Objective  To investigate the effect of silencing phosphoglycerate mutase 1 （PGAM1） gene on the biological function of esophageal carcinoma cells and its possible mechanism. Methods  The expression of PGAM1 was detected by immunohistochemical SP method in 67 fresh esophageal cancer tissues and their adjacent normal tissues from July 2016 to June 2017. In order to analyze the effect of PGAM1 gene silencing on the apoptosis and proliferation of Eca-109 cells， PGAM1 shRNA （shPGM1 group） or shRNA-NC （NC group） was transfected into Eca-109 cells. QPCR and Western blotting were used to detect the effect of PGAM1 on the key molecules in Akt／mTOR signaling pathway. Results The high expression rate of PGAM1 in esophageal carcinoma was 58.2％ （39／67）， which was higher than that in adjacent tissues （31.3％）， and the difference was statistically significant （P＜0.05）. The expression of PGAM1 was correlated with clinical stage， differentiation degree and depth of invasion （P＜0.05）， but not with age， sex and lymph node metastasis （P＞0.05）. The expression of PGAM1 mRNA in shPGAM1 group and NC group were 0.48±0.10 and 1.01±0.14 respectively， and the difference was statistically significant （P＜0.05）. MTT assay showed that after 24， 48， 72 and 96 hours of culture， the proliferation rates Eca-109 cells in shPGAM1 group were （87.65±7.42）％， （79.34±9.11）％， （70.17± 6.84）％ and （60.36±7.95）％ respectively， which were significantly lower than those of NC group （P＜0.05）. The apoptosis rates of Eca-109 cells in shPGAM1 group and NC group were （45.36±5.38）％ and （24.81±4.67）％ respectively after 48 hours （P＜0.05）. The content of glucose in culture supernatant of Eca-109 cells in shPGAM1 group and NC group was （56.84±11.35）％ and （99.87±10.48）％， respectively. The content of lactic acid in culture supernatant of Eca-109 cells in shPGAM1 group and NC group was （48.02±10.18）％ and （99.00±12.35）％， respectively. The difference was statistically significant （P＜0.05）. The expression of PTEN in shPGAM1 group was higher than that in NC group （P＜0.05）， but the expression of p-Akt and p-mTOR was lower than that in NC group （P＜0.05）. Conclusion There are significant evidences that PGAM1 up-regulation would be related with esophageal cancer， which promote the proliferation of Eca-109 cells by activating the Akt／mTOR signaling pathway and Warburg effect.

Objective To investigate the effect of gemcitabine （GEM） on apoptosis and related differential protein expression in esophageal cancer Eca-109 cells and its possible mechanism. Methods The effects of GEM on the proliferation of Eca-109 cells at different concentrations （1， 2， 4， 8， 16 μg／ml） and at different times （12， 24 h） were detected by MTT， and the median inhibitory concentration （IC50） was calculated. Eca-109 cells were treated with 4.26 μg／ml GEM as the treatment group， and the GEM untreated group was also set up. Flow cytometry was used to detect apoptosis in two groups after 24 h. Two groups of proteins were extracted and identified by two-dimensional gel electrophoresis and matrix assisted laser desorption／ionization time of flight mass spectrometry （MALDI-TOF-MS）. The protein types and functions were identified. Western blotting was used to detect the expression of ASC， Mcl-1 and Bax-α protein in two groups after culture for 12 and 24 h. The ultrastructural changes of mitochondria in the two groups were observed by transmission electron microscope. Results GEM inhibited the proliferation of Eca-109 cells in a concentration and time dependent manner. The IC50 of 12 and 24 h were 5.13 μg／ml and 4.26 μg／ml respectively. The differentially expressed proteins of Eca-109 cells induced by GEM were Bax-α， ASC and Mcl-1 respectively. The expression levels of ASC and Bax-α in GEM treated group were higher than those in GEM untreated group after 12 and 24 h， while the expression level of Mcl-1 was opposite. The difference between the two groups was statistically significant （P＜0.01）. Transmission electron microscopy showed that the ultrastructure of mitochondria in GEM treated group changed drastically. Conclusion GEM can inhibit the proliferation and promote apoptosis of esophageal cancer cells， possibly due to the regulation of ASC， Mcl-1 and Bax-α expression by mitochondrial apoptotic pathway.

Objective To investigate the effect and molecular mechanism of HIF-1α on migration and invasion of hepatocellular carcinoma（HCC） cells induced by hypoxia. Methods  Human normal hepatocyte line WRL68， HCC cell line HepG2 and SMMC7721 were cultured under hypoxia and normal culture conditions. Real time quantitative PCR （QPCR） and Western blotting were used to detect the expression of HIF-1α mRNA and protein. HepG2 cells were transfected with NC nonsense nucleic acid sequence （NC group）， siHIF-1α（HIF-1α group） and siIL-8 （IL-8 group）， respectively. Western blotting was used to detect the expression of HIF-1α， IL-8 and NF-κB protein. The changes of migration and invasion ability of HepG2 were detected by interfering with HIF-1α and IL-8. Results Under hypoxia， the levels of HIF-1α mRNA and protein in HepG2 and SMMC7721 cell lines were significantly higher than those in normal human hepatocytes. Compared with the control group and NC group， the expression of HIF-1 alpha protein in HIF-1 alpha group decreased significantly to 0.39±0.077 （P＜0.05）. Under hypoxia， the expression of IL-8 protein in HIF-1α group was 0.31±0.043，significantly lower than that in blank control group and NC group， and the difference was statistically significant （P＜0.05）. The number of HepG2 migrating and invading cells in NC group were 91.2±8.2 and 121.1±6.7 respectively， which were significantly higher than those in HIF-1α group （36.3±5.9 and 47.7±3.3），and the difference was statistically significant （P＜0.05）；which were significantly higher than those in IL-8 group （49.4±5.6 and 39.6±5.1），and the difference was statistically significant （P＜0.05）.Conclusion HIF-1α promotes the migration and invasion of hypoxia induced hepatocellular carcinoma cells through regulating IL-8 expression.

Objective To investigate the role and possible mechanism of miR-590 in epithelial-mesenchymal transition （EMT） of cholangiocarcinoma cells. Methods  Fluorescence quantitative PCR （QPCR） was used to detect the expression of miR-590 in human normal intrahepatic bile duct epithelial cell line HIBEC， human cholangiocarcinoma cell line HUCCT1， HCCC-9810 and RBE. Dual luciferase reporter assay was used to evaluate the regulatory effect of miR-590 on SIP1. MiR-590 mimics （transfected group） and nonsense nucleic aicd sequence （NC group） were transfected into HUCCT1 cells， and Western blotting was used to detect the expression of EMT related protein in two groups. SIP1 siRNA was transfected into HUCCT1 cells and Western blotting was used to detect EMT related protein expression after interfering SIP1. Results The expression levels of miR-590 in HUCCT1， HCCC-9810 and RBE cell lines were 0.37±0.084，0.31±0.071 and 0.53±0.089， which was significantly lower than that of normal intrahepatic bile duct epithelial cell line HIBEC （1.12±0.201）， and the difference was statistically significant （P＜0.05）. MiR-590 mimics significantly reduced luciferase expression in the psiCHECK2-SIP1-3’UTR group （0.37±0.041， P＜0.001），while not affecting the expression of the psiCHECK2-SIP1-3’UTR-MUT group （1.21±0.211， P＞0.05）. Overexpressed of miR-590 could down-regulated the mesenchymal proteins Vimentin， N-cadherin， ZEB1， ETS1， SNAIL1， TWIST1 and up-regulated the epithelial marker E-cadherin. SIP1 silencing could up-regulate the expression of E-cadherin protein and down-regulate the expression of Vimentin and N-cadherin protein. Conclusion MiR-590 blocked its translation by targeting SIP1-3’UTR and ultimately inhibited epithelial mesenchymal transition of cholangiocarcinoma cells.

Objective To investigate the effect and possible mechanism of resveratrol （RES） on the resistance of gastric cancer cell to apatinib. Methods  SGC7901 and SGC7901／AR cells were cultured in vitro. MTT assay and scratch test were used to detect the effects of different concentrations of apatinib or combined with RES on proliferation and migration of SGC7901 and SGC7901／AR cells. Resistance index， reversal multiple （RF） and relative reversal rate （RRR） of SGC7901 and SGC7901／AR cells were calculated respectively. Real-time fluorescence quantitative PCR （QPCR） was used to detect the miR-122， p-VEGFR2， p-Akt mRNA in these cells. Results Apatinib significantly inhibited the proliferation and migration of SGC7901 cells in a concentration-dependent manner （P＜0.05）， and the resistance index was 15.57. Apatinib combined with 50.0 μmol／L RES significantly inhibited the proliferation and migration of SGC7901 and SGC7901／AR cells in a concentration-dependent manner （P＜0.05）. The resistance index was 2.13， the reversal ratio of RES was 7.91 times， and the relative reverse rate was 93.4％. The expression levels of miR-122， p-VEGFR2， p-Akt mRNA in untreated SGC7901 cells were 0.74±0.11， 0.76±0.13 and 0.67±0.09， respectively， which were significantly higher than those in SGC7901／AR cells （P＜0.05）. The expression levels of p-VEGF R2 and p-Akt mRNA in SGC7901 cells decreased significantly after treatment with 10 μmol／L apatinib （P＜0.05）. After treatment with 10 μmol／L apatinib and 50.0 μmol／L RES， the expression of miR-122 in SGC7901 and SGC7901／AR cells increased significantly （P＜0.05）， while the expression of p-VEGFR2 and p-Akt mRNA decreased significantly （P＜0.05）. Conclusion Resveratrol can reverse the drug resistance of gastric cancer cell lines to apatinib， possibly by up-regulating the level of miR-122 and inhibiting the phosphorylation of VEGFR2 and Akt.

Objective To investigate the effect of miR-93 and the sensitivity of colon cancer HT-29 cells on 5-FU and its possible mechanism. Methods  miR-93 inhibitor was transfected into HT-29 cells， and blank control group and negative control group （NC） were also set up. Cell proliferation was detected by MTT assay. The apoptosis， invasion and migration activities of HT-29 cells in the miR-93 inhibitor group， blank control group and NC group were detected by flow cytometry， Transwell cell invasion test and scratch test respectively. Double luciferase reporter gene method was used to verify the relationship between PTEN and miR-93. Real-time fluorescence quantitative PCR （QPCR） was used to detect the expression of miR-93 and the effect on the expression of p-VEGFR2， p-Akt and PTEN mRNA in the three groups. Results The relative expression of miR-93 in the miR-93 inhibitor group was 0.40±0.05， significantly lower than that in the blank control group and NC group （1.13±0.08，1.12±0.09）， and the difference was statistically significant （P＜0.05）. The proliferation inhibition rate of HT-29 cells treated with 1， 4， 16， 64， 256 μg／ml 5-FU in miR-93 inhibitor group was higher than that in the NC group and the blank control group （P＜0.05）. The apoptosis rate， invasion rate and healing rate of HT-29 cells treated with 16 μg／ml 5-FU in the inhibitor group were （52.75 ±7.44）％， （45.76 ±15.85）％， （12.64 ±3.29）％ respectively， which were significantly different from those in the control group and NC group （P＜0.05）. PTEN might be a target protein of miR-93 which was verified by the dual luciferase reporter gene system. The expression levels of p-VEGF R2， p-Akt and PTEN in HT-29 cells treated with inhibitor of miR-93 were 1.28±0.09，0.85±0.08 and 1.22±0.09， respectively. Compared with control group and NC group， the phosphorylation levels of VEGFR2 and Akt were down-regulated and the expression of PTEN was up-regulated. Conclusion Down-regulation of miR-93 can increase the expression of PTEN， inhibit the phosphorylation of VEGFR-2 and Akt， and thus enhance the sensitivity of colon cancer cells to 5-FU.

Objective To investigate the role and possible mechanism of CELF1 in the proliferation of glioma cells. Methods  CELF1 mRNA and protein expression in glioma cell lines U87， U251， SHG44 and human normal astrocyte line HA1800 was detected by fluorescence quantitative PCR （QPCR） and Western blotting. U87 cells were transfected with nonsense nucleic acid NC （NC group）， siCELF1 （siCELF1 group） and siCELF1＆siCDKN1B （siCELF1＆siCDKN1B group）. Cell viability was detected by CCK-8 assay， and cell cycle changes were detected by flow cytometry. The protein expression of CELF1， CDKN1B and Cyclin D1 was detected by Western blotting. Results The relative expression levels of CELF1 mRNA in glioma cell lines U87， U25 1 and SHG44 were 3.1±0.074， 4.2±0.137 and 3.6±0.023， respectively， which were higher than those in normal astrocyte line HA 1800， and the differences were statistically significant （P＜0.05）. The protein expression of CELF1 detected by Western blotting was consistent with that of mRNA. Silence CELF1 can significantly reduce U87 cell viability. The proportion of G0／G1 phase cells in siCELF1 group was （63.5±1.33）％， significantly higher than that in NC group （39.4±1.24）％；while proportion of S phase cells in siCELF1 group was （14.3±0.095）％， significantly lower than that in NC group （22.8±1.97）％ （P＜0.05）. The relative expression of CDKN1B protein in group siCELF1 was 2.37±0.088， which was significantly lower than that in NC group （P＜0.05）. The relative expression of Cyclin D1 protein in group siCELF1 was 0.274±0.039， which was significantly lower than that in siCELF1＆siCDKN1B group （P＜0.05）. Cell viability in group siCELF1＆siCDKN1B was higher than that in group siCELF1 （P＜0.05）. The proportion of G0／G1 phase cells in siCELF1-siCDKN1B group was （42.1±1.76）％， significantly lower than that in siCELF1 group （62.4±1.92）％ （P＜0.05）， while the proportion of S phase cells in siCELF1-siCDKN1B group was （20.3±0.077）％， which was not significantly different from that in NC group （22.8±1.97）％. Conclusion CELF1 mediates the expression of Cyclin D1 by inhibiting CDKN1B， and promotes glioma proliferation.

Objective To investigate the expression of microRNA-328 （miR-328） in nasopharyngeal carcinoma tissues and its effect on invasion and migration of CNE-2 cells. Methods  The quantitative real-time PCR （QPCR） was used to detect the levels of miR-328 in 86 cases of nasopharyngeal carcinoma tissues and 15 cases of chronic nasopharyngitis as well as nasopharyngeal carcinoma cell lines CNE-2， HK1 and normal nasopharyngeal epithelial cell line NP69. The relationship between the levels of miR-328 and the clinicopathological features （age， sex， clinical stage， lymph node metastasis， recurrence and survival status） of nasopharyngeal carcinoma was analyzed. MiR-328 mimics or negative control （NC） were transfected into CNE-2 cells at logarithmic phase by liposome Lipofectamine 2000. The miR-328 level was detected by QPCR at 48 h after transfection to evaluate the transfection efficiency. The numbers of penetrating cells of CNE-2 cells were detected by Transwell migration and invasion assay. Results The Results  of QPCR showed that the miR-328 levels in nasopharyngeal carcinoma cell lines CNE-2 and HK1 were lower than those in normal nasopharyngeal epithelial cell line NP69 （P＜0.05）， and the miR-328 levels in 86 cases of nasopharyngeal carcinoma tissues were lower than those in 15 cases of chronic nasopharyngitis （P＜0.05）. The miR-328 level was related to the recurrence （P=0.037）， clinical stage （P=0.005） and survival （P=0.012）， but not to age， sex and lymph node metastasis （P＞0.05）. After 48-h transfection， the miR-328 level in cells transfected with mimics was significantly higher than that in cells transfected with NC （P＜0.05）. Transwell assay showed that the numbers of CNE-2 cells transfected with mimics were significantly lower than those with NC （P＜0.05）. Conclusion miR-328 is lowly expressed in both nasopharyngeal carcinoma tissues and cells， and participates in the occurrence and development of nasopharyngeal carcinoma. Up-regulating its level can inhibit the migration and invasion process， which has a certain value in the prevention and treatment of nasopharyngeal carcinoma.

Objective To investigate the effect of long non-coding RNA GAS5 （lncRNA GAS5） on proliferation and apoptosis of laryngeal carcinoma Hep2 cells and its possible mechanism. Methods  Real-time fluorescence quantitative PCR （QPCR） was used to detect the expression of GAS5 in laryngeal carcinoma and adjacent normal tissues. The relationship between the expression of GAS5 and the clinicopathological features of laryngeal carcinoma was analyzed. Hep2 cells were transfected with pcDNA3.1-GAS5 or siGAS5， and pcDNA3.1-NC or siNC respectively as control. MTT assay was used to detect the proliferation activity of Hep2 cells after transfection， and Hep2 cell cycle and apoptosis were detected by flow cytometry. QPCR and Western blotting were used to detect the expression of E2F1 and BTF3 mRNA and protein. Results The expression levels of GAS5 in laryngeal carcinoma and adjacent normal tissues were 0.56±0.10 and 0.98±0.11 respectively， and the difference was statistically significant（P＜0.05）. The expression of GAS5 was related to the degree of differentiation and TNM stage. The survival rate of Hep2 cells in pcDNA3.1-GAS5 group at 24， 48， 72 and 96 hours was significantly lower than that in pcDNA3.1-NC group （P＜0.05）， and that in siGAS5 group was significantly higher than that in siNC group （P＜0.05）. The proportion of G1 phase cells transfected with pcDNA3.1-GAS5 was（68.14±4.33）％ higher than that of pcDNA3.1-NC group（P＜0.05）. The apoptotic rate in group pcDNA3.1-GAS5 was higher than that in group pcDNA3.1-NC， and the difference was statistically significant （P＜0.05）. The mRNA and protein levels of E2F1 and BTF3 in pcDNA3.1-GAS5 transfection group were significantly lower than those in pcDNA3.1-NC group （P＜0.05）； the mRNA and protein levels of E2F1 and BTF3 in siGAS5 transfection group were significantly higher than those in siNC group （P＜0.05）. Conclusion GAS5 can negatively regulate the expression of E2F1 and BTF3， and thus participate in the regulation of laryngeal cancer cell proliferation and apoptosis.

Objective To investigate the expression of vascular endothelial growth factor （VEGF）， dendritic cell （DC） differentiation and regulatory T cells （Treg） in oral cancer， and to analyze the factors that affect the recurrence of oral cancer. Methods  The clinical data of 67 patients from January 2015 to June 2015 were collected. The recurrence of the patients was followed up. The expression of VEGF， CD83， CD1αand Foxp3 in oral cancer tissues was detected by immunohistochemical SP， and the relationship between the expression and recurrence of oral cancer was analyzed. The independent factors affecting the recurrence of oral cancer were analyzed by Cox regression model. Results The positive expression rate of VEGF in oral cancer tissues was 59.7％ （40／67）， which was related to tumor location， TNM stage and tumor volume （P＜0.05）. The positive expression rates of CD83 and Foxp3 were 52.2％ （35／67） and 38.8％ （28／67）， respectively， which were related to TNM staging and lymph node metastasis （P＜0.05）. The positive expression rate of CD1 alpha was 41.8％ （26／67）， which was related to TNM stage （P＜0.05）. The mean follow-up period was （31.45±6.23） months， and 21 patients relapsed. There were significant differences in TNM staging， lymph node metastasis， VEGF expression， CD1α， CD1 alpha+ dendritic cell distribution and the distribution of Foxp3+T cells in recurrent and non recurrent patients （P＜0.05）. The Spearman rank correlation analysis showed that VEGF expression was negatively correlated with the distribution of CD83+ dendritic cells， but positively correlated with the distribution of Foxp3+T cells （P＜0.05）， and the distribution of CD83+and CD1α+ dendritic cells was negatively correlated （P＜0.05）， and the distribution of Foxp3+T cells was positively correlated with the distribution of CD1α+ dendritic cells （P＜0.05）. The analysis of multiple factor Cox regression model showed that TNM staging， lymph node metastasis， VEGF positive expression， CD1α+ low distribution and high Foxp3+distribution were independent risk factors for postoperative recurrence （P＜0.05）. Conclusion VEGF in the tumor microenvironment is related to the decrease in the number of mature DCs， but the distribution of immature DCs is positively correlated with the distribution of Treg cells， which can be used as a reference index to judge the prognosis of oral cancer patients.

Objective To evaluate the efficacy and safety of apatinib and S-1 on advanced gastric cancer as second-line and above treatment in order to provide reference for clinical medication. Methods  The pertinent randomized controlled trials （RCTs） about apatinib group and S-1 group as second-line and above treatment for advanced gastric cancer. Studies were retrieved from Cochrane Library， Pubmed， CNKI and Wanfang Database from inception to December 2017. The quality of included studies was evaluated according to modified Jadad scale. Then the related data was extracted and meta-analysis was performed by using Rev Man 5.3 statistical software. Results A total of 8 RCTs were included，involving 456 patients. The Results  of meta-analysis showed that the Objective  response rate was significantly improved in apatinib group compared with S-1 group （RD=0.12， 95％CI： 0.03-0.20， P=0.008）. The disease control rate （RD=0.05， 95％CI：-0.03-0.13， P=0.23） and the quality of life （RD=0.11， 95％CI：-0.00-0.22， P=0.22） had no difference between the two groups. The incidence of hypertension was increased in apatinib group compared with S-1 group （OR=15.27， 95％CI： 2.79-83.76， P=0.002）. However， nausea and vomiting was decreased with statistically significant difference in apatinib group （OR=0.38， 95％CI： 0.18-0.82， P=0.01）. The occurrence of proteinuria， neutropenia， hand-foot syndrome and other adverse reaction had no difference between the two groups. Conclusion Apatinib can improve overall response rate more effectively compared with S-1 as second-line and above treatment for advanced gastric cancer. Meanwhile， the adverse reactions of apatinib were comparable to S-1.

Objective To investigate the relationship between preoperative derived neutrophil-to-lymphocyte ratio （dNLR） and clinicopathological characteristics， as well as prognosis of patients with triple negative breast cancer. Methods  The data of 161 patients with triple negative breast cancer receiving operation from 2000 to 2010 were retrospectively reviewed. The optimal cutoff level for the dNLR was calculated with receiver operating characteristics curve （ROC）. The patients were divided into two groups according to the preoperative dNLR： high dNLR and low dNLR. Overall survival （OS） and disease-free survival （DFS） were assessed using the Kaplan-Meier method. Univariate and multivariate Cox regression models were performed to evaluate the prognostic relevance. Results ROC curve showd that the cutoff value of preoperative dNLR was 2.0 and 161 patients were then divided into high dNLR group （n=78） and low dNLR group （n=83）. Preoperative dNLR was associated with tumor size and histological grade （P＜0.05）， but not with age and lymph node metastasis （P＞0.05）. Patients in high dNLR group had shorter median OS （45.9 months vs. 78.1 months） and DFS （18.1months vs. 24.8 months） compared with patients in low group （P＜0.001）. Cox multivariate analysis showed that histological grade and preoperative dNLR were independent factors influencing DFS； while tumor size， histological grade and preoperative dNLR were independent factors influencing OS. Conclusion Preoperative dNLR can be considered as an independent factor influencing survival in patients with triple negative breast cancer.

Objective To investigate the effect of radiotherapy initiation time on prognosis of patients with early breast cancer after breast conserving surgery. Methods  The clinical data of 142 patients with early breast cancer who underwent breast conserving surgery in our hospital from October 2012 to May 2013 were retrospectively analyzed， including 18 patients in group A received first radiotherapy and then chemotherapy； 99 patients in group B received first chemotherapy and then radiotherapy； 25 patients received chemotherapy-radiotherapy-chemotherapy sandwich therapy. The clinicopathological characteristics and disease-free survival （DFS） of the three groups were compared. Recursive partitioning analysis （RPA） was used to stratify the time points from surgery to radiotherapy， and the differences of DFS were compared. Results In 142 patients， 5-year DFS rate was 81.69％. 5-year DFS rate of group A， group B and group C was 83.3％ （15／18），79.8％ （79／99） and 88.0％ （22／25）. There was no significant difference among the three groups. Multivariate COX risk regression analysis showed that age， vascular tumor thrombus and N stage were independent factors affecting 5-year DFS （P＜0.05）. The patients were divided into two groups by RPA： the interval between operation and radiotherapy was ≤11 weeks （n=53 cases） and ＞11 weeks （n=89 cases）. The 5-year DFS rates of the two groups were 90.6％ and 76.4％ respectively （P =0.389）. Patients in group B were divided into two groups： the interval between operation and radiotherapy was less than 23 weeks （n=89 cases） and more than 23 weeks （n=35 cases）. The 5-year DFS rates of the two groups were 89.9％ and 60.0％ respectively （P＜0.05）. Patients in group C were divided into operation to radiotherapy interval ＜4.8 weeks （n=11 cases） and ＞4.8 weeks （n=7 cases）， The 5-year DFS rates of the two groups 90.9％ and 71.4％ respectively （P =0.291）. Conclusion Breast conserving surgery combined with postoperative radiotherapy and chemotherapy has a good clinical effect on early breast cancer， but radiotherapy is recommended as early as possible to improve the prognosis of patients with chemotherapy.

Objective To investigate the effect of parenteral nutrition intervention on the curative effect and quality of life of patients with upper gastrointestinal malignant tumor undergoing radiotherapy. Methods  Eighty patients with upper gastrointestinal malignancies who received radiotherapy and chemotherapy in our houspital from Nov. 2014 to Jun. 2017 were randomly divided into control group （n=40） and observation group （n=40）. All patients were given conventional intensity modulated radiation therapy （IMRT） and TP regimen. Patients in the observation group were given intravenous drip of 20.0％ fat emulsion， compound amino acid and 10.0％ glucose from Monday to Friday. The daily nutritional energy was 30-40 kcal／kg until the end of radiotherapy and chemotherapy. The patients in the control group ate their own foods， and were treated with symptomatic treatment when severe mucosal reactions or electrolyte disturbances occurred. The short-term efficacy and adverse reactions of the two groups were compared， and the nutritional indicators and quality of life before and after treatment were compared. Results The total effective rates of the observation group and the control group were 90％ and 72.5％ respectively， and the difference was statistically significant （P=0.042）. After treatment， the levels of HB， ALB and TLC in the observation group were （109.52±6.13） g／L， （31.06±3.29） g／L and TLC （2.90±0.56）×109／L higher than those in the control group（98.40±6.65） g／L， （24.91±3.63） g／L， （1.81±0.52）×109／L， respectively， and the difference was statistically significant （P＜0.05）. The scores of general health， physical function， social function， emotional function， cognitive function and role function in the observation group were 66.03±7.58， 64.96±6.81， 66.18±6.23， 69.74±6.95， 63.24±6.07 and 65.58±6.26 respectively， which were higher than those in the control group 52.92±8.47， 54.10±5.39， 51.38±5.70， 57.25±6.13， 54.76±5.98 and 50.90±5.62，the difference was statistically significant （P＜0.05）. After 4 weeks of treatment and at the end of treatment， the body mass and KPS scores of the observation group were（66.72±5.83）kg， （65.87±5.75） kg and 66.14±8.49，64.93±7.74 respectively， which were significantly higher than those of the control group （P＜0.05）. The number of 3-4 grade adverse reactions such as gastrointestinal symptoms， oral mucosal injury， skin reaction， anemia and thrombocytopenia in the observation group was significantly less than that in the control group. Conclusion Parenteral nutrition can improve the curative effect of radiotherapy and chemotherapy for upper gastrointestinal malignancies， improve the nutritional status of the body， reduce the occurrence of adverse reactions of radiotherapy and chemotherapy， and improve the quality of life of patients， which is worthy of clinical promotion.

Objective To observe the sensitizing effect and safety of thalidomide on preoperative intensity modulated radiotherapy （IMRT） for stage Ⅱ／Ⅲ rectal cancer. Methods  From January 2016 to December 2017， 60 patients with stage Ⅱ／Ⅲ rectal cancer receiving preoperative radiotherapy were randomly divided into experimental group （n=30） and control group （n=30）. Both 2 groups received IMRT combined with capecitabine oral concurrent chemotherapy before operation. On this basis， the experimental group was given thalidomide 100 mg／d every night in the first week of radiotherapy， and the second week was added to maintain the target dose of 200 mg／d until the end of radiotherapy. Radical resection of rectal cancer was performed at 6-8 weeks after radiotherapy. The changes of serum vascular endothelial growth factor （VEGF） before and after radiotherapy， the variations of tumor stage， the R0 resection rate， the rate of anus preserving and the pathologic regression degree of the tumor were compared between the two groups. The incidence of acute radiation injury during radiotherapy was recorded and the adverse reactions of thalidomide were evaluated. Results Before radiotherapy， the levels of serum vascular endothelial growth factor in experimental group and control group were （542.47±107.06）pg／ml and （536.36±97.32）pg／ml， with no significant difference （P＞0.05）. The levels of serum vascular endothelial growth factor （VEGF） in the experimental group and the control group were 419.61±77.80）pg／ml and（503.52±87.31）pg／ml after radiotherapy （P＜0.05）. The level of serum VEGF before and after radiotherapy in the experimental group was significantly different （P＜0.05）. After treatment， the T and N staging rate， anal preservation rate， tumor pathological complete remission rate and good rate of tumor regression in the experimental group were significantly higher than those in the control group （P＜0.05）. Nine patients in the experimental group developed nausea and vomiting， 22 patients developed radiation proctitis， and 28 patients in the control group and 30 patients in the control group， respectively. In the experimental group， dizziness and lethargy occurred in 16 cases， while only 6 cases in the control group. Conclusion Thalidomide combined with preoperative IMRT in the treatment of stage Ⅱ／Ⅲ rectal cancer has a synergistic effect， which can significantly reduce the tumor stage， improve the complete pathological remission rate and the good rate of tumor regression. More patients have the chance of anus preservation， and the synergistic mechanism may be related to the reduction of the level of VEGF to regulate angiogenesis. It can reduce the incidence of nausea， vomiting and radiation proctitis.

Neoadjuvant chemoradiotherapy combined with total mesorectal excision have become standard management for locally advanced rectal cancer. Neoadjuvant chemoradiotherapy could develop significant tumor regression and downstaging to achieve chances of sphincter preservation leading to pathological complete response. But surgery accompanied with mortality， complications and dysfunction. Thus the non-operative treatment such as organ preservation and watch-and-wait strategy might lead a new way.

Advanced breast cancer is the first malignant tumor that seriously threathens the health of women worldwide. Comprehensive treatment is the current major treatment， including chemotherapy， endocrine therapy and targeted therapy. Short-term recurrence and metastasis are the most crucial risk that restrict clinical efficacy and lead to poor prognosis. However， imaging and traditional serum markers are difficult to monitor the recurrence of tumor cell levels in a timely manner， leading to delayed clinical decision-making. Therefore， the development of sensitive， accurate， none／low invasive efficacy monitoring method is critical. Circulating tumor DNA （ctDNA） is a kind of DNA free from plasma and derived from tumor cells during the process of necrosis， apoptosis and secretion. A number of studies have shown that it has a huge potential in detection of ctDNA mutation levels in the early diagnosis of cancer， medication guidance， relapse monitoring. This review summarizes recent research progress on it.