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   <dc:title>Vitamin D receptor levels in colorectal cancer. Possible role of BsmI polymorphism</dc:title>
   <dc:creator>Parisi Capdevila, Eva</dc:creator>
   <dc:creator>Reñé Espinet, Josep Maria</dc:creator>
   <dc:creator>Cardús i Figueras, Anna</dc:creator>
   <dc:creator>Valcheva, Petya</dc:creator>
   <dc:creator>Piñol Felis, Carme</dc:creator>
   <dc:creator>Valdivielso Revilla, José Manuel</dc:creator>
   <dc:creator>Fernández i Giráldez, Elvira</dc:creator>
   <dc:subject>Vitamin D</dc:subject>
   <dc:subject>Colon cancer</dc:subject>
   <dc:subject>VDR</dc:subject>
   <dc:subject>Bsml</dc:subject>
   <dcterms:abstract>A high expression of vitamin D receptor (VDR) in colorectal cancer (CRC) tumoral tissue has been related&#xd;
to a good prognosis and it has been proposed that it could be a good biological marker of CRC progression.&#xd;
Nevertheless, there are no previous studies that compare the VDR expression in tumoral towards normal&#xd;
tissue of the same CRC patient in relation to VDR BsmI genotype.&#xd;
We collected normal and tumoral tissue samples, as well as blood samples, from CRC patients (n = 170)&#xd;
and controls (n = 122). VDR genotyping was performed and BsmI homozygous patients were selected&#xd;
(CRC = 50, Cont = 32). VDR mRNA and protein levels were analyzed. We also measured 25-Hydroxyvitamin&#xd;
D serum levels.&#xd;
We found no differences in the polymorphism distribution in tumoral versus normal tissue (control:&#xd;
BB = 15.7%, bb = 41.3%, Bb = 43%; CRC: BB = 14.2%, bb = 41.9%, Bb = 43.9%). Furthermore, VDR levels decreased&#xd;
in colonic cancer tissue (mean: 3.03) versus normal mucosa (11.62) from the same patient (p &lt; 0.001),&#xd;
but this decrease was similar in both genotypes. There were differences in 25-Hydroxyvitamin D3 levels&#xd;
between the CRC and the control group (CRC = 8.65 ng/ml, Cont = 18.15 ng/ml).&#xd;
In conclusion, we found a decrease in VDR levels in tumoral compared with normal mucosa from the&#xd;
same patient. This difference is independent of the BsmI polymorphism.</dcterms:abstract>
   <dcterms:abstract>This work was supported by Fundacio Dr Pifarré grants, FIS ´ PI07/0427, PI06/0010 and REDINREN (16/06).</dcterms:abstract>
   <dcterms:dateAccepted>2024-12-05T22:07:02Z</dcterms:dateAccepted>
   <dcterms:available>2024-12-05T22:07:02Z</dcterms:available>
   <dcterms:created>2024-12-05T22:07:02Z</dcterms:created>
   <dcterms:issued>2016-06-06T11:01:37Z</dcterms:issued>
   <dcterms:issued>2025-01-01</dcterms:issued>
   <dcterms:issued>2008</dcterms:issued>
   <dc:type>article</dc:type>
   <dc:type>publishedVersion</dc:type>
   <dc:identifier>http://hdl.handle.net/10459.1/57167</dc:identifier>
   <dc:relation>Reproducció del document publicat a https://doi.org/10.1016/j.jsbmb.2008.05.001</dc:relation>
   <dc:relation>Journal of Steroid Biochemistry &amp; Molecular Biology, 2008, vol. 111, núm. 1-2, p. 87-90</dc:relation>
   <dc:rights>(c) Elsevier, 2008</dc:rights>
   <dc:rights>info:eu-repo/semantics/restrictedAccess</dc:rights>
   <dc:publisher>Elsevier</dc:publisher>
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