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ABSTRACT: Castleman's disease is a slowly progressive and rare lymphoproliferative disorder. Here, we report a 55-year-old woman with superior mediastinal Castleman's disease being misdiagnosed for a long term. We found a 4.3 cm mass localized in the superior mediastinum accompanied with severe clinical symptoms. The patient underwent an exploratory laparotomy, but the mass failed to be totally excised. Pathologic examination revealed a mediastinal mass of Castleman's disease. After radiotherapy of 30 Gy by 15 fractions, the patient no longer presented previous symptoms. At 3 months after radiotherapy of 60 Gy by 30 fractions, Computed tomography of the chest showed significantly smaller mass, indicating partial remission. Upon a 10-month follow-up, the patient was alive and free of symptoms.
Chinese journal of cancer 05/2011; 30(5):351-6.
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Yue-Min Li,
San-Tai Song,
Ze-Fei Jiang,
Qi Zhang,
Chang-Qing Su,
Guo-Qing Liao,
Yi-Mei Qu,
Guo-Qing Xie,
Ming-Ying Li,
Fei-Jiao Ge,
Qi-Jun Qian
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ABSTRACT: To evaluate the therapeutic efficiency of replicative adenovirus CNHK300 targeted in telomerase-positive hepatocellular carcinoma.
CNHK300, ONYX-015 (55 kDa protein deleted adenovirus) and wtAd5 (wild type adenovirus 5) were compared, and virus proliferation assay, cell viability assay, Western blot and fluorescence microscopy were used to evaluate the proliferation and cytolysis selectivity of CNHK300.
The replicative multiples in Hep3B and HepG II after 48 h of CNHK300 proliferation were 40625 and 65326 fold, respectively, similar to that of wtAd5. However, CNHK300 exhibited attenuated replicative ability in normal fibroblast cell line BJ. CNHK300 could lyse hepatocellular carcinoma cells at a low multiplicity of infection (MOI), but could not affect growth of normal cells even at a high MOI.
CNHK300 is a cancer-selective replication-competent adenovirus which can cause oncolysis of liver cancer cells as well as wtAd5 (wild type adenovirus 5), but had severely attenuated replicative and cytolytic ability in normal cells. This novel strategy of cancer treatment offers a promising treatment platform.
World Journal of Gastroenterology 03/2008; 14(8):1274-9. · 2.47 Impact Factor
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ABSTRACT: ObjectiveChemotherapy is an effective means of treating breast cancer, and cancer-specific replicative adenovirus is also a promising
antitumor agent in recent years. Our investigation aims to demonstrate that CNHK300 can mediate selective antitumor efficacy
and produce synergistic cytotoxicity with chemotherapy on HER-2 over-expressing breast cancer.
MethodsWe engineered the telomerase-dependent replicative adenovirus CNHK300 by placing the E1A gene under the control of the human
hTERT promoter. By analysis of E1A expression, we proved the fidelity of hTERT promoter in adenovirus genome and the selective
expression of E1A in telomerase-positive breast cancer cells but not in normal fibroblast cells. By proliferation test, we
further showed efficient replication of CNHK300 in breast cancer cells with apparently attenuated proliferation in normal
fibroblast cells. Finally, we demonstrated by MTT methods that CNHK300 virus caused potent cytolysis and produced synergistic
cytotoxicity with chemotherapy in breast cancer cells with attenuated cytotoxicity on normal cells.
ResultsIn this virus, the E1A gene is successfully placed under the control of the human hTERT promoter. CNHK300 virus replicated
as efficiently as the wild-type adenovirus and caused intensive cell killing in HER-2 over-expressing breast cancer cells
in vitro. In contrast, telomerase-negative normal fibroblast cells, which expressed no hTERT activity, were not able to support CNHK300
replication. Combined treatment of CNHK300 with paclitaxel improved cytotoxicity on cancer cells.
ConclusionWe conclude that CNHK300 can produce selective antitumor efficacy and enhance the in vitro response of chemotherapy on HER-2
overexpressing breast cancer.
Chinese Journal of Cancer Research 05/2007; 19(2):76-81. · 0.18 Impact Factor
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ABSTRACT: To evaluate the safety and efficacy of gefitinib as second-line or even third-line treatment for previously treated patients with locally advanced or metastatic non-small cell lung cancer (NSCLC).
156 patients with locally advanced NSCLC which were about to undergo progression after previous chemotherapy were eligible for this study. The regimen was oral intake of gefitinib 250 mg once daily in the morning or afternoon until the disease progression or toxicity has become intolerable. The drug was provided by AstroZeneca Company by its Expanded Access Program.
154 such patients were evaluable for response and toxicity assessment. The overall rate of objective response and disease control was 28.6% (44/154) and 89.6% (138/154). The median duration of response was 7. 5 months. The median time to disease progression (TTP) was 5. 1 months and the median overall survival time (OS) 10.0 months. The actuarial 1-year survival was 41. 0%. The response rate in adenocarcinoma was significantly higher than that in squamous carcinoma (P = 0. 026). The risk of disease progression in patients with squamous carcinoma was 1. 7 times as much as that of adenocarcinoma patients ( P = 0. 011) , and the risk of death in male was 2. 0 times as much as that in female ( P = 0. 002). At least one of these adverse events would be observed in 40.9% (63/154) of these patients, which, however was mild and reversible. Conclusion Gefitinib is effective and safe as a second-line or third-line treatment for previously treated patients with locally advanced or metastatic non-small cell lung cancer.
Zhonghua zhong liu za zhi [Chinese journal of oncology] 02/2007; 29(1):66-9.
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ABSTRACT: To assess the optimal regimen and its mechanism of ZD1839 in combination with SN38, the active metabolite of irinotecan (CPT-11), in the colon cancer cell lines HT-29 and LoVo.
Chou and Talalay method was used to analyze the combination effects of sequencing of ZD1839 and SN38. Western blotting and immunoprecipitation were used to determine the effects of ZD1839 and/or SN38 on their targeted enzymes and downstream markers. Apoptosis was assayed by analyzing histone-associated DNA fragment.
Sequential SN38 followed by ZD1839 produced a synergistic effect. In contrast, SN38 following ZD1839 exhibited an antagonist effect. SN38 markedly inhibited topoisomerase I (Topo-I) activity. ZD1839 did not alter epidermal growth factor receptor (EGFR) expression, but resulted in a complete inhibition of EGFR phosphorylation. Sequential ZD1839 followed by SN38 did not show any enhanced inhibition effect on Topo-I activity, phosphorylation of EGFR and one of its downstream markers MAPK. However, simultaneous SN38 plus ZD1839, and sequential SN38 followed by ZD1839 administrations showed modest inhibition effect on EGFR's another downstream marker AKT. The combination schedules also showed prominent influence on cell cycle distribution. ZD1839 maintained SN38-induced DNA damage and apoptosis.
Sequential SN38 followed by ZD1839 may be a favorable combination schedule.
Zhonghua zhong liu za zhi [Chinese journal of oncology] 09/2006; 28(8):578-82.
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ABSTRACT: Basic research of gefitinib (Iressa, ZD1839) has demonstrated the combination effects of gefitinib and chemotherapy were sequence-dependent. To evaluate the efficacy of sequential administration of gefitinib following a minor response or partial response to two to three cycles of chemotherapy, a phase II clinical trial was done in Chinese patients with advanced non-small-cell lung cancer (NSCLC).
Thirty-three consecutive patients with advanced NSCLC that had been pretreated with at least one chemotherapeutic regimen and were responding to chemotherapy following 2 to 3 cycles of treatment, entered the trial from May 2004 to February 2006. Patients received gefitinib at an oral dose of 250 mg once daily for 4 weeks.
Thirty-three patients were evaluable for response and toxicity. The objective response rate was 24.2% (8 of 33) (95% CI, 11% to 42%). The symptom improvement rate was 54.5% (18 of 33) (95% CI, 41% to 69%). The median duration of response was 7 months (95%CI, 4.0 to 13.2 months). The median time to disease progression (TTP) was 6.5 months (95%CI, 0.7 to 16.6 months). The median overall survival time (OS) was 9.8 months (range, 2.1 to 18.0 months), and the actuarial 1-year survival was 36.4%. Toxicity was relatively mild and included only one patient (3.0%) with grade 4 diarrhea, 1 (3.0%) with grade 3 rash, 1 (3.0%) with grade 3 nausea, and 1 with grade 3 vomiting (3.0%).
Preliminary results suggest that sequential administration of gefitinib following a response to chemotherapy may be beneficial for Chinese patients with advanced NSCLC. Further randomized clinical trials are needed.
BMC Cancer 02/2006; 6:288. · 3.01 Impact Factor
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ABSTRACT: To evaluate the therapeutic efficiency of replicative adenovirus CNHK300 targeted at telomerase-positive hepatocellular carcinoma.
Human liver cancer cell line HepGII and Hep3B, human embryonic kidney cell line 293, and normal human fibroblasts of the line BJ were cultured and added with adenoviruses CNHK300, ONYX-015 (55 000 protein deleted adenovirus), or wtAd5 (wild type 5) with different multiplicity of infection (MOI) for 7 days. 293 cells were used to measure the titer of the filial generation virus from different cells. The cell survival rate was calculated by MTT method 2, 4, 6, and 8 days after. Different cells were added with CNHK300 virus and then the E1A protein in the cytoplasm was measured by western blotting. Fluorescence microscopy was used to observe the CNHK300-EGFP proliferation after the cells were cultured and added with the virus for 1.5 hours.
The replicative viruses CNHK300 and wtAd5 proliferated rapidly in HepGII and Hep3B cells since 24 hours after inoculation and proliferated 40625 and 65326 times respectively with a proliferation potential similar to that of the wild-type adenovirus and much higher than that of the ONYX-015 virus. CNHK300 of the MOI of 0.0002 killed half of the cancer cells, especially those of the line Hep3B, within 5 approximately 6 days, and CNHK300 virus of the MOI of 0.5 pfu/cell killed almost all the HepGII cells in the 8th day, with a killing power lower than that of the wild-type virus and higher than that of the ONYX-015 cells. The IC(50) was as low as MOI of 0.002 pfu/cell for the Hep3B cell and was as high as MOI of 100 pfu/cell for the BJ cell. CNHK300 was a less powerful killer of fibroblasts than wild-type virus. E1A expression was shown by western blotting in 293 cells and CNHK300-infected liver cancer cells, but not in the CNHK300-infected normal human fibroblasts. Fluorescence microscopy showed only isolated fluorescence-positive fibroblasts till the 10th day of infection, but obvious proliferation of CNHK300-EGFP virus since the 3rd day and fluorescence-positive cells in sheets by the 7th day, however, the fluorescent intensity was weakened since the 10th day.
Tumor-selective adenovirus CNHK300 replicates in telomerase-positive liver cancer cells efficiently as well as wtAd5 and causes oncolysis, but has severely attenuated proliferation and cytolysis in normal cells.
Zhonghua yi xue za zhi 03/2005; 85(7):468-72.
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ABSTRACT: Different environment illuminations have a great impact on face detection. We present a solution based on face relighting technology. The basic idea is that there exists nine harmonic images that can be derived from a 3D model of a face, and by which we can estimate the illumination coefficient of any face sample. Using an illumination radio image, we can produce images under new lighting conditions. To detect the faces under certain lighting condition, we relight the original face samples to get more new faces under different kinds of possible lighting condition, and add them to the training set. Our experimental results on support vector machine (SVM) turns out that the relighting subspace is effective in face detection under various lighting conditions. Moreover, if we relight original face samples to the new samples under different illuminations, the collected example sets are multiplied. We use the expanded database to train an AdaBoost-based face detector and test it on the MIT+CMU frontal face test set. The experimental results show that the data collection can be efficiently speeded up by the proposed methods. The later experiment also verifies the generalization capability of the proposed method.
Machine Learning and Cybernetics, 2004. Proceedings of 2004 International Conference on; 09/2004
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ABSTRACT: To study the feasibility of adenoviral transduction of Herceptin complete antibody gene and its effect on Her2 over-expressing cancer.
The genes of VH and VL from the monoclonal antibody Herceptin were cloned into the genome of replication-defective adenovirus by viral recombination technology to produce the recombinant adenovirus Ad-SG-Her. Normal human liver cells of the line L-02 were transfected with Ad-SG-Her and ELISA was used to detect the expression of Herceptin antibody 3 and 7 days after. Forty BALB/c nude mice were inoculated with Her2 high-expressing oophoroma cells of SK-OV-3 line and were randomized into 4 equal groups: group A injected with Ad-SG-Her at the dosage of: 2 x 10(9) plaque forming unit (pfu) through the caudal vein, group B injected with Ad-SG-Her at the dosage of 1 x 10(9) pfu, group C injected with Ad-SG-Her at the dosage of 5 x 10(8) pfu, and control group. On the days 3, 7, 10, 14, 21, 28, and 35 after the injection of virus, the antibody expression in the serum was measured by ELISA and the size of tumor was measured vernier caliper. Western blot and IFA was used to detect the specificity for Her2-overexpressing ovarian cancer cell lines SK-OV-3 and the integrity of complete antibody. Anti-tumor effects were also observed in nude mice bearing SK-OV-3 tumors.
The constructed recombinant adenovirus Ad-SG-Her could express Herceptin efficiently both in vitro and in vivo. The biological activity of the expressed antibody was similar to that of the commercial Herceptin as shown by Western blotting, IFA, and ELISA. Herceptin expression of Ad-SG-Her was detected since day 3 after treatment in the groups A, B, and C and reached the peak on days 7 - 10. The expression lasted for four weeks or so. The expression level was significantly different between group A and the groups B and C (all P < 0.05), however, without a significant difference between the group B and group C. The antibody expression of group A might increase to 103.5 micro g/ml, high enough to inhibit tumor growth and induce tumor cell apoptosis. The antibody expression of the group B was below 40 micro g/ml, and that of the group C was below 30 micro g/ml. Furthermore the expressed antibody doses were statistically significantly different at different time points. Almost no tumor growth was seen in the group A during the observation period in comparison with the groups B and C and the control group (all P < 0.05). The tumor growth was almost not influenced in the group B and C and the control group.
Ad-SG-Her efficiently expresses humanized complete Herceptin with effective bioactivity and induces long-term stable expression both in vitro and in vivo. The system may serve as a new antitumoral gene therapy strategy in antibody field.
Zhonghua yi xue za zhi 07/2004; 84(14):1147-51.
