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Objective To analyze the clinical efficacy of different anti-tumor therapies for recurrence and metastasis after liver transplantation for primary liver cancer (liver cancer). Methods Clinical data of 145 recipients undergoing liver transplantation for liver cancer were retrospectively analyzed. The overall survival and recurrence and metastasis after liver transplantation for liver cancer were analyzed. The clinical efficacy of different anti-tumor therapies for recipients with recurrence and metastasis were compared. Results Sixty-five recipients (44.8%) developed recurrence and metastasis. The median recurrence time was 6 months. Among them, 1 case underwent secondary liver transplantation after recurrence and died of intestinal perforation. Twenty-four recipients (37%) received targeted drug therapy with a median tumor-bearing survival of 22 months. Eleven recipients (17%) received radiotherapy or chemotherapy with a median tumor-bearing survival of 11 months. Nine recipients (14%) received local treatment (surgical resection or radiofrequency ablation), and the median tumor-bearing survival was 8 months. Twenty recipients (31%) abandoned anti-tumor therapy, and the median tumor-bearing survival was 3 months. The tumor-bearing survival of recipients receiving anti-tumor therapy was significantly longer than that of recipients without anti-tumor therapy (P < 0.001). The tumor-bearing survival of recipients receiving targeted drug therapy was significantly longer than that of those receiving other anti-tumor therapies (P=0.03). The tumor-bearing survival of recipients receiving local treatment, radiotherapy and chemotherapy was considerably longer than that of those who abandoned anti-tumor therapy (P=0.004). Conclusions Surgical resection and radiofrequency ablation are the optimal therapies for recipients with recurrence and metastasis after liver transplantation for liver cancer. For recipients with multi-focal tumors who fail to receive local treatment, those receiving targeted drug therapy obtain the longest survival. In addition, radiotherapy and chemotherapy can also prolong the survival of recipients with recurrence and metastasis.
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Ovarian cancer is one of the highest mortality rate of gynecologic malignant tumors. Chemotherapy can improve the survival rate of the traditional ovary. In recent years, PARP [poly(ADP-ribose)polymerase]inhibitors in breast cancer susceptibility gene (breast cancer susceptibility gene, BRCA) mutations in patients with ovarian cancer can significantly improve the disease-free survival, may change the prognosis of patients with ovarian cancer. This part of PARP [poly(ADP-ribose)polymerase] inhibitors, inhibiting the repairment of DNA damage in tumor cell, causing DNA damage accumulation, eventually killing tumor cells.In breast cancer susceptibility gene 1 (breast cancer susceptibility gene1, BRCA1)/BRCA2 mutation patients with ovarian cancer, PARP inhibitors and BRCA mutation of the synthetic lethal effect provides a new direction for the development of anti-cancer drugs. Now, many highly selective and sensitive PARP inhibitors have been developed and applied in clinical trials.Although PARP inhibitor monotherapy can produce a therapeutic effect in BRCA mutation in patients with ovarian cancer, but the clinical application is still used in combination with other chemotherapy or radiotherapy. This review is focused on the recent progress in clinical trials of PARP inhibitors in combination with common chemotherapeutic agents.
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Objective To explore the clinical and pathological characters of Xp1 1.2 translocation renal cell carcinoma.Method We screened patients of renal cell carcinoma of PUMCH between Jan.2011 and Dec.2015,6 patients with Xp11.2 translocation renal cell carcinoma were found.There were 2 males and 4 females,with average age of 39 (ranging from 16 to 73 years old).Diameter of tumor ranged from 1.9cm to 19.0cm,and 9.6cra in average.Among which,3 cases were detected by routine physical examination,1 by severe anemia (Hb 66g/L),1 by gross hematuria,and 1 by flank discomfort.Before treatment,2 cases had local metastasis (local lymph node,renal pelvis invasion),1 had distant metastasis (pulmonary metastasis).CT examination showed that the tumors had soft tissue density / low density,with significant enhancment or uneven enhancement in enhanced scanning,and were all considered malignancy.6 patients were all treated with surgeries,of which 5 patients received radical nephrectomy,1 patient received nephron sparing surgery.Result Pathologically,most clear cells arranged in a papillary,nest like structure,with psaamoma bodies in them.Immunohistochemical examination showed that all patients were positive for TFE3.AE1/AE3,RCC,Vimentin,CD10,EMA,P504 were positive in different degree.According to pathological result,all 6 patients were proved to be Xp1 1.2 translocation renal cell carcinoma.After surgery,2 patients received immunotherapy,2 received targeted drug therapy,and 1 received local radiotherapy.The follow-up duration ranged from 9 to 56 months (average 37 months).Among which,1 patient died from tumor recurrence and multiple metastasis 22 months after surgery,1 had pulmonary metastasis 12 months after surgery,and the tumor had no significant progress after receiving targeted drug therapy.All the other patients survive without tumor recurrence.Conclusions Xp1 1.2 translocation renal cell carcinoma predominantly occurs in children and adults younger than 40 years.Arterial phase enhancement is slightly lower for Xp1 1.2 translocation renal cell carcinoma in CT scan than that of renal clear cell carcinoma.Histological features and immunohistochemical staining of TFE3 positive expression are important means of diagnosis of this disease.If necessary,gene detection could be done to make better diagnose.Surgery is preferred treatment option.Metastatic leads to poor prognosis,and need to be supplemented by targeted drug therapy.
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Objective To obtain a chimera composed of annexin Bl (AnxBl) and melittin (MLT) and to investigate its inhibitory effect on phosphatidylserine liposome activity and SMMC7721 and HepG2 cell proliferation. Methods A fusion gene AnxBl-MLT was constructed by overlap extension gene splicing and then was inserted into plasmid pGEX-5T. The recombinant plasmid was transformed into E. coli strain K802 and induced by IPTG at low temperature. The expression condition was optimized and GST affinity chromatography column was used for purification. Calcium-dependent phospholipid binding assay was used to determine whether the chimera kept the activity of AnxBl. CCK8 analysis was employed to investigate the effect of AnxBl-MLT on SMMC7721 and HepG2 cell proliferation. Results After being inserted into the expression plasmid, AnxBl-MLT protein expressed in K802 cells, with a high level recombinant protein induced by 0. 2 mmol/ L IPTG at 22-24»C for 4 h. The protein AnxBl-MLT was purified by using GST affinity chromatography column (a band at 63 000) and the purification of the final purified protein was >95%. AnxBl-MLT was able to bind to phosphatidylserine liposome in a calcium-dependent manner. CCK8 analysis indicated that AnxBl-MLT inhibited SMMC7721 and HepG2 cell proliferation at a dose-dependent manner. Conclusion We have successfully constructed a chimera AnxBl-MLT, which retains the calcium-dependent phospholipid binding activity of AnxB1, and can inhibit the proliferation of hepatic cancer cell lines SMMC7721 and HepG2.
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Neovascular age-related macular degeneration (AMD) is the main cause of vision loss in AMD patient.Now,the application of anti-vascular endothelial growth factor(VEGF) has become the preferred therapy for the treatment of neovascular AMD,and it has been proved to improve the visual acuity and reduce the blindness rate.But the formation of choroidal neovascularization (CNV) in AMD is a comprehensive and integrated pathological process.It is difficult to cure the CNV with only anti-VEGF drug for all the neovascular AMD patients.Therefore,the targeting drugs toward other signal pathway associated with CNV are being in different phases of clinical trials.Resent years,with the development of science and technology,small interference RNA(siRNA) and genome technology has been applied to treat neovascular AMD and show a potential prospect,and gene therapy and stem cell therapy are the most remarkable and predominant ways for AMD.Doubtlessly,these therapies offer novel choice for the management of neovascular AMD.