PMID- 27631728
OWN - NLM
STAT- MEDLINE
DCOM- 20170515
LR  - 20181113
IS  - 1432-1211 (Electronic)
IS  - 0093-7711 (Linking)
VI  - 69
IP  - 2
DP  - 2017 Feb
TI  - Association of the genetic diversity of killer cell immunoglobulin-like receptor 
      genes and HLA-C ligand in Saudi women with breast cancer.
PG  - 69-76
LID - 10.1007/s00251-016-0950-x [doi]
AB  - Breast cancer (BC) progression and metastases have been linked to antitumor 
      immunity inefficiency and particularly to natural killer (NK) cells. Killer cell 
      immunoglobulin-like receptors (KIRs) are the most polymorphic receptors of NK 
      cells. Through their interactions with human leukocyte antigen (HLA)-C ligands, 
      they modulate NK and T cell actions against target cells. Therefore, we studied 
      the combinatorial effect of KIR genes and their HLA-C ligands on the 
      susceptibility to development of BC in Saudi women. The presence of KIR genes and 
      HLA-C1 and HLA-C2 groups was typed in 50 Saudi patients living in Riyadh and 65 
      healthy controls using polymerase chain reaction with sequence-specific primers. 
      Our results indicated a protective effect by the KIR2DS2, 2DS3, and 2DL5A genes 
      against BC (OR = 0.25, 0.21, and 0.27, respectively, and p < 0.01). The 
      synergistic action of the three genes was observed when they occurred together, 
      and the absence of the three genes increased BC occurrence by 6.5-fold. 
      Distribution of the HLA-C1/C2 ligand between patients and controls showed an 
      increase in the risk of BC occurrence for the heterozygote C1/C2 (OR = 2.33; 95 % 
      CI = 1.08-5.02; p = 0.037) and a protective effect of the homozygote C2C2 
      (OR = 0.03; 95 % CI = 0.009-0.098; p < 0.001). Combinatory analyses of KIR genes 
      and their HLA-C ligands showed protective effects of KIR2DL2 and 2DL3 in the 
      absence of their HLA-C1 ligand. These results suggested that KIR-gene content 
      combined with their ligand could influence the risk of BC development in women in 
      Saudi Arabia.
FAU - Alomar, Suliman Y
AU  - Alomar SY
AD  - Zoology Department, College of Sciences, King Saud University, Post Office Box 
      2455, Riyadh, 11451, Saudi Arabia.
FAU - Alkhuriji, Afrah
AU  - Alkhuriji A
AD  - Zoology Department, College of Sciences, King Saud University, Post Office Box 
      2455, Riyadh, 11451, Saudi Arabia.
FAU - Trayhyrn, Paul
AU  - Trayhyrn P
AD  - Zoology Department, College of Sciences, King Saud University, Post Office Box 
      2455, Riyadh, 11451, Saudi Arabia.
AD  - Clore Laboratory, Buckingham Institute for Translational Medicine, University of 
      Buckingham, Buckingham, UK.
FAU - Alhetheel, Abdulkarim
AU  - Alhetheel A
AD  - Department of Microbiology/Pathology, King Khalid University Hospital, College of 
      Medicine King Saud University, Riyadh, Saudi Arabia.
FAU - Al-Jurayyan, Abdullah
AU  - Al-Jurayyan A
AD  - Immunology and HLA section, Pathology and Clinical Laboratory Medicine, King 
      Fahad Medical City, Riyadh, Saudi Arabia.
FAU - Mansour, Lamjed
AU  - Mansour L
AD  - Zoology Department, College of Sciences, King Saud University, Post Office Box 
      2455, Riyadh, 11451, Saudi Arabia. lamjed.mansour@gmail.com.
AD  - Faculty of Sciences of Gabes, University of Gabes, Erriadh City, 6072, Zrig 
      Gabes, Tunisia. lamjed.mansour@gmail.com.
LA  - eng
PT  - Journal Article
DEP - 20160915
PL  - United States
TA  - Immunogenetics
JT  - Immunogenetics
JID - 0420404
RN  - 0 (HLA-C Antigens)
RN  - 0 (Receptors, KIR)
SB  - IM
MH  - Adult
MH  - Breast Neoplasms/epidemiology/*genetics/immunology
MH  - Case-Control Studies
MH  - Female
MH  - Genetic Predisposition to Disease
MH  - Genetic Variation/*genetics
MH  - Genotype
MH  - HLA-C Antigens/*genetics
MH  - Humans
MH  - Killer Cells, Natural/immunology/metabolism
MH  - Polymerase Chain Reaction
MH  - Receptors, KIR/*genetics
MH  - Saudi Arabia/epidemiology
OTO - NOTNLM
OT  - Genetic association
OT  - HLA ligands
OT  - Malignant diseases
OT  - Natural killer cells
EDAT- 2016/09/16 06:00
MHDA- 2017/05/16 06:00
CRDT- 2016/09/16 06:00
PHST- 2016/06/18 00:00 [received]
PHST- 2016/08/31 00:00 [accepted]
PHST- 2016/09/16 06:00 [pubmed]
PHST- 2017/05/16 06:00 [medline]
PHST- 2016/09/16 06:00 [entrez]
AID - 10.1007/s00251-016-0950-x [pii]
AID - 10.1007/s00251-016-0950-x [doi]
PST - ppublish
SO  - Immunogenetics. 2017 Feb;69(2):69-76. doi: 10.1007/s00251-016-0950-x. Epub 2016 
      Sep 15.