EVALUATION OF COMBINED EBNA1-IgA AND EA-IgG ASSAYS IN SEROLOGICAL DIAGNOSIS OF NASOPHARYNGEAL CARCINOMA

Objective: To evaluate the value of combined assays of serum EBNA1-IgA and EA-IgG for serological diagnosis of nasopharyngeal carcinoma (NPC). Methods: The serum EBNA1-IgA and EA-IgG were tested by use of ELISA for 56 patients with NPC and 58 healthy adults. The sensitivity, specificity, positive predictive value, accuracy rate and odds ratio of the 2 tests used singly or in combination were compared with each other. Results: The sensitivity of EBNA1-IgA test (91.09%) was higher than that (87.50%) of EA-IgG test. The specificity of EA-IgG test (87.93%) was higher than that (84.48%) of EBNA1-IgA test. The combined usage of EBNA1-IgA and EA-IgG could enhance the specificity (94.83%), predictive value of a positive test (0.9375), likelihood ratio of a positive test (15.5435) and odds ratio (75.0) for serological diagnosis of NPC. Forty-five NPC patients showed positivity to EBNA1-IgA and EA-IgG concurrently. A positive EA-IgG reaction was demonstrated in 4 out of 5 NPC patients with negative EBNA1-IgA result and a positive EBNA1-IgA reaction in 6 out of 7 NPC patients with negative EA-IgG result as well. Conclusion: Though high sensitivity and specificity could be obtained by EBNA1-IgA and EA-IgG test, respectively, the combined use of these 2 tests is able to enhancing the reliability of serological diagnosis of NPC. The majority of NPC patients showed positivity to ENBA1-IgA and EA-IgG concurrently. There is a complementary effect through using EBNA1-IgA and EA-IgG for serological diagnosis of NPC.

Targeted and personalized therapy for cancer:Theory and practice in China

Molecular targeted therapy (MTT), using chemicals of low molecular weight, monoclonal antibodies, and/or polypep- tides to interfere with specific signaling pathways in cancer cells, causes inhibition of tumor progression. Clinical evi- dence has demonstrated that MTT has promising potential in not only killing tumors but also inducing tumor cells to differentiate into normal cells, leading to cure of the patients. Furthermore, MTT leads to potent inhibition of oncogenic signals. The delay of tumor progression makes the patients "survive with tumor". Thus, in the future it is possible that cancer becomes a chronic disease much like diabetes and hypertension. This article reviews the theory on molecular targeted therapy, its features and future direction, and con- tributions in the field from Chinese scientists.

ZNF582 hypermethylation promotes metastasis of nasopharyngeal carcinoma by regulating the transcription of adhesion molecules Nectin-3 and NRXN3

Background:Epigenetic regulation plays an important role in the development and progression of nasopharyngeal carcinoma(NPC).However,the epigenetic mechanisms underlying NPC metastasis remains poorly understood.We aimed to find functional genes which regulate the metastasis of NPC and identify therapeutic targets for NPC treatment.Methods:Bisulfite pyrosequencing was used to analyze zinc finger protein 582(ZNF582)methylation in NPC tissues and cell lines.Quantitative reverse transcription-polymerase chain reaction(qRT-PCR)and Western blotting were used to determine the expression of ZNF582.In vitro and in vivo experiments were performed to evaluate the biological function of ZNF582 in NPC.ZNF582-targeting genes were identified by chromatin immunoprecipitation sequencing(ChIP-seq)and were confirmed by ChIP-qPCR and luciferase assay.Results:ZNF582 promoter was hypermethylated in NPC,and both the mRNA and protein levels of ZNF582 were down-regulated in NPC tissues and cell lines.The restoration of ZNF582 inhibited NPC migration,invasion,and metastasis,while the knockdown of ZNF582 promoted NPC migration,invasion,and metastasis in vitro and in vivo.ZNF582 directly regulated the transcription and expression of adhesion molecules Nectin-3 and NRXN3.Both Nectin-3 and NRXN3 were identified as functional targets of ZNF582,and the restoration or abrogation of these genes reversed the tumor suppressor effect of ZNF582 in NPC metastasis.Conclusions:ZNF582 acts as a tumor suppressor gene in NPC by regulating the transcription and expression of adhesion molecules Nectin-3 and NRXN3,which may provide novel therapeutic targets for NPC treatment.

Translational medicine promising personalized therapy inoncology

Translational medicine has newly emerged to bridge the gap between bench-related basic science research and bedside clinical practice.From early diagnosis to late-stage disease treatment,translational medicine has transformed the clinical practice by making personalized medicine possible.Attributing to the progress in translational medical research,cancer therapy has evolved from non-specific cytotoxic drugs against both tumor and normal proliferating cells to more specific small molecule chemical and immunotherapy approaches.Small molecular agents are directed at unique pathogenesis of cancer cells,whereas immunotherapeutic agents target the cancer immune response.Both approaches aim to produce less toxicity with high effectiveness.Therapeutic regimens with these agents in biomarker-classified sensitive populations promises a personalized approach in modern oncology.

Correction to: ZNF582 hypermethylation promotes metastasis of nasopharyngeal carcinoma by regulating the transcription of adhesion molecules Nectin-3 and NRXN3

Following publication of this article[1],the authors noticed that the mismatched images were inadvertently included in Figure 5(migration assays of SUNE1-shNRXN3-#2 group in Figure 5I)and Figure 6(invasion assays of SUNE1-ZNF582+Nectin3 group in Figure 6A).This error has now been corrected online.