Background: Radiofrequency coagulation (RFC) is being promoted as a novel technique with a low morbidity rate in the treatment of liver tumours. The purpose of this study was to assess critically the complication rates of RFC in centres with both large and limited initial experience, and to establish causes and possible means of prevention and treatment. The morbidity and mortality of RFC, while low, is higher than previously assumed. With adequate knowledge, many complications are preventable.
As an alternative to standard surgical resection for the treatment of malignant tumors, radiofrequency ablation (RFA) has rapidly evolved into the most popular minimally invasive therapy. To help readers gain the relevant background knowledge and to better understand the other reviews in this Feature Section on the clinical applications of RFA in different abdominal organs, the present report covers the general aspects of RFA. After an introduction, we present a simple definition of the energy applied during RFA, a brief historical review of its technical evolution, and an explanation of the mechanism of action of RFA. These basic discussions are substantiated with descriptions of RFA equipment including those commercially available and those under preclinical development. The size and geometry of induced lesions in relation to RFA efficacy and side effects are discussed. The unique pathophysiologic process of thermal tissue damage and the corresponding histomorphologic manifestations after RFA are detailed and cross-referenced with the findings in the current literature. The crucial role of imaging technology during and after RFA is also addressed, including some promising new developments. This report finishes with a summary of the key messages and a perspective on further technologic refinements and identifies some specific priorities.
Radiofrequency coagulation by laparoscopy or laparotomy results in superior local control, independent of tumor size. The percutaneous route should mainly be reserved for patients who cannot tolerate a laparoscopy or laparotomy. The short-term benefits of less invasiveness for the percutaneous route do not outweigh the longer-term higher risk of local recurrence.
N6-methyladenosine (m6A), and its reader protein YTHDF1, play a pivotal role in human tumorigenesis by affecting nearly every stage of RNA metabolism. Autophagy activation is one of the ways by which cancer cells survive hypoxia. However, the possible involvement of m6A modification of mRNA in hypoxia-induced autophagy was unexplored in human hepatocellular carcinoma (HCC). In this study, specific variations in YTHDF1 expression were detected in YTHDF1-overexpressing, -knockout, and -knockdown HCC cells, HCC organoids, and HCC patient-derived xenograft (PDX) murine models. YTHDF1 expression and hypoxia-induced autophagy were significantly correlated in vitro; significant overexpression of YTHDF1 in HCC tissues was associated with poor prognosis. Multivariate cox regression analysis identified YTHDF1 expression as an independent prognostic factor in patients with HCC. Multiple HCC models confirmed that YTHDF1 deficiency inhibited HCC autophagy, growth, and metastasis. Luciferase reporter assays and chromatin immunoprecipitation demonstrated that HIF-1α regulated YTHDF1 transcription by directly binding to its promoter region under hypoxia. The results of methylated RNA immunoprecipitation sequencing, proteomics, and polysome profiling indicated that YTHDF1 contributed to the translation of autophagy-related genes ATG2A and ATG14 by binding to m6A-modified ATG2A and ATG14 mRNA, thus facilitating autophagy and autophagy-related malignancy of HCC. Taken together, HIF-1α-induced YTHDF1 expression was associated with hypoxia-induced autophagy and autophagy-related HCC progression via promoting translation of autophagy-related genes ATG2A and ATG14 in a m6A-dependent manner. Our findings suggest that YTHDF1 is a potential prognostic biomarker and therapeutic target for patients with HCC.
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