RESUMEN
Gastric cancer (GC) used to be one of the most common malignancies in the world and still is the second leading cause of malignancy-related death in the Far East. The most significant factors that were found to be associated with the clinical outcome in patients with non-metastatic (M0) gastric cancer is tumor's depth of invasion, the presence and the extend of lymphnode involvement, as well as the histological type according to Lauren (intestinal or diffuse). Although it is generally accepted that D2 gastrectomy is the procedure of choice to achieve adequate oncologic excision, there are quite many concerns for its use in patients with early gastric cancer (EGC), where No or N1 specimens are frequently reported. The last two decades, with the evolvement of cancer cell detection techniques, the attend of the medical community is focused on GC patients with solitary lymphnode metastasis (SLN) or micrometastasis (mM). There is a discussion whether SLN should be attributed as the "real" sentinel node (SN) and its projection on patients' survival. The aim of this study is to review the recent literature and attempt to clarify the clinical significance of SLN in gastric cancer.
RESUMEN
Hepatitis C virus (HCV) chronic infection induces liver fibrosis and cirrhosis but is also responsible for a significant portion of hepatocellular carcinoma (HCC) occurrence. Since it was recognized as a causative factor of chronic hepatitis, there have been multiple efforts towards viral eradication, leading to the first-generation HCV treatment that was based on interferon (IFN)-α and its analogs, mainly PEGylated interferon-α (PEG IFNα). Sustained virological response (SVR), defined as the absence of detectable RNA of HCV in blood serum for at least 24 wk after discontinuing the treatment, was accepted as a marker of viral clearance and was achieved in approximately one-half of patients treated with PEG IFNα regimens. Further research on the molecular biology of HCV gave rise to a new generation of drugs, the so-called direct antiviral agents (DAAs). DAA regimens, as implied by their name, interfere with the HCV genome or its products and have high SVR rates, over 90%, after just 12 wk of per os treatment. Although there are no questions about their efficacy or their universality, as they lack the contraindication for advanced liver disease that marks PEG IFNα, some reports of undesired oncologic outcomes after DAA treatment raised suspicions about possible interference of this treatment in HCC development. The purpose of the present review is to investigate the validity of these concerns based on recent clinical studies, summarize the mechanisms of action of DAAs and survey the updated data on HCV-induced liver carcinogenesis.
