Mesenteric ischemia: Pathogenesis and challenging diagnostic and therapeutic modalities

Leiomyosarcoma of the inferior vena cava (IVCL) is a rare malignant tumour originating from the smooth muscle cells of the media with intra- or extra-luminal growth. The type of the lesion is further divided into three levels in relation to hepatic and renal veins respectively. The aim of this review was to evaluate the results of surgical treatment of IVCL with special reference to the extent of its histological spread and to analyse the recent literature in order to provide an update on the current concepts of diagnostic and therapeutic management of this entity. IVCL's patients may present with non-specific complaints such as dyspnoea, malaise, weight loss, nausea, vomiting, fever and abdominal pain. Haematogenous metastasis is frequent. At a later stage, IVCL may also spread through lymphatic. Multiple diagnostic imaging techniques have been proposed for accurate preoperative diagnosis, including Doppler ultrasonography (US), computed tomography (CT) and magnetic resonance imaging (MRI), individually or in combination with cavography echocardiography or CT-guided biopsy. Despite recent research on the therapeutic strategies against IVCL, surgical resection appears the only potentially curative approach. Unfortunately, a mere minority of patients is eligible to undergo surgical intervention. In addition, surgical removal of IVCL does not necessarily guarantee patient's long-term survival. Alternative therapies, such as radio- and chemo-therapy often proved insufficient. Debate continues regarding the optimal management of the IVC after tumour resection, with primary repair, ligation and IVC reconstruction all have been utilized with varying success.

Chemotherapy resistance is a rising concern in Gastric Cancer (GC) and has led to the investigation of various cellular compounds. Α functional equilibrium of histone acetylation and deacetylation was discovered in all cells, regulated by Histone Acetyltransferases and Deacetylases (HDACs), controlling chromatin coiling status and changing gene expression appropriately. In accordance with recent research, this equilibrium can be dysregulated in cancer cells aiding in the process of carcinogenesis and tumor progression by altering histone and non-histone proteins affecting gene expression, cell cycle control, differentiation, and apoptosis in various malignancies. In addition, increased HDAC expression in GC cells has been associated with increased stage, tumor invasion, nodal metastases, increased distant metastatic potential, and decreased overall survival. HDAC inhibitors could be used as treatment regimens for GC patients and could develop important synergistic interactions with chemotherapy drugs. The aim of this article is to review the molecular identity and mechanism of action of HDAC inhibitors, as well as highlight their potential utility as anti-cancer agents in GC.