Abstract
In this study, we aim to investigate oxidative stress in hepatocellular carcinoma (HCC) tissues in patients receiving preoperative transcatheter arterial chemotherapy (TAC) and its association with prognosis. A total of 89 HCC patients enrolled in this study, 39 received preoperative TAC 1 week before surgery (pTAC group) and 50 did not (non-pTAC group). All patients underwent hepatectomy and postoperative TAC and were followed up to 400 weeks. Samples of liver tissue without HCC and hepatitis (n = 15) served as normal controls. Cellular levels of 8-hydroxy-2′-deoxyguanosine (8-OHdG), TP53, and p21waf1/cip1 were measured in both cancer and surrounding tissues using an immunohistochemistry assay. Taken together, our data suggested that preoperative TAC might postpone postoperative HCC relapse within 1 year via suppression of tumor cells by induction of high levels of oxidative stress.
Highlights
Hepatocellular carcinoma (HCC) is one of the most common malignancies in China [1]
Our study showed that regardless of whether HCC patients received preoperative transcatheter arterial chemotherapy (TAC) or not, 8-OHdG
We found that 8-OHdG levels in HCC tissues were significantly lower in the preoperative transcatheter arterial chemotherapy (pTAC) group than in the non-pTAC group, probably because the active metabolism and chemoresponsiveness of HCC cells were inhibited by the antitumor pTAC drugs
Summary
Hepatocellular carcinoma (HCC) is one of the most common malignancies in China [1]. Transcatheter arterial chemoembolization (TACE) is a palliative treatment for patients with unresectable intrahepatic tumors to obtain degradation and possible consequential resection [2]. When applying transcatheter arterial chemotherapy (TAC) without embolization agents rather than TACE for the treatment of patients with HCC and main portal vein thrombosis(MPVT), TAC as an adjunctive therapy significantly improved survival in HCC patients[4]. Preoperative TAC is safer than the TACE for resectable HCC patients, but whether it could improve surgical outcomes was not fully studied so far. The anti-tumor effect of TAC is attributed to oxidative stress induced by anti-neoplastic agents [7] via generation of both high and low levels of reactive oxygen species (ROS) [8]. Chemotherapy could trigger DNA repair in HCC, raising the hypothesis that the overall efficacy of TAC on HCC depends on the cellular response to oxidative stress caused by chemotherapeutic agents in both cancerous and surrounding tissues. We investigated oxidative stress in liver tissues in HCC patients receiving preoperative TAC to determine the effect of oxidative stress on changes in HCC tissue and its association with prognosis
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