Association of the maternal 14-bp insertion/deletion polymorphism in the histocompatibility leukocyte antigen G gene with recurrent implantation failure

Implantation failure of blastocyst is one of the main reasons of failure to become pregnancy following use of Assisted Reproductive Techniques. HLA-G, one of the non-classic HLA subtypes, seems to have a vital role in neutralizing of mother immune system. According to importance of ins/del polymorphism of HLA-G in regulation of HLA-G expression, it seems that this polymorphism has an important effect in immune response against embryo, and so success of embryo implantation. In this experiment we try to evaluate association of HLA-G ins/del polymorphism with risk of occurrence of RIF in ART treated infertile women. To evaluating insertion/deletion polymorphism association with RIF we design a case-control study. We select 40 women with history of recurrent failure to become pregnant following IVF as RIF case group. Forty women with pregnancy following IVF were selected as control. Members of both groups were assessed to rule out of anatomical, immunological and known genetical cause of infertility. Presence of 14 bp insertion/deletion alleles was assessed using PCR-PAGE technique. The data were analyzed by means of SPSS software using Chi-Square tests at the significant level of p<0.05. Our data shows that frequency of heterozygote genotype [ins/del] was significantly higher in case group. Furthermore presence of HLA-G insertion/deletion genotype shows association with increase of implantation failure risk by 3.85 fold. According our results, Heterozygote genotype of ins/del leads to increase of RIF risk. It seems that by genotyping of HLA-G polymorphism, we can predict risk of implantation failure in infertile women after use of ART

Robertsonian translocation between chromosomes [no.21/14] in relation to the history of spontaneous abortion in a family

Background: Approximately 205 million pregnancies occur each year in the worldwide. On the other hand, Spontaneous abortion has been reported in 15-20% of all diagnosed pregnancies. The most common cause of spontaneous abortion is chromosomal abnormalities of the embryo. Robertsonian translocation carriers specially 21-14 are the most common balanced rearrangement among the carrier couples with the history of spontaneous abortion. In order to search for balanced chromosomal rearrangement and cytogenetic disorders, 10 members of related family with consanguinity marriage with the history of recurrent miscarriage were assessed

Case: Cytogenetic evaluation on the basis G-banding technique at high resolution was performed in 3 couples and their related family with the history of idiopathic RSA in order to postulate any balanced chromosomal rearrangement

Conclusion: six members of them appeared with robertsonian balanced translocation between chromosome No.21 to No. 14 with the karyotype of 45, XX, t [14, 21] and 45, XY, t [14, 21], which this results are in agreement with several similar works which claimed that the risk of spontaneous abortion in couples with balanced chromosomal rearrangements is higher compared with general population. Considering to results of present study, it seems as if the cytogenetic analysis of couples with the history of recurrent abortions should be suggested compulsory to estimate the probable presence of any chromosomal rearrangement. This offer wills valuable information for genetic consulting

role of tumor protein 53 mutations in common human cancers and targeting the murine double minute 2-P53 interaction for cancer therapy

The gene TP53 [also known as protein 53 or tumor protein 53], encoding transcription factor P53, is mutated or deleted in half of human cancers, demonstrating the crucial role of P53 in tumor suppression. There are reports of nearly 250 independent germ line TP53 mutations in over 100 publications. The P53 protein has the structure of a transcription factor and, is made up of several domains. The main function of P53 is to organize cell defense against cancerous transformation. P53 is a potent transcription factor that is activated in response to diverse stresses, leading to the induction of cell cycle arrest, apoptosis or senescence. The P53 tumor suppressor is negatively regulated in cells by the murine double minute 2 [MDM2] protein. Murine double minute 2 favors its nuclear export, and stimulates its degradation. Inhibitors of the P53- MDM2 interaction might be attractive new anticancer agents that could be used to activate wild-type P53 in tumors. Down regulation of MDM2 using an small interfering RNA [siRNA] approach has recently provided evidence for a new role of MDM2 in the P53 response, by modulating the inhibition of the cyclin-dependent kinase 2 [cdk2] by P21/WAF1 [also known as cyclin-dependent kinase inhibitor 1 or CDKinteracting protein 1]