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Objective To construct a nomogram prognostic model for predicting the survival of patients with lung adenocarcinoma based on the large sample data from the SEER database. Methods We retrospectively analyzed the clinical data of patients who were diagnosed with lung adenocarcinoma from 2010 to 2015 in the SEER database. A nomogram model was created based on independent parameters influencing the prognosis of patients with lung adenocarcinoma using Lasso Cox regression analysis. The C-index and calibration curve were utilized to assess the ability to distinguish and calibrate the nomogram. NRI and DCA curves were used to evaluate the prediction ability and net benefit of the nomogram. Results A total of 15 independent risk factors affecting the prognosis of lung adenocarcinoma were identified and integrated into the nomogram model. The C-index of the prediction model was 0.819 in the training cohort and 0.810 in the validation cohort. The predicted specific survival rate of the 1-, 3- and 5-year calibration curves of the training cohort and the validation cohort were consistent with the actual specific survival rate. In comparison to the 7th edition of the AJCC TNM staging system, the NRI and DCA curves demonstrated a considerable boost to the predictive capacity and net benefits achieved by the nomogram model. The risk stratification model constructed with this nomogram model was able to distinguish the patients with different risks well (P < 0.0001). Conclusion A nomogram prognostic model is successfully developed and validated, which provides a simple and reliable tool for the survival prediction of the patients with lung adenocarcinoma. Meanwhile, the risk stratification model constructed by the prediction model can conveniently screen patients with different risks, which is important for the individualized treatment of lung adenocarcinoma patients.
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Objective To analyze the expression of long non-coding RNA ( lncRNA) in renal clear cell carcinoma ( RCCC ) , the association of lncRNA with RCCC, as well as the role of lncRNA in the diagnosis and treatment of RCCC.Methods Forty fresh RCCC tissues and their normal adjacent tissues were collected from March 2012 to June 2013, and total RNA was extracted using Trizol reagents, purified and tested by denaturing agarose gel electrophmesis and NanoDrop 1000.Through Arraystar Human LncRNA Microarray, the different expression of lncRNA between RCCC and normal adjacent tissues was screened. RT-qPCR was used to verify the expression of lncRNA in 40 pair RCCC tissues and normal adjacent tissues. The receiver-operating characteristic ( ROC ) curve was adopted to verify the diagnostic efficiency of the selected lncRNA.Results LncRNA expression profile showed 1 787 lncRNA with expression alteration in two fold or above, up-regulated and down-regulated candidate lncRNAs were 941 and 846 respectively. Compared with the adjacent tissues, NR_034095 and NR_038974 were up-regulated in RCCC, and ENST00000571724 and ENST00000566575 were down-regulated, which were consistent with the microarray analysis.By the ROC curves of NR_034095, NR_038974, ENST00000571724 and ENST00000566575 to discriminate the RCCC from normal adjacent tissue, the area under curve was 0.928 ( 95%CI 0.873 -0.984), 0.759 (95%CI 0.647-0.871), 0.833 (95%CI 0.747-0.919) and 0.887 (95%CI 0.815-0.959 ) , respectively.Conclusions NR _ 034095, NR _ 038974, ENST00000571724 and ENST00000566575 are significantly differently expressed in RCCC.The different expressed lncRNA might be closely related to the process of RCCC, and may be used as a new candidate target for molecular diagnosis and gene therapy of RCCC.
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Objective:To investigate the effects of HLA-B?1502 genetic polymorphism on cyclosporine( CsA)-induced liver injury in Chinese renal transplant recipients. Methods:HLA-B?1502 genotypes were determined by polymerase amplification chaln reaction of sequence-specific primers( PCR-SSP) in a total of 339 renal transplant recipients receiving CsA. All the subjects were divided into the CsA-induced liver injury group, non-CsA-induced liver injury group and the control group according to the liver injury occurrence. Results:In the 339 renal transplant recipients, the frequency of HLA-B?1502 mutation allele was 22. 64%. The distribution frequen-cy of HLA-B?1502 mutation allele had no significant difference among the three groups. There were no significant differences in the clinical characteristics of HLA-B?1502 genotypes among three groups(P>0. 05). Conclusion: No association is observed between HLA-B?1502 genetic polymorphism and cyclosporine-induced liver injury in Chinese renal transplant recipients.
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OBJECTIVE To explore the dyna mic change of lncRNA expression during lung carcino-genesis induced by urethane.METHODS A total of 40 BALB/c mice received weekly ip injection of urethane 1 g·kg -1 for four continuous weeks,mice were euthanized at 12th week or 24th week after the first urethane treat ment,respectively.The RNA of lung tissues were isolated and used for microarray analysis.Based on the results of the microarray we selected lncRNA-AK017233 for additional qPCR analysis in individual mouse.RESULTS The incidence of lung cancer were 85% and 100% at 12th week and 24th week after the first ad ministration of urethane,respectively.The multiplicity and dia meter of lung tu mors in 24 weeks treated group were statistically significant fro m those in 12 weeks treated group (P<0.01 ),and pathological analysis showed that tu mors were classifiable as moderately differ-entiated adenocarcino ma.Total of 26 Down-regulated lncRNAs in which lncRNA-AK017233 stand for the most down-regulated lncRNA were identified by microcarray analysis.qPCR detected that the lncRNA-AK017233 was significantly altered by 0.33 ti mes in lung tu mors of urethane treated group at 12th week, co mpared to parallel lung tissues in urethane treated group at 12th week.AK017233 expression of ure-thane treated group was significantly reduced by 0.22 ti mes at 24th week,co mpared to parallel lung tis-sues in urethane treated group at 24th week.CONCLUSION LncRNA-AK017233 was consistently down-regulated during urethane induced lung carcinogenesis.