Vitamin D receptor expression in invasive breast tumors and breast cancer survival.
Breast cancer
Mortality
Survival
Tissue microarray
Vitamin D receptor
Journal
Breast cancer research : BCR
ISSN: 1465-542X
Titre abrégé: Breast Cancer Res
Pays: England
ID NLM: 100927353
Informations de publication
Date de publication:
29 07 2019
29 07 2019
Historique:
received:
12
02
2019
accepted:
15
07
2019
entrez:
31
7
2019
pubmed:
31
7
2019
medline:
25
1
2020
Statut:
epublish
Résumé
Vitamin D has been suggested to prevent and improve the prognosis of several cancers, including breast cancer. We have previously shown a U-shaped association between pre-diagnostic serum levels of vitamin D and risk of breast cancer-related death, with poor survival in patients with the lowest and the highest levels respectively, as compared to the intermediate group. Vitamin D exerts its functions through the vitamin D receptor (VDR), and the aim of the current study was to investigate if the expression of VDR in invasive breast tumors is associated with breast cancer prognosis. VDR expression was evaluated in a tissue microarray of 718 invasive breast tumors. Covariation between VDR expression and established prognostic factors for breast cancer was analyzed, as well as associations between VDR expression and breast cancer mortality. We found that positive VDR expression in the nuclei and cytoplasm of breast cancer cells was associated with favorable tumor characteristics such as smaller size, lower grade, estrogen receptor positivity and progesterone receptor positivity, and lower expression of Ki67. In addition, both intranuclear and cytoplasmic VDR expression were associated with a low risk of breast cancer mortality, hazard ratios 0.56 (95% CI 0.34-0.91) and 0.59 (0.30-1.16) respectively. This study found that high expression of VDR in invasive breast tumors is associated with favorable prognostic factors and a low risk of breast cancer death. Hence, a high VDR expression is a positive prognostic factor.
Sections du résumé
BACKGROUND
Vitamin D has been suggested to prevent and improve the prognosis of several cancers, including breast cancer. We have previously shown a U-shaped association between pre-diagnostic serum levels of vitamin D and risk of breast cancer-related death, with poor survival in patients with the lowest and the highest levels respectively, as compared to the intermediate group. Vitamin D exerts its functions through the vitamin D receptor (VDR), and the aim of the current study was to investigate if the expression of VDR in invasive breast tumors is associated with breast cancer prognosis.
METHODS
VDR expression was evaluated in a tissue microarray of 718 invasive breast tumors. Covariation between VDR expression and established prognostic factors for breast cancer was analyzed, as well as associations between VDR expression and breast cancer mortality.
RESULTS
We found that positive VDR expression in the nuclei and cytoplasm of breast cancer cells was associated with favorable tumor characteristics such as smaller size, lower grade, estrogen receptor positivity and progesterone receptor positivity, and lower expression of Ki67. In addition, both intranuclear and cytoplasmic VDR expression were associated with a low risk of breast cancer mortality, hazard ratios 0.56 (95% CI 0.34-0.91) and 0.59 (0.30-1.16) respectively.
CONCLUSIONS
This study found that high expression of VDR in invasive breast tumors is associated with favorable prognostic factors and a low risk of breast cancer death. Hence, a high VDR expression is a positive prognostic factor.
Identifiants
pubmed: 31358030
doi: 10.1186/s13058-019-1169-1
pii: 10.1186/s13058-019-1169-1
pmc: PMC6664551
doi:
Substances chimiques
Biomarkers
0
Receptors, Calcitriol
0
VDR protein, human
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
84Références
Cancer Res. 1986 Oct;46(10):5406-8
pubmed: 3019526
Horm Res. 1981;15(4):263-9
pubmed: 6100940
Endocr Relat Cancer. 2017 Apr;24(4):181-195
pubmed: 28213567
J Clin Epidemiol. 2009 Nov;62(11):1202-9
pubmed: 19364635
Eur J Epidemiol. 2017 Sep;32(9):765-773
pubmed: 28983736
Breast Cancer Res Treat. 2013 Oct;141(3):331-9
pubmed: 24104883
J Natl Cancer Inst. 2007 Nov 7;99(21):1594-602
pubmed: 17971526
Clin Lab. 2016 Aug 1;62(8):1461-1468
pubmed: 28164608
Cancer Res. 1987 Dec 15;47(24 Pt 1):6793-9
pubmed: 2824042
Endocrine. 2016 Nov;54(2):556-559
pubmed: 27393303
BMC Cancer. 2010 Sep 11;10:483
pubmed: 20831823
J Cancer. 2016 Jan 05;7(3):232-40
pubmed: 26918035
Breast Cancer Res Treat. 2016 May;157(1):77-90
pubmed: 27120467
Int J Cancer. 2008 Sep 1;123(5):1146-53
pubmed: 18528862
J Clin Endocrinol Metab. 1988 Sep;67(3):607-13
pubmed: 2842365
Cancer Res. 1991 Jan 1;51(1):239-44
pubmed: 1846309
Oncotarget. 2017 Apr 18;8(16):26687-26701
pubmed: 28460457
Int J Oncol. 2004 Oct;25(4):1183-91
pubmed: 15375571
Histochem J. 2002 Jan-Feb;34(1-2):35-40
pubmed: 12365798
J Bone Miner Res. 1998 Mar;13(3):325-49
pubmed: 9525333
J Clin Invest. 2014 Feb;124(2):859-70
pubmed: 24463450
JAMA Oncol. 2017 Mar 1;3(3):351-357
pubmed: 27832250
Proc Natl Acad Sci U S A. 2017 Mar 14;114(11):E2186-E2194
pubmed: 28242709
Mol Cell Endocrinol. 2018 Sep 5;472:18-25
pubmed: 29183808
Breast Cancer Res Treat. 2017 Oct;165(3):645-657
pubmed: 28643022
J Clin Pathol. 1997 Oct;50(10):801-4
pubmed: 9462258
Arch Biochem Biophys. 2010 Feb 15;494(2):166-77
pubmed: 19951695
Cancer Res. 1984 Apr;44(4):1677-81
pubmed: 6322984
Int J Cancer. 2007 May 15;120(10):2202-7
pubmed: 17278089
J Histochem Cytochem. 2012 Feb;60(2):121-9
pubmed: 22108646
Anticancer Res. 2002 May-Jun;22(3):1919-24
pubmed: 12168894
Clin Cancer Res. 2017 Jan 1;23(1):97-103
pubmed: 27407090
Cancer Causes Control. 2014 Sep;25(9):1131-40
pubmed: 24952509