Primary central nervous system lymphoma (PCNSL) is a rare form of non-Hodgkin lymphoma (NHL) and has aggressive biological behavior.Due to absence of typical clinical presentation,heterogeneity of pathological morphology and multiple neuroimaging appearance and so on,the immunohistochemistry and molecular biology are of vital importance in accurate diagnosis of PCNSL.The development of regimen based on high-dose MTX leads to significant changes in the PCNSL treatment and it has become a generally recognized regimen.Compared with single radiotherapy,the survival rate has evidently been raised.Early diagnosis and surgical removal of the tumors combined with effective radiotherapy and chemotherapy are the key to extending survival period and improving living quality of patients with PCNSL.

Epidermal growth factor receptor (EGFR) inhibitors targeted therapy is the forward position means for non-small cell lung cancer.However,acquired resistance to EGFR inhibitors limits the development of targeted drugs.Using existing data on drug resistance in EGFR-mutant lung cancer,this review discusses three basic approaches for overcoming resistance to EGFR-targeted therapies:intensification of EGFR inhibition,combination of EGFR inhibitors with other targeted therapies,and altering clinical management via alternate pathways.

As a kind of rare central nervous system malignant tumor, primary central nervous system lymphoma (PCNSL) has poor prognosis, and the main treatment include surgery, radiotherapy and chemotherapy.Stereotactic biopsy has become a routine diagnostic method of PCNSL, because of which has the advantage of minimally invasive and convenient.Whole brain radiotherapy is a standardized treatment method for the multifocal PCNSL, which can delay the progress of tumor in a short term.The therapeutic regimen based on high dose methotrexate leads to significant changes in the PCNSL treatment and it has become an effective treatment measure.Effective comprehensive treatment is the key to extending survival time and improving the quality of life for the patients with PCNSL.

Objective To explore the clinical efficacy of paclitaxel(taxol,TAX)and capecitabine scheme(capecitabine,CAPE)in treatment ofⅣperiod lung adenocarcinoma.Methods 90 patients with Ⅳ period lung adenocarcinoma from March 2011 to August 2013 were collected and randomly divided into two groups,control group(n =45 )were given CAPE treatment and experimental group (n =45 )were given CAPE +TAX combination therapy.After treatment,the clinical efficacy and side effects in two groups were observed and compared. Results Evaluation of recent efficacy:the efficacy(response rate,RR)of experimental group was 46.67%,the disease control rates(DCR)was 77.78%,while RR of control group was 48.89%and DCR was 73.33%,there was no statistical significance between two groups.Evaluation of long-term efficacy:progression-free survival (PFS )in experimental group was(6.18 ±3.12)months,while in control group was(3.09 ±2.29)months,the difference was statistically significant(P<0.05). Overall survival(OS)in experimental group was(9.19 ±2.04)months,while in control group was(8.63 ±3.93)months,there was no statistical significance between two groups.Evaluation of adverse reaction:in terms of hematology change,white blood cell count(WBC),neutrophil counts(NE)in experimental group were decreased significantly than control group,the difference were statistically significant(P<0.05 ),but not the PLT.In terms of the hematology change,alopecia in experimental group was more than in control group,the difference was statistically significant(P<0.05 ),but there were no changes in nausea and vomiting,the brotherhood of syndrome,liver damage,oral cavity mucous membrane inflammation.Conclusion CAPE and TAX has good clinical efficacy in treatment of stage Ⅳ lung adenocarcinoma.It can increase the progression-free surial,and side effects is in hematology change.

EGFR-TKI plays an important role in the treatment of non-small-cell lung cancer. However, some researchers find that there are still some patients with primary or acquired resistance to EGFR-TKI. The present known mechanisms of acquired drug resistance finally lead to the re-activation EGFR downstream signa-ling pathways. Liver X receptor agonist has inhibition function to several critical steps of EGFR downstream sig-naling pathways PI3K-Akt-NF-κB,which makes it possible to overcome the drug resistance.

Epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) is one of the most important targeted drugs for lung cancer patients carrying EGFR sensitive mutations.However,almost all patients that are effective to this treatment will eventually develop secondary resistance to EGFR-TKI.The most accepted mechanisms of resistance mainly include T790M mutation,MET amplification,PIK3CA mutation,down-regulation of PTEN expression and activation of Fas-transcription factor-κB.Recent years,many new drugs are developed to overcome this resistance.Although most of drugs are in the stages of cell or animal experiment,some new drugs get positive clinical results.

Objective:To transfer human endostatin gene into umbilical cord CD34 + hematopoietic stem cells and detect its expression and excretion. Methods: Human endostatin gene was transferred into human umbilical cord CD34 + hematopoietic stem cells by retroviral pLNCX to build endostatin-transferred cell line.RT-PCR and Western blot analysis were applied to examine the transfection and expression of endostatin gene. Results:RT-PCR proved that genome of endostatin-transferred CD34 + hematopoietic stem cells contained a 550 bp fragment of human endostatin .The expression and excretion of human endostatin from endstatin-transferred hematopoietic stem cells were confirmed by Western blot analysis. Conclusion:Human endostatin gene can be transferred into CD34 + hematopoietic stem cells.

Long non-coding RNA urothelial carcinoma associated 1 (UCA1) is initially discovered and named in bladder cancer tissue,which is highly expressed in multi types of tumor tissues,such as bladder cancer,ovarian cancer,lung cancer,suggesting that UCA1 acts as oncogene.UCA1 is confirmed to regulate tumor cell proliferation,apoptosis,invasion and migration,which plays an important role in the occurrence and development of cancers.UCA1 is expected to become a new biomarker for diagnosis,prognosis and drug susceptibility,which may be a promising therapeutic target of cancer.

Objective To study the prognostic factors of primary duodenal papilla carcinoma.Methods The clinical data of 73 patients with primary duodenal papilla carcinoma who were admitted to the Dongnan Hospital of Xiamen University from June 1995 to June 2005 were retrospectively analyzed.Ten factors including gender,age,jaundice,tumor size,course of disease,total bilirubin,tumor differentiation,lymphatic metastasis,type of surgery and degree of resection were analyzed by Log-rank test.Prognostic factors with significant difference were further analyzed by the Cox regression model.The survival curve was drawn by using the Kaplan-Meier method.Results The median survival time of the patients was 34 months.Age,jaundice,tumor size,course of disease,total bilirubin,tumor differentiation,lymphatic metastasis,type of surgery and degree of resection were correlated with the prognosis (x2 =18.315,4.562,7.989,10.660,11.138,7.995,5.423,114.464,83.383,P＜0.05),while no significant difference was found between gender and prognosis ( x2 =1.720,P ＞ 0.05 ).Multivariate analysis demonstrated that tumor differentiation,type of surgery and degree of resection were the factors influencing the prognosis of patients with duodenal papilla carcinoma (RR =2.039,2.178,5.798,P＜0.05).Conclusions Tumor differentiation,type of surgery and degree of resection are the dependent factors influencing the prognosis of patients with duodenal papilla carcinoma.The standard type of surgery and degree of resection are important for the prognosis of patients.

Objective To investigate the relationship between genetic polymorphisms of ERCC1 and survival rate in advanced non-small cell lung cancer (NSCLC) patients treated with platinum based chemotherapy.Methods A total of 204 patients with advanced NSCLC were routinely treated by platinbased chemotherapy.The polymorphic genotypes were analyzed by MALDI-TOF-MS nethod using DNA samples isolated from peripheral blood before treatment.Besides,5 ％ samples werc extracted randomly for sequencing to test the accuracy of this method.To explored the association between SNP of ERCC1 (118) and prognosis to platinum-based chemotherapy in advanced NSCLC patients.Results Among 204 patients,61 achieved partial response,116 achieved stable response,and 27 achieved progressive disease.The overall response rate was 29.9 ％ (61/204).The effective rates of patients with the ERCC1 (118) C/C genotype,C/T + T/T genotype were 24.0 ％ (29/121) and 38.6 ％ (32/83),respectively,with significant difference (P ＜ 0.05).The response rate of ERCC1 (118) C/T allele carriers was 1.992-fold than that of C/C allele carriers (95 ％ confidence interval:1.083-3.650,P =0.025).MST,1-year survival and 2-year survival rates of patients with the ERCC1 (118) C/C genotype,C/T + T/T genotype were 9.0 months,34.7 ％ (42/121) and 4.1％ (5/121) vs 12.0 months,60.2 ％ (50/83) and 12.0 ％ (10/83),respectively,with significant difference (P ＜ 0.05).Conclusions Polymorphisms of ERCC1 might be associated with overall survival period in patients with advanced NSCLC after treatment with platin-based chemotherapy,which might be the predictive markers for overall survival.