PMID- 26561054
OWN - NLM
STAT- MEDLINE
DCOM- 20161014
LR  - 20190728
IS  - 1873-4286 (Electronic)
IS  - 1381-6128 (Linking)
VI  - 22
IP  - 3
DP  - 2016
TI  - Dendritic Cells in Esophageal Adenocarcinoma: The Currently Available Information 
      and Possibilities to use Dendritic Cells for Immunotherapeutic Approaches.
PG  - 307-11
AB  - Esophageal adenocarcinoma (EAC) is the second frequent cancer of the esophagus. 
      Barrett's esophagus (BE) takes precedence over EAC. BE is a metaplastic change of 
      the stratified squamous epithelium to the intestinal columnar epithelium due to 
      the acidic gastrointestinal reflux. Further, the disease takes the hyperplastic 
      stage followed by EAC. An initial immune response is an essential reaction of a 
      body to an occurrence of alien/modified cells to be removed. It has been 
      appreciated that an inflammatory reaction occurs in the early stages of EAC or 
      even in BE. Dendritic cells (DCs) play a key role in a frontier of an immune 
      response due to their advanced ability to recognize foreign antigens and mobilize 
      naive T cells to effectors. However, in a cancer condition, tumor-delivered 
      immunosuppression occurs in a variety of mechanisms that alter/switch the 
      functionality of DCs from immune activating to immune suppressive cells. In this 
      brief review, we consider tumor-induced paths of a capacity of tumor cells to 
      down-regulate DCs, with a focus on EAC, and also discuss a possibility to use DCs 
      for immunotherapeutic approaches. Indeed, DCs represent a promising tool for 
      developing new immunotherapeutic approaches for cancer treatment including EAC. 
      It has been reported to achieve effective DC-mediated immune responses by raising 
      anti-tumor cytotoxic T cell responses against multiple cancer antigens through 
      loading DCs with total tumor RNA. However, more studies should be performed in 
      order to understand a precise role in tumor-induced mechanisms of DC suppression 
      in BE/EAC. Likely, these mechanisms should involve general carcinogenic and 
      EAC-specific pathways.
FAU - Chistiakov, Dimitry A
AU  - Chistiakov DA
FAU - Orekhov, Alexander N
AU  - Orekhov AN
FAU - Bobryshev, Yuri V
AU  - Bobryshev YV
AD  - Faculty of Medicine, University of New South Wales, Sydney, NSW 2052, Australia. 
      y.bobryshev@unsw.edu.au.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United Arab Emirates
TA  - Curr Pharm Des
JT  - Current pharmaceutical design
JID - 9602487
RN  - 0 (Antigens, Neoplasm)
RN  - 0 (Cancer Vaccines)
SB  - IM
MH  - Adenocarcinoma/immunology/*therapy
MH  - Animals
MH  - Antigens, Neoplasm/immunology
MH  - Barrett Esophagus/immunology
MH  - Cancer Vaccines/*therapeutic use
MH  - Dendritic Cells/cytology/*immunology
MH  - Esophageal Neoplasms/immunology/*therapy
MH  - Humans
MH  - T-Lymphocytes, Cytotoxic/cytology/immunology
MH  - Tumor Microenvironment/immunology
EDAT- 2015/11/13 06:00
MHDA- 2016/10/16 06:00
CRDT- 2015/11/13 06:00
PHST- 2015/08/01 00:00 [received]
PHST- 2015/11/11 00:00 [accepted]
PHST- 2015/11/13 06:00 [entrez]
PHST- 2015/11/13 06:00 [pubmed]
PHST- 2016/10/16 06:00 [medline]
AID - CPD-EPUB-71806 [pii]
AID - 10.2174/1381612822666151112153620 [doi]
PST - ppublish
SO  - Curr Pharm Des. 2016;22(3):307-11. doi: 10.2174/1381612822666151112153620.