One of the most common complications during pregnancy is gestational diabetes mellitus (GDM), hyperglycemia that occurs for the first time during pregnancy. The condition is multifactorial, caused by an interaction between genetic, epigenetic, and environmental factors. However, the underlying mechanisms responsible for its pathogenesis remain elusive. Moreover, in contrast to several common metabolic disorders, molecular research in GDM is lagging. It is important to recognize that GDM is still commonly diagnosed during the second trimester of pregnancy using the oral glucose tolerance test (OGGT), at a time when both a fetal and maternal pathophysiology is already present, demonstrating the increased blood glucose levels associated with exacerbated insulin resistance. Therefore, early detection of metabolic changes and associated epigenetic and genetic factors that can lead to an improved prediction of adverse pregnancy outcomes and future cardio-metabolic pathologies in GDM women and their children is imperative. Several genomic and epigenetic approaches have been used to identify the genes, genetic variants, metabolic pathways, and epigenetic modifications involved in GDM to determine its etiology. In this article, we explore these factors as well as how their functional effects may contribute to immediate and future pathologies in women with GDM and their offspring from birth to adulthood. We also discuss how these approaches contribute to the changes in different molecular pathways that contribute to the GDM pathogenesis, with a special focus on the development of insulin resistance.

Introduction: ASPS is a rare, soft tissue tumor which represents 0.2-1 % of soft tissue sarcomas. A characteristic nonreciprocal translocation is found in nearly all cases. The resulting ASPSCR1-TFE3 fusion gene is postulated to be involved in the pathogenesis of this tumor. Case report: 29 years-old female presented with abdominal pain for few months. MRI and CT revealed a large necrotic abdominopelvic mass, which is extra-uterine, extra-ovarian, and peritoneal nodules. Exploratory laparotomy revealed a large mass arising from the distal part of the descending colon involving the mesentery and the surrounding peritoneum. She underwent left colectomy with primary anastomosis, and resection of the involved adjacent peritoneal and mesenteric surface nodules. Histopathology revealed ASPS involving the outer serosal layer of the large bowel wall negative margins. It also involved the resected mesenteric fat, greater omentum, and peritoneum. No further treatment was received as the patient traveled to home country. Discussion: The treatment of early-stage ASPS involves radical surgical excision of the primary tumor. Traditionally, patients with advanced ASPS have limited therapeutic options because of the resistance of the tumor to conventional cytotoxic chemotherapy, however, it is a targetable sarcoma. The response rate of metastatic ASPS to targeted therapy is clinically meaningful, and comparable to that of first-line chemotherapy. Most patients who received targeted therapy achieved disease control. Patients who had refractory or progressive disease to one targeted agent demonstrated a response to other agents. More randomized trials are warranted to expand treatment options and compare them to standard care regimens. Conclusion: In conclusion, while radical surgical excision remains crucial for early-stage ASPS, the landscape for advanced cases is evolving with targeted therapies showing promising results. However, further randomized trials are necessary to broaden the treatment options available and to evaluate these new therapies against existing standard care regimens. This ongoing research is vital to improving outcomes for patients with ASPS and tailoring more effective treatment strategies. Highlights: