PMID- 29388277
OWN - NLM
STAT- MEDLINE
DCOM- 20190418
LR  - 20190418
IS  - 1521-2254 (Electronic)
IS  - 1099-498X (Linking)
VI  - 20
IP  - 2-3
DP  - 2018 Feb
TI  - Promoter polymorphisms in TGFB1 and IL10 genes influence tumor dendritic cells 
      infiltration, development and prognosis of colorectal cancer.
PG  - e3005
LID - 10.1002/jgm.3005 [doi]
AB  - BACKGROUND: Anti-inflammatory cytokines such as interleukin (IL)-10 and 
      transforming growth factor (TGF)-beta1 have a complex role in the development of 
      colorectal cancer (CRC). Dendritic cells (DCs) are the cellular component of the 
      inflammatory microenvironment in the tumor and infiltration of tumors by DCs is 
      associated with better prognosis and fewer metastases. METHODS: In the present 
      study, we explored the role of two single nucleotide polymorphisms (SNPs) in the 
      promoter regions of TGFB1 and IL10 genes and their associations with infiltrating 
      DCs in CRC.A case-control study was designed. Genotyping was performed via the 
      polymerase chain reaction-restriction fragment length polymorphism method and DC 
      infiltration was determined immunohistochemically. RESULTS: For the TGFBeta1 -509C/T 
      SNP, we found that the T allele was less frequent in patients than in controls (p 
      = 0.031) and the TT-genotype had a 2.74-fold lower risk for CRC than the 
      CC-genotype (odds ratio = 0.365, 95% confidence interval = 0.15-0.88, p = 0.015). 
      Additionally, the TT carriers had the shortest median survival (14.4 months) (p = 
      0.045). The C-allele genotypes had a significantly longer survival compared to TT 
      carriers (p = 0.018). The CC genotype was associated with a lower cellular 
      density of CD11c in the invasive margin of the tumor (p = 0.033), whereas there 
      was an opposite finding for CD83+ DCs (p = 0.037). Carriers of A-allele genotypes 
      of the IL10 -1080A/G SNP had significantly lower CD83+ cells (p = 0.046) in the 
      tumor invasive margin. CONCLUSIONS: The T-allele of the TGFB1 -509C/T SNP might 
      be a protective factor for development of CRC, although, in the course of the 
      disease, this variant allele might be associated with more unfavorable prognosis 
      of the patients.
CI  - Copyright (c) 2018 John Wiley & Sons, Ltd.
FAU - Gulubova, Maya
AU  - Gulubova M
AD  - Department of General and Clinical Pathology, Forensic Medicine and Deontology, 
      Medical Faculty, Trakia University, Stara Zagora, Bulgaria.
FAU - Aleksandrova, Elina
AU  - Aleksandrova E
AD  - Department of General and Clinical Pathology, Forensic Medicine and Deontology, 
      Medical Faculty, Trakia University, Stara Zagora, Bulgaria.
AD  - Department of Medical Chemistry and Biochemistry, Medical Faculty, Trakia 
      University, Stara Zagora, Bulgaria.
FAU - Vlaykova, Tatyana
AU  - Vlaykova T
AD  - Department of Medical Chemistry and Biochemistry, Medical Faculty, Trakia 
      University, Stara Zagora, Bulgaria.
LA  - eng
PT  - Journal Article
DEP - 20180305
PL  - England
TA  - J Gene Med
JT  - The journal of gene medicine
JID - 9815764
RN  - 0 (IL10 protein, human)
RN  - 0 (TGFB1 protein, human)
RN  - 0 (Transforming Growth Factor beta1)
RN  - 130068-27-8 (Interleukin-10)
SB  - IM
MH  - Aged
MH  - Alleles
MH  - Colorectal Neoplasms/*genetics/pathology
MH  - Dendritic Cells/pathology
MH  - Disease-Free Survival
MH  - Female
MH  - Genetic Association Studies
MH  - *Genetic Predisposition to Disease
MH  - Genotype
MH  - Humans
MH  - Interleukin-10/*genetics
MH  - Male
MH  - Middle Aged
MH  - Polymorphism, Single Nucleotide/genetics
MH  - Prognosis
MH  - Transforming Growth Factor beta1/*genetics
OTO - NOTNLM
OT  - colon cancer
OT  - gene polymorphism
OT  - rectal cancer
EDAT- 2018/02/02 06:00
MHDA- 2019/04/19 06:00
CRDT- 2018/02/02 06:00
PHST- 2017/07/17 00:00 [received]
PHST- 2017/12/08 00:00 [revised]
PHST- 2017/12/27 00:00 [accepted]
PHST- 2018/02/02 06:00 [pubmed]
PHST- 2019/04/19 06:00 [medline]
PHST- 2018/02/02 06:00 [entrez]
AID - 10.1002/jgm.3005 [doi]
PST - ppublish
SO  - J Gene Med. 2018 Feb;20(2-3):e3005. doi: 10.1002/jgm.3005. Epub 2018 Mar 5.