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CONCLUSION: LCVP is easily achievable in technique.Maintenance of CVP ≤ 4 mmHg can help reduce blood loss during hepatectomy, shorten the length of hospital stay, and has no detrimental effects on hepatic or renal function. INTRODUCTIONHepatectomy remains as the treatment of choice for hepatocellular carcinoma (HCC). Intra-operative blood loss is one of the major causes for post-operative morbidity and mortality. Various techniques, such as Pringle's maneuver and unilateral hepatic hilum occlusion, have been used to control bleeding from hepatic arterial and portal venous systems during hepatectomy in clinical settings. However, for excision of HCC adjacent to major blood vessels, hepatic system could be the major source of hemorrhage, especially after the application of Pringle's maneuver. Hence, effective control of hepatic venous hemorrhage is crucial to minimize intraoperative blood loss. This prospective randomized clinical trial aims at evaluating the role of low central venous pressure (LCVP) in reducing blood loss during hepatectomy for HCC. MATERIALS AND METHODS Patients'data and groupingFrom June 2002 to December 2003, a total of 50 consecutive patients with HCC (40 men and 10 women) underwent hepatectomy by the same group of surgeons at our hospital. By the sealed envelope method, the patients were blindly randomized into LCVP group (n = 25) and control group (n = 27) at the beginning of the operation. Two patients in the control group were excluded from the study because hepatectomy was given up due to cardiac arrest in one and unclear tumor demarcation in the other. Eventually, there were 25 patients in each group. The demographic data of the patients are shown in Table 1

Percutaneous microwave ablation and radiofrequency ablation are both effective methods in treating hepatocellular carcinomas. The local tumor control, complications related to treatment, and long-term survivals were equivalent for the two modalities.

The proinflammatory IL-17–producing CD8+ T cells (Tc17 cells) have recently been detected in tumors, but the nature and regulation of these cells in human tumors are presently unknown. We have recently found that IL-17+ cells are accumulated in human hepatocellular carcinomas (HCC), where they promote disease progression by fostering angiogenesis. In this study, we showed that Tc17 cells constitute a remarkable portion of IL-17–producing cells in human HCC. Although most circulating Tc17 cells were negative for IFN-γ, >80% of Tc17 cells in HCC tissues were positive for IFN-γ, and they were enriched predominantly in invading tumor edge. Most CD68+ cells located in invading tumor edge exhibited an activated phenotype and, accordingly, the activated monocytes isolated from HCC tissues were significantly superior to those isolated from nontumor tissues in inducing expansion of Tc17 cells in vitro with phenotypic features similar to those isolated from tumors. Compared with IL-17−IFN-γ+CD8+ cells, these IFN-γ+Tc17 cells have significantly higher expression of proinflammatory cytokines (IL-2, IL-22, and TNF-α), but reduced expression of granzyme B and perforin. Moreover, we found that tumor-activated monocytes secreted a set of key cytokines (IL-1β, IL-6, and IL-23) to trigger the proliferation of Tc17 cells. These data reveal an intriguing mechanism in which human Tc17 cells are generated by a fine-tuned collaborative action between different types of immune cells in distinct tumor microenvironments.

The ability of cancer cells to evade apoptosis may permit survival of a recombinant vaccinia lacking antiapoptotic genes in cancer cells compared with normal cells. We have explored the deletion of two vaccinia virus host range/ antiapoptosis genes, SPI-1 and SPI-2, for their effects on the viral replication and their ability to induce cell death in infected normal and transformed cells in vitro. Indeed, in three paired normal and transformed cell types, the SPI-1 and SPI-2 gene-deleted virus (vSP) preferentially replicates in transformed cells or p53-null cells when compared with their normal counterparts. This selectivity may be derived from the fact that vSP-infected normal cells died faster than infected cancer cells. A fraction of infected cells died with evidence of necrosis as shown by both flow cytometry and detection of high-mobility group B1 protein released from necrotic cells into the culture supernatant. When administered to animals, vSP retains full ability to replicate in tumor tissues, whereas replication in normal tissues is greatly diminished. In a model of viral pathogenesis, mice treated with vSP survived substantially longer when compared with mice treated with the wild-type virus. The mutant virus vSP displayed significant antitumoral effects in an MC38 s.c. tumor model in both nude (P < 0.001) and immunocompetent mice (P < 0.05). We conclude that this recombinant vaccinia vSP shows promise for oncolytic virus therapy. Given its enhanced tumor selectivity, improved safety profile, and substantial oncolytic effects following systemic delivery in murine models, it should also serve as a useful vector for tumor-directed gene therapy. (Cancer Res 2005; 65(21): 9991-8)