Shaobo Hu

Huazhong University of Science and Technology, Wu-han-shih, Hubei, China

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Publications (3)0 Total impact

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    ABSTRACT: Objective Rupture of hepatocellular carcinoma (HCC) following transarterial embolization/chemoembolization (TAE/TACE) is a rare but life-threatening complication. The aim of the study was to explore the incidence, risk factors, clinical characteristics, treatment, and outcomes of this complication. Methods We described two cases and reviewed all cases of ruptured HCC after TAE/TACE reported in the literature. Results Our search yielded 32 cases of ruptured HCC after TAE/TACE. The overall incidences were 0.45% per patient and 0.21% per session. The mean age of the patients was 57.4 years (range 28–90 years, n = 26, No. of cases with available information). Males accounted for 81% of cases (21/26). The 50% of the cases had histories of primary hypertension, diabetes or peripheral artery disease (6/12). Mean diameter of the tumors was 11.4 cm (range 3–20 cm, n = 27). The 100% of cases had superficial or exophytic tumors (23/23). Portal vein thrombosis was presented in 61.5% of patients (8/13). The median interval between TAE/TACE and rupture was 2 days (range 0 hour — 30 days, n = 31). Management choices included emergency TAE, surgery, and conservative treatment. The overall median survival time was 7 days (n = 19). Conclusion Rupture of HCC following TAE/TACE is relatively rare but potentially life-threatening. The management is difficult and prognosis is poor. Large tumor size, superficial or exophytic tumors as well as portal vein thrombosis and comorbidities such as primary hypertension, diabetes or peripheral artery disease may be predisposing factors for rupture.
    The Chinese-German Journal of Clinical Oncology 02/2013; 12(2).
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    ABSTRACT: ObjectiveThe aim of the study was to report an anemia patient with melena for five years caused by duodenal gastrointestinal stromal tumor (GIST), who required surgical treatment. MethodsA 44-year old man present with anemia appearance was admitted to our center (Department of Hepatobiliary Surgery, Union Hospital, Huazhong University of Science and Technology, China) due to sustaining melena for five years. Endoscopy found no special mucosal abnormalities in the duodenal lumen. Computed Tomography showed a well-demarcated mass, 7.4 cm in diameter, located between the C loop of duodenum and pancreatic head. Pylorus-preserving pancreaticoduodenectomy and right hemicolectomy were performed when the patient’s general conditions were improved. He recuperated successfully and was discharged on the 21st postoperative day. No complications happened during the period of hospital stay. ResultsHistological and immunohistochemical study revealed a high risk invasive duodenal GIST which was positive for CD117, CD34, α-smooth muscle actin and negative for S-100. ConclusionDuodenal GIST can be a source of upper gastrointestinal hemorrhage; surgical treatment is still a reasonable choice for the patients with invasive duodenal GIST. Key wordsduodenum-gastrointestinal stromal tumor (GIST)-CD117-hemorrhage-surgery
    The Chinese-German Journal of Clinical Oncology 04/2010; 9(4):243-245.
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    ABSTRACT: ObjectiveThe aim of this study was to study the effect of human papilloma virus (HPV) type 16 E7 protein expression on growth of RMA cells in vitro and in vivo. MethodsThe recombination vector pcDNA3.1-E7 carrying wild type HPV 16 E7 was identified by sequencing. The recombination vector pcDNA3.1-E7 was transfected into mouse lymphadenoma cell line RMA by liposome, and the monoclonal cells transfected stably were obtained by antibiotics G418 sieving and limiting dilution assay. RT-PCR method was used to detect the expression of HPV 16 E7 mRNA in RMA-E7 cells. The growth of RMA cells and RMA-E7 cells cultured in vitro was tested by Cell Count Kit-8. RMA-E7 cells and RMA cells were subcutaneously inoculated in syngeneic mice respectively, the tumor size was measured by sliding caliper twice a week, and the E7 protein expression in tumor tissue of mice was detected by Western blot after tumor formation. The kinetics of cytolytic activity of E7 specific T cells in tumor-bearing mice was measured by LDH kit. ResultsSequencing of recombination vector showed the target gene which was inserted into the recombinant was correct, and RMA-E7 cells expressing E7 protein stably were obtained by limited dilution assay. There were no obvious differences in morphous and growth velocity between RMA cells and RMA-E7 cells in vitro. RMA-E7 cells grew in syngeneic mice were significantly slower than RMA cells. The E7 protein was expressed stronger in RMA-E7 cells in vivo than in vitro. The cytolytic ability of E7-specific CTL was activated at the early stage, reached the maximum at the middle stage, and lost at the end stage. RMA-E7 cells isolated from the tumor-bearing mice were more resistant to E7-specific CTL killing than RMA-E7 cells cultured in vitro. ConclusionThe E7 protein expression has no obvious influence on growth of RMA-E7 cells in vitro, and can suppress growth of RMA-E7 cells in vivo. The activity curve of E7 specific CTL approximately presents “bell” shape. The RMA-E7 cells grew in vivo had a high expression levels of E7 protein, and more resistant to E7-specific CTL killing than those cultured in vitro. The E7 protein expression in vivo not only initiates immune activation, but also induces immune tolerance. Key wordscytotoxic T lymphocyte-human papilloma virus (HPV) type 16 E7-immune tolerance
    The Chinese-German Journal of Clinical Oncology 01/2010; 9(2):73-78.