PMID- 28710021
OWN - NLM
STAT- MEDLINE
DCOM- 20190312
LR  - 20190312
IS  - 1879-1220 (Electronic)
IS  - 0960-0760 (Print)
IS  - 0960-0760 (Linking)
VI  - 177
DP  - 2018 Mar
TI  - Identification of tumor-autonomous and indirect effects of vitamin D action that 
      inhibit breast cancer growth and tumor progression.
PG  - 155-158
LID - S0960-0760(17)30167-X [pii]
LID - 10.1016/j.jsbmb.2017.07.003 [doi]
AB  - Several epidemiological studies have found that low vitamin D levels are 
      associated with worse prognosis and poorer outcomes in patients with breast 
      cancer (BCa), although some studies have failed to find this association. In 
      addition, prior research has found that BCa patients with vitamin D deficiency 
      have a more aggressive molecular phenotype and worse prognostic biomarkers. As 
      vitamin D deficiency is common in patients diagnosed with BCa, elucidating the 
      cause of the association between poor outcomes and vitamin D deficiency promises 
      to have a significant impact on improving care for patients with BCa including 
      enabling the development of novel therapeutic approaches. Here we review our 
      recent findings in this area, including our data revealing that reduction of the 
      expression of the vitamin D receptor (Vdr) within BCa cells accelerates primary 
      tumor growth and enables the development of metastases, demonstrating a tumor 
      autonomous effect of vitamin D signaling to suppress BCa metastases. We believe 
      that these findings are likely relevant to humans as we discovered evidence that 
      a mechanism of VDR regulation identified in our mouse models is conserved in 
      human BCa. In particular, we identified a negative correlation between serum 
      25(OH)D concentration and the level of expression of the tumor progression factor 
      ID1 in primary tumors from patients with breast cancer.
CI  - Copyright (c) 2017 Elsevier Ltd. All rights reserved.
FAU - Aggarwal, Abhishek
AU  - Aggarwal A
AD  - Department of Pediatrics, Stanford School of Medicine, Stanford University, CA 
      94305, United States.
FAU - Feldman, David
AU  - Feldman D
AD  - Department of Medicine, Stanford School of Medicine, Stanford University, CA 
      94305, United States; Stanford Cancer Institute, Stanford University, CA 94305, 
      United States.
FAU - Feldman, Brian J
AU  - Feldman BJ
AD  - Department of Pediatrics, Stanford School of Medicine, Stanford University, CA 
      94305, United States; Stanford Cancer Institute, Stanford University, CA 94305, 
      United States. Electronic address: feldman@stanford.edu.
LA  - eng
GR  - R01 DK114217/DK/NIDDK NIH HHS/United States
GR  - UL1 TR001085/TR/NCATS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20170711
PL  - England
TA  - J Steroid Biochem Mol Biol
JT  - The Journal of steroid biochemistry and molecular biology
JID - 9015483
RN  - 1406-16-2 (Vitamin D)
SB  - IM
MH  - Animals
MH  - Breast/metabolism/pathology
MH  - Breast Neoplasms/*metabolism/pathology
MH  - Female
MH  - Humans
MH  - Vitamin D/*metabolism
PMC - PMC5764828
MID - NIHMS893247
OTO - NOTNLM
OT  - Breast cancer
OT  - ID1
OT  - Metastasis
OT  - Microenvironment
OT  - Stromal cells
OT  - Vitamin D
OT  - Vitamin D receptor
OT  - calcitriol
EDAT- 2017/07/16 06:00
MHDA- 2019/03/13 06:00
PMCR- 2019/03/01
CRDT- 2017/07/16 06:00
PHST- 2017/05/05 00:00 [received]
PHST- 2017/06/29 00:00 [revised]
PHST- 2017/07/03 00:00 [accepted]
PHST- 2017/07/16 06:00 [pubmed]
PHST- 2019/03/13 06:00 [medline]
PHST- 2017/07/16 06:00 [entrez]
PHST- 2019/03/01 00:00 [pmc-release]
AID - S0960-0760(17)30167-X [pii]
AID - 10.1016/j.jsbmb.2017.07.003 [doi]
PST - ppublish
SO  - J Steroid Biochem Mol Biol. 2018 Mar;177:155-158. doi: 
      10.1016/j.jsbmb.2017.07.003. Epub 2017 Jul 11.