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Showing 2 results for Endometriosis

Shokrzadeh Sh, Saidijam M, Dehghan A, Esna-Ashari F, Farimani Sanoee M, Bahmanzadeh M, Alizadeh Z,
Volume 69, Issue 10 (1-2012)
Abstract

Normal 0 false false false EN-US X-NONE AR-SA MicrosoftInternetExplorer4 Background: The techniques used in assisted reproductive technologies have progressed considerably, but many embryos do not implant after transfer upon the use of these techniques. One of the causes of infertility is repeated implantation failure due to decreased endometrial receptivity. Furthermore, in clinical conditions such as endometriosis and myoma, implantation decreases after embryo transfer. In this case-control study the expression patterns of HOXA-10 and BTEB1 mRNAs were evaluated at the time of implantation in patients with myoma and endometriosis.
Methods : In this study performed in Hamadan University of Medical Sciences during 1389, the cases included 16 patients with endometriosis and myoma (8 in each group) and the control group consisted of 8 fertile women. Endometrial sampling was performed at mid-secretory phase. Later, the expression patterns of HOXA-10 and BTEB1 mRNAs were evaluated using a semi-quantitative RT-PCR method.
Results : The optimal PCR cycles determined were 30, 32 and 26 for HOXA10, BTEB1 and β-actin, respectively. Endometrial HOXA-10 and BTEB1 mRNA expression levels (normalized to ß-actin expression) at the time of implantation were significantly decreased in the endometrium of infertile patients with endometriosis compared with that of healthy fertile controls (P<0.05). A similar pattern was seen in patients with myomas for both HOXA10 and BTEB1 genes, (P<0.05).
Conclusion: It seems that lower expression of HOXA-10 and BTEB1 mRNAs in the implantation window of endometrium that increase normally, could account for some aspects of infertility in patients with endometriosis and myoma.


Reihaneh Asadi , Parisa Mohamadynejad , Fatemeh Davari Tanha , Mahdi Safarpour , Ahmad Ebrahimi ,
Volume 72, Issue 12 (3-2015)
Abstract

Background: The major issue to address in endometriosis etiology is to identify the genetic changes in the disease and their occurrence in different populations. Uncovering these genetic changes may be important in developing potential biomarkers for early diagnosis and prognosis of endometriosis. Among all endometriosis susceptibility genes studied before, convincing association has been found with variants in the estrogen receptor alpha (ESR1) gene and this disease however, the contributions of these genetic variants in different populations and ethnic groups are not similar. Accordingly, this study was carried out to replicate the previous findings to assess whether this polymorphism is associated with endometriosis in Iranian women. Methods: A case-control study was designed to determine the possible association between ESR1-351A>G variant and occurrence of endometriosis. The study group consisted of 100 subjects diagnosed with endometriosis as case group and 100 fertile women without endometriosis as controls recruited from subjects referred to the Tehran Women’s General Hospital between January to September 2013. All subjects were genotyped for this marker using amplification refractory mutation system- polymerase chain reaction (ARMS-PCR). Association of risk allele (G) with endometriosis was as-sessed using PLINK software after age adjustment. Results: The results showed that the genotype frequencies were in Hardy-Weinberg Equilibrium (HWE) in both case (F=0.04, P:0.67) and control (F=0.02, P:0.83) groups. In addition, there were no significant differences between case and control groups in terms of genotype frequencies (P=0.17). Moreover, the results indicated that the presence of risk allele (G) did not significantly increase risk of endometriosis (OR: 1.43, 95%CI: 0.96-2.13, P=0.07). Conclusion: The results do not support the previous findings of an association between -351A>G genetic polymorphism in ESR1 gene and endometriosis. Therefore, comprehensive genetic approaches including linkage analyses and family-based tests, together with a number of replication studies with large sample size, are needed to make conclusive claims about the role of this genetic polymorphism in susceptibility to endometriosis.

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