Objective. To analyze the diagnosis and treatment of patients with concomitant malignant tumors after organ transplantation by compiling data from organ transplantation patients. Methods. By searching CNKI and PubMed databases, we made a systematic analysis of the studies of postorgan transplantation complicating malignant tumors in the last decade. Results. There were 10 articles on malignant tumors after renal transplantation, 8 articles on liver transplantation, 2 articles on heart transplantation, and 1 article on lung transplantation. The incidence of malignant tumors complicating renal transplantation is 10.4% in Europe, with skin cancer and Kaposi’s sarcoma being common; the incidence in the United States is 3.4%, with PTLD having the highest incidence; the incidence of malignant tumors is relatively lowest in Asia, with gastrointestinal malignancies being the main ones. The mean time to complication of malignancy after renal transplantation is 3.83 years. The incidence of concurrent malignancies after liver transplantation is 8.8% in Europe, where skin cancer and Kaposi’s sarcoma are common; 5.6% in Asia, where gastrointestinal tract tumors are prevalent; and 4.5% in the United States, where gastrointestinal tract tumors, PTLD, and hematologic diseases are predominant. The mean time to complication of malignancy after liver transplantation is 4.79 years. The incidence of malignancy after heart transplantation is 6.8-10.7%. The incidence of malignancy after lung transplantation is about 10.1%. Minimization of immunosuppression or modification of immunosuppression regimens may be a key component of cancer prevention. mTOR inhibitors and phenolate (MMF) reduce the incidence of de novo malignancies in patients after solid organ transplantation. Surgical treatment improves survival in patients with early malignancies. The use of external beam radiation therapy in the treatment of hepatocellular carcinoma is limited due to the risk of radiation liver disease. Conclusions. The risk of concomitant malignancy needs to be guarded for 5 years of immunosuppressive therapy after organ transplantation surgery. Adjusting the immunosuppressive treatment regimen is an effective way to reduce concurrent malignancies. Systemic chemotherapy or radiotherapy requires vigilance against the toxic effects of drug metabolism kinetics on the transplanted organ.
Objective. To evaluate the safety of bevacizumab combined with platinum-based thoracic perfusion for treating lung cancer-related malignant pleural effusion (MPE) through meta-analysis. Methods. The CNKI, PubMed, Cochrane Library, Embase, Chinese Science and Technology Journal Database (VIP), and Wanfang Databases were searched for randomized controlled trials (RCTs) of bevacizumab combined with platinum-based thoracic perfusion for the treatment of MPE. The references included in the articles were manually searched for additional studies. A meta-analysis of the RCTs was conducted using the RevMan 5.3 application. Results. A total of 8 studies involving 540 patients (271 cases in the test group and 269 cases in the control group) were included in the meta-analysis. The test group had a significantly greater risk of elevated blood pressure as well as a higher rate of complete remission (CR) compared to the control group ( P < 0.05 ). In contrast, the incidence of partial remission (PR) was only slightly higher in the test group ( P > 0.05 ), and the risks of leukopenia, vomiting or nausea, rhinorrhea, diarrhea, gastrointestinal bleeding or hemoptysis, proteinuria, abnormal kidney and liver function, arrhythmia, and rashes were not significantly different between the test and control groups ( P > 0.05 ). Conclusion. Bevacizumab combined with platinum-based thoracic perfusion can achieve CR of MPE in patients with advanced lung cancer without significantly increasing the risk of adverse effects. The rate of PR was similar for the combination treatment and platinum-based infusion.
Recently, it was covered that cellular retinoic acid-binding protein 2 (CRABP2) is upregulated in ovarian cancer and participates in tumor progression, however, the specific mechanism remains to be explored. The pcDNA-CRABP2 or si-CRABP2 was transfected into SKOV3 and OVCAR3 ovarian cancer cells, respectively, and we observed that overexpression of CRABP2 inhibited cell apoptosis, promoted cell invasion and expression of epithelial mesenchymal transition (EMT) marker proteins, and transfection of si-CRABP2 had the opposite effect. Furthermore, we predicted that EZH2 interacted with CRABP2, and overexpression of CRABP2 promoted EZH2 expression, knockdown of CRABP2 inhibited EZH2 expression, and coimmunoprecipitation assay confirmed their binding relationship. The SKOV3 and OVCAR3 cells were then incubated with pcDNA-CRABP2 alone together with si-EZH2, and we found that si-EZH2 reversed the effect of pcDNA-CRABP2 on promotion of EZH2 expression, cell invasion and EMT maker protein levels. Next, we found that EZH2 could bind to DNMT1, and overexpression of EZH2 inhibited TRIM16 expression and knockdown of EZH2 promoted TRIM16 expression. Moreover, the promoter of TRIM16 contains the CpG island, and ChIP assay observed enriched DNMT1 on the promoter of TRIM16, and overexpression of EZH2 increased the promoter methylation level of TRIM16 and knockdown of EZH2 suppressed the methylation. The SKOV3 cells were incubated with si-EZH2 alone or combined with si-TRIM16, and we found that si-TRIM16 reversed the effect of si-EZH2. In vivo studies showed that knockdown of CRABP2 inhibited tumor volume and weight, suppressed the expression of EZH2 and EMT related proteins vimentin and snail, and increased the expression of TRIM16 and E-cadherin.
The present study was designed to investigate the association between the effect of controlled fluid resuscitation on massive hemorrhage and expression of human neutrophil lipocalin (HNL). A total of 112 patients confirmed with traumatic hemorrhage were enrolled as study subjects and were randomly divided into the control group (n=56) and observation group (n=56). The control group was treated with rapid fluid resuscitation, and the observation group was treated with controlled fluid resuscitation. The success rate of resuscitation, incidence rate of complications, and HNL levels were compared both before and after resuscitation at multiple time intervals. The success rate of resuscitation showed a significant improvement while the incidence rate of complications were decreased. The HNL levels in both groups revealed increase after resuscitation at 3–10 h, thereby, they showed decline following peak point. However, the peak reduction in the observation group appeared earlier, while the HNL levels at 24 and 72 h were significantly lower than those in the control group. The study concluded that the effect of controlled fluid resuscitation on massive hemorrhage was superior to that of rapid fluid resuscitation. Moreover, controlled fluid resuscitation was also able to decrease the level of HNL as well as inflammatory response.
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