2026-04-17T05:41:21Zhttps://recercat.cat/oai/request
oai:recercat.cat:10459.1/571672024-12-05T22:07:02Zcom_2072_3622col_2072_479130
RECERCAT author Parisi Capdevila, Eva author Reñé Espinet, Josep Maria author Cardús i Figueras, Anna author Valcheva, Petya author Piñol Felis, Carme author Valdivielso Revilla, José Manuel author Fernández i Giráldez, Elvira 2024-12-05T22:07:02Z 2024-12-05T22:07:02Z 2016-06-06T11:01:37Z2025-01-012008 http://hdl.handle.net/10459.1/57167 A high expression of vitamin D receptor (VDR) in colorectal cancer (CRC) tumoral tissue has been related to a good prognosis and it has been proposed that it could be a good biological marker of CRC progression. Nevertheless, there are no previous studies that compare the VDR expression in tumoral towards normal tissue of the same CRC patient in relation to VDR BsmI genotype. We collected normal and tumoral tissue samples, as well as blood samples, from CRC patients (n = 170) and controls (n = 122). VDR genotyping was performed and BsmI homozygous patients were selected (CRC = 50, Cont = 32). VDR mRNA and protein levels were analyzed. We also measured 25-Hydroxyvitamin D serum levels. We found no differences in the polymorphism distribution in tumoral versus normal tissue (control: BB = 15.7%, bb = 41.3%, Bb = 43%; CRC: BB = 14.2%, bb = 41.9%, Bb = 43.9%). Furthermore, VDR levels decreased in colonic cancer tissue (mean: 3.03) versus normal mucosa (11.62) from the same patient (p < 0.001), but this decrease was similar in both genotypes. There were differences in 25-Hydroxyvitamin D3 levels between the CRC and the control group (CRC = 8.65 ng/ml, Cont = 18.15 ng/ml). In conclusion, we found a decrease in VDR levels in tumoral compared with normal mucosa from the same patient. This difference is independent of the BsmI polymorphism.This work was supported by Fundacio Dr Pifarré grants, FIS ´ PI07/0427, PI06/0010 and REDINREN (16/06). (c) Elsevier, 2008 info:eu-repo/semantics/restrictedAccess Vitamin D Colon cancer VDR Bsml Vitamin D receptor levels in colorectal cancer. Possible role of BsmI polymorphism article publishedVersion