in the
Netherlands. No major factors in the aetiology of glioma have been identified,
and for &gt;95% of the patients, the cause is unknown. The objective of this thesis
was to explore aetiological factors for glioma. 

In the studies for environmental and genetic risk factors, we used several
different approaches in both population-based and family-based designs. In the
first part of the thesis, the aim was to obtain additional insights in
environmental risk factors for glioma. By the use of classical and novel
methods, hypotheses were formulated about mechanisms that possibly play a role
in the development of glioma. The second part of the thesis aimed at the genetic
basis of the disease by studying both families and more distantly related
patients from genetically isolated communities.</description>
    </item> <item>
      <title>Hypertension as a risk factor for glioma? Evidence from a population-based study of comorbidity in glioma patients. (Article)</title>
      <link>http://repub.eur.nl/res/pub/13472/</link>
      <pubDate>2004-08-01T00:00:00Z</pubDate>
      <description>BACKGROUND: Little is known about the aetiology of glioma. Research is often hampered by the low incidence and high mortality of the disease. Concomitant diseases in glioma patients may indicate possible aetiological pathways. We therefore studied comorbidity in glioma patients. PATIENTS AND METHODS: We performed a case-control study using population-based data from the Eindhoven Cancer Registry. We compared prevalences of concomitant diseases in 510 glioma patients with two reference cancer populations from the same registry. RESULTS: Compared with all other cancer patients, a significantly higher prevalence of hypertension was found in glioma patients for age categories 60-74 years [odds ratio (OR) 1.37; 95% confidence interval (CI) 1.02-1.84] and 75+ years (OR 2.37; 95% CI 1.34-4.21). The association was most pronounced in elderly men and in astrocytic glioma, with a maximum in age category 75+ years (OR 5.86; 95% CI 2.20-15.7). The prevalence of cerebrovascular disease was higher in glioma patients &gt;45 years old (OR 1.67; 95% CI 1.12-2.47), whereas the prevalence of other cancers was lower (OR 0.64; 95% CI 0.48-0.87). No consistent associations were detected for several other concomitant diseases. CONCLUSIONS: Our data suggest an association between hypertension and glioma, although questions remain about causality and the possible mechanisms. We hypothesise that this association is mediated through potentially neurocarcinogenic effects of antihypertensive medication.</description>
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