Evaluation of germline sequence variants within the promoter region of RANTES gene in a cohort of women with endometriosis from Spain
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⤵ 6 in-corpus citations
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This study genotyped promoter variants in the RANTES gene in Spanish women with endometriosis and found no association with the disease.
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Abstract
The RANTES (regulated upon activation normal T cells expressed and secreted) chemokine, is known to be expressed in endometriotic lesions in a concentration correlating with the severity of endometriosis. Since it has been widely demonstrated that endometriosis has a genetic basis, we postulated that the gene encoding RANTES could be a good candidate gene for the disease. We have used fluorescence resonance energy transfer (FRET) technology to genotype and evaluate the role of the variants -403G-->A and -28C-->G, located within the promoter region of the gene, as susceptibility factors in a cohort of Spanish women with endometriosis. No differences have been found in the allelic frequencies of both variants nor in the haplotype/ genotype distribution between patients and controls. These data are consistent with the lack of association between these polymorphisms and endometriosis in our population. They do not exclude completely a possible role of other variants within RANTES gene in this pathology.
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Cited by (6)
- Inflammation and Cytokines in Endometriosis 2014
- Functional genetic polymorphisms and female reproductive disorders: part II--endometriosis 2008
- Endometriosis and genetic polymorphisms 2007
- Genetics of endometriosis: current status and prospects 2007
- Analysis of the involvement of CCR5-Delta32 and CCR2-V64I variants in the development of endometriosis 2004
- Peritoneal macrophages induce RANTES (regulated on activation, normal T cell expressed and secreted) chemokine gene transcription in endometrial stromal cells 2004
Source provenance
- europepmc
- last seen: 2026-10-16T06:09:50.462052+00:00
- openalex
- last seen: 2026-06-10T17:14:06.276822+00:00
- pubmed
- last seen: 2026-10-08T21:01:06.509505+00:00
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