PMID- 14981141
OWN - NLM
STAT- MEDLINE
DCOM- 20040505
LR  - 20061115
IS  - 1360-9947 (Print)
IS  - 1360-9947 (Linking)
VI  - 10
IP  - 3
DP  - 2004 Mar
TI  - Analysis of the involvement of CCR5-Delta32 and CCR2-V64I variants in the 
      development of endometriosis.
PG  - 155-7
AB  - Several arguments support the proposal that the cytokine network plays a critical 
      role in the aetiology of endometriosis. Among various chemokines, 
      regulated-on-activation, normal-T-cell-expressed and -secreted (RANTES) and 
      monocyte chemotactic protein 1 (MCP-1) concentrations have been shown to be 
      increased in the peritoneal fluid of women with endometriosis. Some studies have 
      demonstrated that, in the context of endometriosis, these chemokines are involved 
      in apoptosis, angiogenesis and/or chemotaxis. Since the chemokines exert their 
      effects by binding to their receptors, it would be plausible that factors 
      affecting such interactions might play a role in the pathogenesis of 
      endometriosis. Thus we postulated that the genes encoding CCR5 and CCR2, which 
      are the receptors for RANTES and MCP-1 respectively, could be good candidate 
      genes for the disease. We have used real-time PCR and FRET technologies to 
      genotype and evaluate the variants CCR5-Delta32 and CCR2-V64I, as susceptibility 
      factors in a cohort of Spanish women with endometriosis. No differences have been 
      found in the frequencies of the two polymorphisms nor in the haplotype/genotype 
      distribution between cases and controls. These data would suggest the lack of 
      association between these polymorphisms and endometriosis in our population, 
      although they do not permit us to discard completely a possible role of other 
      variants within CCR5 and CCR2 genes in this pathology.
FAU - Antinolo, G
AU  - Antinolo G
AD  - Unidad Clinica de Genetica y Reproduccion, Hospitales Universitarios Virgen del 
      Rocio, Avda. Manuel Siurot s/n, 41013 Seville, Spain. 
      guillermo.antinolo.sspa@juntadeandalucia.es
FAU - Fernandez, R M
AU  - Fernandez RM
FAU - Noval, J A
AU  - Noval JA
FAU - Molini, J L
AU  - Molini JL
FAU - Borrego, S
AU  - Borrego S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20040129
PL  - England
TA  - Mol Hum Reprod
JT  - Molecular human reproduction
JID - 9513710
RN  - 0 (Receptors, CCR5)
SB  - IM
MH  - Endometriosis/*genetics/metabolism
MH  - Female
MH  - Haplotypes
MH  - Humans
MH  - Mutation
MH  - Receptors, CCR5/*genetics/metabolism
EDAT- 2004/02/26 05:00
MHDA- 2004/05/07 05:00
CRDT- 2004/02/26 05:00
PHST- 2004/02/26 05:00 [pubmed]
PHST- 2004/05/07 05:00 [medline]
PHST- 2004/02/26 05:00 [entrez]
AID - gah026 [pii]
AID - 10.1093/molehr/gah026 [doi]
PST - ppublish
SO  - Mol Hum Reprod. 2004 Mar;10(3):155-7. doi: 10.1093/molehr/gah026. Epub 2004 Jan 
      29.