AT-rich interaction domain 1A gene (ARID1A) encodes for a subunit of the switch/sucrose non-fermentable (SWI/SNF) complex, a chromatin remodeling complex, and it has been implicated in the pathogenesis of various cancer types. In this review, we discuss how ARID1A is linked to endometrial cancer and what molecular pathways are affected by mutation or inhibition of ARID1A. We also discuss the potential use of ARID1A not only as a prognostic biomarker, but also as a target for therapeutic interventions. The dynamic modification of chromatin structure in a temporal-and spatial-specific manner determines cell fate by regulating expression levels of specific genes. The complexity of this process is further highlighted when considering all the endogenous and exogenous signals received by each cell during development and throughout its life. Numerous molecules (proteins and RNA) and macromolecular complexes are responsible for the organization of nucleosomes (Figure 1), epigenetic modifications, the dynamic change between the 'relaxed' or 'tight' conformation of chromatin (euchromatin and heterochromatin, respectively) and the accessibility of gene promoters determining cellular activities such as gene transcription, DNA repair and cell differentiation. Thus, disruption of normal chromatin remodeling impairs cellular development and homeostasis, and it has been associated extensively with tumorigenesis [reviewed in (1)]. The switch/sucrose non-fermentable (SWI/SNF) complex is a nucleosome-remodeling factor found in both eukaryotes and prokaryotes. It is involved in gene expression through transcriptional regulation and plays a pivotal role in carcinogenesis (2). This complex changes the DNA conformation in nucleosomes, allowing recruitment of transcription factors or other complexes responsible for DNA repair, replication and proliferation. Thus, when the SWI/SNF complex is disrupted, aberrant cell cycling is observed, as well as a loss of control of proliferation (3). SWI/SNF is a multi-subunit complex and many of its subunits, such AT-rich interaction domain 1A (ARID1A), ARID1B, SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily A, member 2 (SMARCA2) and SMARCA4 (Figure 2), have been incriminated as driving mutations in various cancer types due to the high mutation frequencies observed (4). In particular, when considering human primary cancer cases with mutations in the SWI/SNF complex, most of the mutations seen are encountered in the gene encoding ARID1A (5-7). ARID1A and ARID1B genes encode DNA-targeting subunits, while SMARCA2 and SMARCA4 encode ATPase enzymes. The mutation frequency of these subunits in different cancer types seems to be tumor type-specific indicating that there is probably differential participation of the complex in gene regulation in different tissues (4). Loss of ARID1A has been shown in numerous human malignancies, such as uterine endometrioid carcinoma (8-10), ovarian endometrioid carcinoma (11), gastric cancer (12, 13), esophageal adenocarcinoma (14), pan...

Thromboembolic disease during pregnancy is a significant cause of maternal morbidity and mortality involving venous or arterial thrombosis and possible clinical manifestations like clinical symptoms of antiphospholipid antibody syndrome and hyperhomocysteinemia. For diminishing the prevalence of thromboembolic disease, the early identification of pregnant women with various risk factors for thrombosis without clinical symptoms is of great importance. However, the optimal management for asymptomatic pregnant women who have inherited thrombophilia is uncertain and recognized only due to pregnancy complications such as recurrent pregnancy loss and preeclampsia. The clinical approach to thromboembolism is the same in pregnant women with or without thrombophilia. Based on family history, clinical symptoms should begin with simple reliable inexpensive laboratory tests like prothrombin time and activated thromboplastin time to test the status. Early diagnosis and appropriate use of thromboprophylaxis lead to increasing better maternal and perinatal outcomes. Conclusively, it is important to recognize these patients in order to prevent all pregnancy complications.

The detailed research for more information on the very important area of tongue cancer is the purpose of the present study. We report two cases of pregnant women suffering from tongue cancer during pregnancy, the treatment of tongue cancer and information on the outcome of pregnancy. Pregnancy should not be considered an obstacle to the proper treatment of a mother's tongue malignancy. The epidemiological trend in recent years is to increase the overall survival of patients and keep them free of disease for a longer period of time. The reported pregnant women were in the third trimester of pregnancy with tongue cancer symptoms at 37 and 32 weeks, respectively. After detailed information, the cesarean section was performed and the two women treated according to the proposed protocols which were as following: surgical removal of tumors, lymph node dissection in 5 levels and postoperative radiotherapy. The first case of these recurred 3 months later, underwent surgical removal of the tumor and subsequently underwent chemotherapy and immunotherapy. She died one year after the primary diagnosis of tongue cancer. The perinatal effect was perfect in both cases. The lack of systematic randomized prospective studies and the difficulties in carrying them out in general, make bibliographic review even more useful in guidelines, retrospective studies, series of events and individual cases for future scientific studies to be performed in order to establish treatment protocols.

The miscarriages' investigation should include a familiar history, gynecological examination and a full laboratory testing including hormonal control, as well as karyotype, maternal immune control and thrombophilia testing. If the physician suspects the cause of abortions is chromosomal due to heredity, a special blood test (karyotype) for the pair is recommended. Chromosomal abnormalities are the most common reason for first trimester abortions, and are impossible to be prevented. Based on the above data, abortion and the subsequent possible infertility should not be considered as a personal failure for the woman and the treating physician. Nowadays, medical advancement provides many options combined with psychological support can actually reduce the miscarriages' risk.

In recent years an increase in premature births (PB) rate has been noticed, as this pregnancy complication that still remain an important cause of perinatal morbidity and mortality, is multifactorial and prediction is not easy in many cases. There are many bibliographic data supporting the view that PB have also genetic predisposition. The trend of “recurrence” of PB in women as well as its increased frequency in ethnic groups suggests its association with genetic factors, either as such or as an interaction of genes and environment. Immunomodulatory molecules and receptors as well as polymorphisms of various genes and/or single nucleotides (single nucleotide polymorphisms, SNPs) now allow with advanced methods of Molecular Biology the identification of genes and proteins involved in the pathophysiology of PB. From the history of a pregnant woman, the main prognostic factor is a previous history of prematurity, while an ultrasound assessment of the cervix between 18 and 24 weeks is suggested, both in the developed and the developing world. According to the latest data, an effective method of successful prevention of premature birth has not been found. The main interventions suggested for the prevention of premature birth are the cervical cerclage, the use of cervical pessary, the use of progesterone orally, subcutaneously or transvaginally, and for treatment administration of tocolytic medication as an attempt to inhibit childbirth for at least 48 hours to make corticosteroids more effective. Despite the positive results in reducing mortality and morbidity of premature infants, the need for more research in the field of prevention, investigation of the genital code and the mechanism of initiation of preterm birth is important.