Objective  To investigate the mechanism of miR-21 regulating autophagy of non-small cell lung cancer（NSCLC） by targeting autophagy-related target gene 5 （Atg5） and its role in proliferation， migration and invasion of A549 cells. Methods  Nonsense nucleic acid sequence NC （NC group）， miR-21 mimics （miR-21 mimics group） and miR-21 inhibitor（miR-21 inhibitor group） were transfected into A549 cells， respectively. CCK-8 was used to detect the proliferation of A549 cells， scratch test was used to detect the migration ability of A549 cells， and Transwell invasion test was used to detect the invasion ability of A549 cells. Dual luciferase reporter gene assay verified the targeting relationship between miR-21 and Atg5. Western blotting was used to detect the expression of LC3B-II， p62 and Atg5 proteins. Results  Compared with NC group， the proliferation， migration and invasiveness of the cells in the miR-21 mimics group were up-regulated， while the proliferation， migration and invasiveness of the cells in the miR-21 inhibitor group were down-regulated （P＜0.05）. The results of double luciferase report experiment showed that miR-21 significantly inhibited the luciferase activity of wild-type Atg5 3’-UTR plasmid transfected cells （P＜0.05）， but had no effect on the luciferase activity after co-transfection of mutant Atg5 3’-UTR gene report plasmid with miR-21 mimics. The expression of LC3B-II protein in NC group was lower than that in miR-21 mimics group， higher than that in miR-21 inhibitor group （P＜0.05）； the expression of p62 and Atg5 protein in NC group was higher than that in miR-21 mimics group， lower than that in miR-21 inhibitor group  （P＜0.05）. Compared with NC group， 3-MA treatment decreased the proliferation of A549 cells induced by miR-21 mimics transfection （P＜0.05）. Scratch and Transwell experiments showed that 3-MA treatment inhibited the migration and invasion of A549 cells induced by miR-21 mimics transfection （P＜0.05）. Conclusion MiR-21 targeting Atg5 regulates autophagy in non-small cell lung cancer cells and promotes proliferation， migration and invasion of lung cancer cells.

Objective  To investigate the expression of microRNA-582-5p （miR-582-5p） in non-small cell lung cancer （NSCLC） and its effect on proliferation and invasion of A549 cells， as well as the targeting regulation of Rab27a gene. Methods  The expression of miR-582-5p in 33 NSCLC tissues and adjacent tissues， A549 cell line and human normal bronchopulmonary epithelial cell line BEAS-2B was detected by real-time fluorescence quantitative polymerase chain reaction （QPCR）. MiR-582-5p inhibitor （anti-miR-582-5p） and miR-582-5p mimics （mim-miR-582-5p） transfected into A549 cells， and anti-NC and mim-NC were used as negative control. The relationship between Rab27a and miR-582-5p was validated by double luciferase reporter assay. MTT assay and Transwell chamber assay were used to detect the proliferation and invasion ability of A549 cells， QPCR and Western blotting were used to detect the expression of Rab27a gene and protein. Results  The expression of miR-582-5p in NSCLC tissues and adjacent tissues were 0.26±0.09 and 0.83±0.10， respectively. The expression of miR-582-5p in A549 cell lines and BEAS-2B cell lines were 0.63±0.08 and 1.17±0.09， respectively， with statistical significance （P＜0.05）. The proliferation rates of A549 cells in anti-miR-582-5p group after 24， 48， 72 and 96 hours were （115.68±4.34）％， （130.48±5.48）％， （138.95±5.55）％， （147.03±5.69）％， respectively， which were significantly higher than those in anti-NC group （P＜0.05）. The proliferation rates of A549 cells in mim-miR-582-5p group after 24， 48， 72 and 96 hours were （91.31±4.18）％， （86.74±3.23）％， （79.45±3.20）％， （75.22±4.09）％ respectively， which were significantly lower than those in mim-NC group （P＜0.05）. Transwell chamber results showed that the invasion number of A549 cells in anti-miR-582-5p group was 189±19， which was significantly higher than that in anti-NC group； the invasion number of A549 cells in mim-miR-582-5p group was 55±8， which was significantly lower than that in mim-NC group （P＜0.05）. MiR-582-5p inhibited the luciferase activity of wild type Rab27a 3’-UTR reporter gene vector， but had no effect on mutant Rab27a 3’-UTR luciferase activity. The expression of Rab27a mRNA and protein in anti-miR-582-5p group were （2.01±0.29） and （0.85±0.12）， which were higher than anti-NC group （P＜0.05）. The expression of Rab27a mRNA and protein in mim-miR-582-5p group were （0.35±0.08） and （0.21±0.05）， which were lower than mim-NC group （P＜0.05）. Conclusion  Up-regulation of the expression of miR-582-5p can inhibit the expression of Rab27a， thus inhibiting the proliferation and invasive activity of lung cancer A549 cells. MicroRNA-582-5p is expected to become a new therapeutic target for lung cancer.

Objective  To investigate the targeted regulation of mitogen-activated protein kinase 9 （MAP3K9） expression by microRNA-148a-3p （miR-148a-3p） and its effect on proliferation and apoptosis of gastric cancer cells. MethodsGastric cancer MGC-803 cells at the logarithmic growth phase were transfected with miR-148a-3p mimics （mimics group） and negative control （NC group）， and the untransfected MGC-803 cells were used as control group. Real-time quantitative PCR （QPCR） was used to detect the expression of miR-148a-3p after transfection in each group to evaluate the transfection efficiency. MTT proliferation assay was conducted to evaluate the proliferation. Flow cytometry was used to detect apoptosis in each group. The expression of Bcl-2， Bax， caspase-3 and MAP3K9 were detected by QPCR and Western blotting， respectively. The targeting relationship between miR-148a-3p and MAP3K9 was verified by double luciferase report assay. Results The Results  of QPCR showed that the expression of miR-148a-3p in control group， NC group and mimics group were 1.021±0.123， 1.087±0.196 and 2.854±0.368， respectively. Compared with control group and NC group， the expression of miR-148a-3p in mimics group was higher （P＜0.05）. The proliferation activity of MGC-803 cells in mimics group was weaker than that in the other two groups （P＜0.05）. The apoptotic rate in mimics group was （15.2±1.6）％， higher than （3.5±0.9）％ of control group and （4.5±1.1）％ of NC group （P＜0.05）. Compared with other two groups， the expressions of MAP3K9 and Bcl-2 were down-regulated in the mimics group， while the expressions of Bax and caspase-3 were up-regulated significantly （P＜0.05）. Double luciferase assay confirmed that MAP3K9 was the direct target of miR-148a-3p. Conclusion MiR-148a-3p can inhibit the proliferation and induce apoptosis of MGC-803 cells as anti-cancer factor possibly by targeting MAP3K9. MiR-148a-3p／MAP3K9 axis has a certain application prospect in the prevention and treatment of gastric cancer.

Objective  To investigate the effect of silenced chitinase 40 （YKL-40） expression on cisplatin-resistant endometrial cancer cell line Ishikawa／DDP. Methods Ishikawa／DDP drug-resistant cell lines were established by DDP long-term concentration gradient method in vitro， and the expression of MDR1， Bcl-2， Bax and caspase-3 were detected. The proliferation activity of Ishikawa cells and Ishikawa／DDP cells was detected by MTT method， and the half inhibitory concentration （IC50） was calculated. Ishikawa／DDP was transfected with NC negative sequence （NC group） and siRNA YKL-40 （si-YKL-40 group）， respectively. The untransfected cells were set as blank control group. The effects of DDP on proliferation， migration and apoptosis of Ishikawa／DDP cells in si-YKL-40 group were detected by MTT， scratch test and Annexin V／PE double staining. Results Ishikawa／DDP resistant cell lines were successfully established in vitro. The inhibitory rates of 3.125， 6.25， 12.5， 25， 50 and 100 μmol／L DDP on proliferation of Ishikawa／DDP cells were （6.93±2.45）％， （8.14±4.50）％， （11.37±4.62）％， （15.18±3.97）％， （26.29±5.08）％， （41.32±7.64）％， which were significantly lower than those of Ishikawa cells （P＜0.05）. The IC50 were 14.58 μmol／L and 116.70 μmol／L， respectively. The resistance index of Ishikawa／DDP was 8.004. The expression of YKL-40， MDR1 and Bcl-2 in Ishikawa／DDP cells were 1.87±0.40， 2.34±0.46 and 1.52±0.28， which were higher than those in Ishikawa cells （P＜0.05）. The expression of Bax and caspase-3 in Ishikawa／DDP cells were 0.72±0.21 and 0.49±0.17， which were lower than those in Ishikawa cells （P＜0.05）. The inhibitory rates of 3.125， 6.25， 12.5， 25， 50 and 100 μmol／L DDP on the proliferation of si-YKL-40 cells were （10.95±2.74）％， （18.73±5.30）％， （32.79±5.47）％， （52.28±6.58）％， （61.73±5.26）％， （65.45±7.33）％， respectively， which were significantly higher than those of blank control group and NC group （P＜0.05）. The IC50of DDP on si-YKL-40 cells was 22.19 μmol／L. Compared with the blank control group and NC group， the apoptotic rate increased and the healing rate decreased in the si-YKL-40 group， while the expression of YKL-40， MDR1 and Bcl-2 decreased， while the expression of Bax and caspase-3 increased （P＜0.05）. Conclusion Silencing YKL-40 can significantly increase the sensitivity of Ishikawa／DDP cell lines to cisplatin and promote cell apoptosis， which may be related to down-regulation of MDR1， Bcl-2 expression and up-regulation of Bax and caspase-3 expression.

Objective  To detect the expression of long chain non-coding RNA MEG3 in cervical cancer cells， and to detect the effect of MEG3 on the proliferation and migration of HeLa cells and its possible molecular mechanism. Methods The expression of MEG3 in normal cervical epithelial cells HcerEpic and cervical cancer cell lines C-33A， C4-1， Caski， SiHa and HeLa was detected by fluorescence quantitative PCR （QPCR）. MEG3 overexpression plasmid （MEG3 group）， negative control plasmid （NC group） and MEG3+Rac1 overexpression plasmid （MEG3+Rac1 group） were transfected into HeLa cells respectively. MTT assay was used to detect cell proliferation and Transwell assay was used to detect cell migration. The expression of PCNA， E-cadenin， N-cadenin， Vimentin and Rac1 was detected by Western blotting assay. Results The expression levels of MEG3 in C-33A， C4-1， Caski， SiHa and HeLa cells were 0.37±0.044， 0.65±0.075， 0.41±0.071， 0.71±0.053 and 0.42±0.081， which were lower than those in HcerEpic cells （P＜0.05）. MTT assay showed that the proliferation activity of HeLa cells in MEG3 group was significantly lower than that in NC group. The number of migrating cells in MEG3 group was 385±14， which was significantly lower than that in NC group （594±16），and the difference was statistically significant （P＜0.05）. Compared with NC group， the expressions of PCNA， N-cadenin and Vimentin were down-regulated and E-cadenin was up-regulated in MEG3 group. Compared with MEG3 group， MEG3+Rac1 group significantly increased the expression of Rac1 protein， the proliferation activity and the number of migrating cells. Conclusion LncRNA MEG3 inhibits the proliferation and migration of cervical cancer cells by targeting Rac1 signaling pathway.

Objective  To investigate the effect of microRNA122 （miR-122） on apoptosis of glioma cells and its possible molecular mechanism. Methods The expression of miR-122 in human normal astrocyte lines HA1800 and glioma cell lines U251， U87， SHG44 and MO59K was detected by quantitative fluorescence PCR （QPCR）. Dual luciferase reporter assay was used to evaluate the targeting effect of miR-122 on RUNX2. MiR-122 mimics （miR-122 group）and negative control NC（NC group） were transfected into U251 cells. Apoptosis was detected by flow cytometry. Western blotting was used to detect the expression of Bcl-2，Bax and cleaved caspase-3 protein in two groups. MiR-122 mimics and siRUNX2 （MiR-122+siRUNX2 group） were simultaneously transfected into U251 cells. Apoptosis was detected by flow cytometry. Results The expression of miR-122 in U251，U87，SHG44 and MO59K cell lines were 0.34±0.052， 0.65±0.061， 0.59±0.071 and 0.69±0.098， which was significantly lower than that of human normal astrocyte lines HA1800 （1.17±0.173）， and the difference was statistically significant （P＜0.05）.MiR-122 inhibited the luciferase activity of wild-type RUNX2 3’UTR reporter gene vector， but had no effect on the luciferase activity of mutant RUNX2 3’UTR reporter gene vector. The apoptotic rate of U251 cells in miR-122 group was （23.77 ±0.83）％， higher than that in NC group （6.17 ±0.12）％， lower than that in miR-122+siRUNX2 group （70.85±0.35）％.The difference was statistically significant （P＜0.05）. Western blotting Results  showed that the expression of RUNX2 protein in the miR-122 group was 0.57±0.048， which was lower than that in the NC group （1.21±0.19）， with statistical significance （P＜0.05）. Compared with NC group， the expressions of Bax and cleaved caspase-3 were significantly up-regulated in miR-122 group， while Bcl-2 was significantly down-regulated （P＜0.05）. Conclusion MiR-122 can promote the activation of mitochondrial apoptosis pathway by targeting RUNX2， thereby promoting apoptosis of glioma cells.

Objective  Effects of isocryptotanshinone （ICTS） on proliferation， cycle and apoptosis of gastric cancer cell lines BGC-823 and SGC-7901 and its possible mechanism. Methods Gastric cancer cell lines BGC-823 and SGC-7901 were cultured in vitro. After treatment of 0，5，10，20 μmol／L ICTS for 24， 48 and 72 hours， CCK-8 method was used to detect the inhibition rate of cell proliferation. After determining the optimal concentration and time of ICTS inhibiting BGC-823 and SGC-7901 cells， cell cycle and apoptotic rate were detected by flow cytometry. Western blotting was used to detect the expression of Cyclin D1， Bcl-2， p53 and p21 proteins in gastric cancer cells treated with ICTS. Results The inhibition rates of BGC-823 cells treated with 0，5，10，20 μmol／L ICTS for 24 hours were （0.789±0.048）％， （16.74±1.55）％， （33.58±2.26）％ and （54.62±2.61）％. The difference was statistically significant （P＜0.05）. The inhibition rates of SGC-7901 cells treated with 0，5，10，20 μmol／L ICTS for 24 hours were （-0.184±0.023）％， （12.76±1.73）％， （32.95±2.47）％ and （53.80±2.65）％. The difference was statistically significant （P＜0.05）. The inhibition rates of BGC-823 cells treated with 20 μmol／L ICTS at 24， 48 and 72 hours were （54.62±2.61）％， （55.08±2.35）％， （59.72±2.53）％. There was no significant difference （P＞0.05）. The inhibition rates of SGC-7901 cells treated with 20 μmol／L ICTS at 24， 48 and 72 hours were （53.80±2.65）％，（55.76±2.47）％ and （61.83±2.82）％，. There was no significant difference （P＞0.05）. BGC-823 and SGC-7901 cells were treated with 20 μmol／L ICTS for 24 hours. The percentage of G0／G1 phase cells was （78.34±7.13）％ and （79.57±7.34）％， which were higher than those of the control group（P＜0.05）. The apoptotic rates of BGC-823 and SGC-7901 in ICTS treatment group were （24.78±3.42）％ and （28.76±4.21）％， which were higher than those of control group （P＜0.05）. The expression of Cyclin D1 and Bcl-2 protein in ICTS treatment group was significantly lower than that in the control group （P＜0.05）， and the expression of p53 and p21 protein in ICTS treatment group was significantly higher than that in the control group （P＜0.05）. Conclusion ICTS plays an anti-gastric cancer role by increasing the expression of p53 and p21， reducing the expression of Cyclin D1 and Bcl-2， thereby inhibiting cell proliferation， increasing G0／G1 blockade and apoptosis.

Objective  To investigate the effect of mithramycin （MTM） on cell cycle and apoptosis of gastric cancer cells and its possible mechanism. Methods BGC-823， SGC-7901， MKN-28， AGS and normal gastric mucosa GES-1 cells were cultured in vitro. Real-time fluorescence quantitative analysis （QPCR） and Western blotting were used to detect the expression of SP1 mRNA and protein. BGC-823 cells were treated with 0， 25， 50 and 100 nmol／L MTM for 24 hours. The expression of SP1， p53 and p21 were detected by QPCR and Western blotting. Flow cytometry was used to detect the changes of cell cycle and apoptosis in BGC-823 cells treated with 50 nmol／L MTM. Results The expression of SP1 in BGC-823， SGC-7901， MKN-28 and AGS cell lines was 6.12 ±0.15， 5.42±0.24， 3.33±0.21 and 3.01±0.12 by QPCR， which were significantly higher than those in GES-1 cell lines （P＜0.05）. Western blotting showed that the expression of SP1 protein was consistent with that of mRNA. When BGC-823 cells were treated with 0， 25， 50 and 100 nmol／L MTM， the expression of SP1 decreased gradually， while the expression of p53 and p21 increased gradually. Compared with 0 nmol／L MTM group， the expression of SP1 was the lowest and p53 was the highest in 50 nmol／L MTM group and the expression of p21 was the highest in 100 nmol／L MTM group（P＜0.05）. Flow cytometry showed that the G0／G1 ratio and apoptotic rate of BGC-823 cells in 50 nmol／L MTM group were （63.71±2.14）％ and （24.68±1.09）％ respectively， which were significantly higher than those in 0 nmol／L MTM group. Conclusion Mithramycin can increase cell cycle arrest and induce apoptosis by decreasing SP1， increasing p53 and p21 expression.

Objective  To systematically evaluate the efficacy of gemcitabine monotherapy and gemcitabine combined with nab-paclitaxel in the first-line treatment of advanced metastatic pancreatic cancer in East Asian population， in order to provide a reference for the clinical rational use of gemcitabine in the first-line treatment of patients with metastatic pancreatic cancer in China. Methods According to the preset inclusion and exclusion criteria， literatures published from January 2010 to June 2018 were systematically searched in Wanfang， Cochran Library， MEDLINE， PubMed and CNKI databases. The primary endpoint was objective remission rate （ORR）， and the secondary endpoint was progression-free survival （PFS） and overall survival （OS）. Then the related data was extracted and meta-analysis was performed by using Rev Man 3.5.0 statistical software. Results A total of 38 studies involving 1945 patients were included. The ORR of gemcitabine monotherapy for advanced pancreatic cancer was 0.15 （95％ CI： 0.11-0.18）， the median PFS was 3.39 （95％ CI： 2.74-4.05） months， and the median OS was 7.39 （95％ CI： 6.54-8.23） months. The ORR of gemcitabine combined with nab-paclitaxel in the treatment of advanced pancreatic cancer was 0.40 （95％ CI： 0.29-0.52）， the median PFS was 5.68 （95％ CI： 4.30-7.06） months， and the median OS was 9.80 （95％ CI： 7.89-11.71） months. Conclusion Compared with gemcitabine monotherapy， gemcitabine combined with albumin-bound paclitaxel has obvious superiority and is suitable for East Asian population， especially for patients with advanced pancreatic cancer in China.

Objective  To study the relationship between epidermal growth factor receptor （EGFR）， transforming growth factor-α（TGF-α） and different fractional doses of radiotherapy in lung cancer cells and its possible mechanism. Methods Lung cancer cell line A549 cells were irradiated with conventional fractionation （2Gy／day） and large fractionation （4，8 Gy／day）， DT=8 Gy. Real-time fluorescence quantitative PCR （QPCR）， enzyme-linked immunosorbent assay （ELISA） and Western blotting were used to detect EGFR， TGF-α gene and protein expression in A549 cells， respectively. In addition， the expression of γ-H2AX was determined by immunofluorescence assay. Results The expression levels of EGFR mRNA and TGF-α mRNA in A549 cells of 4 Gy／day and 8 Gy／day fractionation groups were significantly lower than those of 2 Gy／day fractionation group （P＜0.05）. The expressions of EGFR and TGF-α proteins in A549 cells of 4 Gy／day and 8 Gy／day fractionation groups were significantly lower than those of 2 Gy／day fractionation group （P＜0.05）. Immunofluorescence assay showed that the expression ofγ-H2AX in A549 cells in 4 Gy／day and 8 Gy／day fractionation groups was significantly higher than that in control group and 2 Gy／day fractionation group. Conclusion The expression of EGFR and TGF-α decreased significantly after high dose fractionated radiotherapy， which increased the sensitivity of A549 cells to radiation. The mechanism may be related to the up-regulation of the expression of histone γ-H2AX in DNA damage repair.

Objective  To investigate the expression and significance of miRNA-138-5p （miR-138-5p） in non-small cell lung cancer （NSCLC）. Methods Real-time fluorescence quantitative PCR （QPCR） was used to detect the expression of miR-138-5p in 102 NSCLC tissues and 98 paracancerous tissues. The relationship between the expression of miR-138-5p and the clinicopathological features of NSCLC （sex， age， TNM stage， tumor size and lymph node metastasis） were analyzed. The survival curve was drawn by Kaplan-Miere method， and the difference was checked by Log-rank test. Cox regression model was used to analyze the factors affecting overall survival（OS）. Results The expression level of miR-138-5p in NSCLC tissues was 0.42±0.11， significantly lower than 1.03 ±0.28 in adjacent tissues （P＜0.05）. The expression of miR-138-5p was correlated with TNM stage， tumor size and lymph node metastasis （P＜0.05）. The median OS of high expression of miR-138-5p was more than 36 months， which was significantly higher than that of low expression of miR-138-5p （P＜0.05）. Cox univariate analysis showed that besides the expression of miR-138-5p， lymph node metastasis， tumor size and TNM stage were also associated with OS （P＜0.05）. Conclusion The expression of miR-138-5p is down-regulated in NSCLC， which is related to the development and prognosis of NSCLC. MiR-138-5p can be used as a new target for diagnosis and prognosis prediction of NSCLC.

Objective  To analyze the methylation status of promoter of O6-methylguanine-DNA methyltransferase （MGMT） gene and its relationship with clinicopathological features and prognosis of glioma. Methods The methylation level of MGMT was detected by methylation specific polymerase chain reaction （MSP） in 70 glioma tissues and 14 normal brain tissues of non-tumor patients who underwent surgical treatment from January 2012 to June 2013. The relationship between MGMT methylation and clinicopathological features was analyzed. Overalll survival （OS） of patients with high and low grade glioma with different MGMT methylation status was compared. Cox proportional regression model was used to analyze the factors affecting OS in low-grade glioma patients. Results Of 70 glioma patients， 48 （68.6％） had MGMT promoter methylation， while only 2 （14.3％） had MGMT methylation in normal brain tissues （P＜0.05）. MGMT methylation was not correlated with age， sex， tumor type， KPS score， p53 and Ki-67 expression （P＞0.05）， but with pathological grade （P＜0.05）. The median OS of MGMT methylated glioma patients was 30 months， significantly longer than that of non-methylated glioma patients for 11 months （P＜0.05）. Univariate analysis showed that WHO pathological grade， alkylating agent chemotherapy and MGMT methylation were associated with OS in low-grade glioma patients （P＜0.05）. Multivariate analysis showed that WHO grade Ⅱ， non-alkylation chemotherapy and MGMT non-methylation were independent risk factors for OS in low-grade glioma patients （P＜0.05）. Conclusion MGMT methylation is related to the occurrence and development of glioma. It has certain value in judging the malignancy of glioma， evaluating prognosis and guiding clinical treatment.

Objective  To analyze the effect of intensity modulated radiotherapy （IMRT） on long-term survival and immune function after breast conserving surgery for breast cancer. Methods Two hundred and fifty-four breast-conserving breast cancer patients were divided into observation group （n=147） and control group （n=147）. The patients were treated with whole breast irradiation 50 Gy／25 times after operation. In the supplementary radiotherapy of tumors， the control group was treated with electronic radiation， while the observation group was treated with X-ray IMRT. The prescription doses were 10-16 Gy／5-8 times. Dosimetry of target area， dosimetry of heart， dosimetry of affected lung， side effects， 5-year disease-free survival rate， 5-year survival rate and T cell subsets before and after radiotherapy were compared between the two groups. Results There was no significant difference in V95％ of target area of the tumor bed between the two groups （P＞0.05）. The V105％， V110％， cardiac irradiation dose and dose of affected side lung irradiation in observation group were （11.26±2.59）％， （3.15±0.84）％， （3.72±1.16） Gy and （7.51±2.06） Gy， which were lower than control group. The difference was significant （P＜0.05）. There was no significant difference in the incidence of acute skin reaction， late skin reaction， bone marrow suppression， radiation pneumonia and radiation esophagitis between the two groups （P＞0.05）. The 5-year disease-free survival rate of the observation group was 98.55％， which was higher than 94.16％ of the control group （P＜0.05）. The 5-year survival rate was 95.65％ in the observation group and 94.89％ in the control group， with no significant difference （P＞0.05）. After radiotherapy， the levels of CD+3， CD+4 and CD+4／CD+8 in the observation group were lower than those in the control group， and the level of CD+8 were higher than those in the control group （P＜0.05）. Conclusion X-ray IMRT after breast-conserving surgery for breast cancer can achieve better tumor-free survival， with little impact on immune function. It may be related to the uniform distribution of dose in the target area of the tumor bed and the reduction of radiation dose in the heart and lung of the affected side， which is worthy of clinical application.

Objective  To evaluate the value of peripheral blood neutrophil to lymphocyte ratio （NLR） before radiotherapy in evaluating the efficacy and prognosis of senile patients with esophageal squamous cell carcinoma（ESCC）. Methods One hundred and twenty-eight senile ESCC patients treated with radiotherapy alone or concurrent radiotherapy and chemotherapy were retrospectively analyzed. The relationship between the level of NLR in peripheral blood before radiotherapy and the clinicopathological features and prognosis of ESCC patients was analyzed. Cox proportional hazard regression model was used to analyze the factors affecting total survival （OS）. Results The receiver operator characteristics （ROC） curve showed that the best cut-off value of NLR before radiotherapy was 3.13. One hundred and twenty-eight patients were divided into low NLR group （n=75） and high NLR group （n=53）. The level of NLR before radiotherapy was not related to age， sex， TNM stage and treatment modality （P＞0.05）. The effective rate of radiotherapy was 96.0％ in low NLR group and 69.8％ in high NLR group. The difference was statistically significant （P＜0.05）. Univariate analysis showed that NLR， N stage and TNM stage were the factors affecting OS in elderly patients with esophageal squamous cell carcinoma. Multivariate analysis showed that NLR and N staging were independent factors affecting OS in senile ESCC patients. Conclusion The high NLR level suggests that the radiotherapy effect and prognosis of elderly patients with esophageal squamous cell carcinoma are poor.

Objective  To summarize the clinicopathological characteristics， diagnosis and therapy as well as the prognostic factors of patients with thymic squamous cell carcinoma （TSCC）. Methods Twenty-four patients with TSCC admitted to Beijing Chest Hospital from January 2006 to April 2013 were retrospectively analyzed. Among them， 15 cases received surgical treatment （10 cases of combined radiotherapy and chemotherapy after operation， 3 cases of chemotherapy after operation， 1 case of radiotherapy after operation and 1 case without adjuvant treatment after operation） and 9 cases received palliative radiotherapy and chemotherapy. The clinical data of TSCC patients were analyzed. Follow-up data were collected and survival analysis was performed by Kaplan-Meier method. Results All patients were followed up for 1.0 to 139.0 months with a median follow-up time of 53.2 months. The overall survival （OS） was 2.5-139.0 months with a median OS of 68.1 months. The 1-， 3- and 5-year survival rates were 70.8％， 54.2％ and 41.7％， respectively. Kaplan-Meier univariate analysis indicated that Masaoka stage （P=0.018）， surgical resection （P=0.016） and surgical resection integrity （P=0.017） were the prognostic factors of TSCC patients. Postoperative radiotherapy did not prolong the patients’ prognosis （P=0.401）. Conclusion The clinical manifestation of TSCC is lack of specificity. Surgery is the main treatment. Masaoka stage and surgery have an impact on the prognosis of patients. Radical surgery has a better prognosis than palliative surgery. Postoperative radiotherapy has not been able to benefit patients’ survival. Clinical treatment should be formulated according to the physical condition of patients and the integrity of tumor resection.

Objective  To investigate the relationship between c-ros oncogene 1（ROS1） fusion gene mutation and epidermal growth factor receptor（EGFR） mutation and clinicopathological characteristics in non-small cell lung cancer（NSCLC）. Methods Real-time fluorescence quantitative PCR（QPCR） was performed to examine gene rearrangement of ROS1 fusion gene in 3487 NSCLC patients of Northwest China from December 2014 to December 2017. EGFR mutation was detected by ARMS method for patients with ROS1 fusion gene mutation. The clinicopathological features of patients with double mutations were analyzed. Results Among the 3487 patients， 54 patients（1.5%） occurred ROS1 fusion gene mutation. ROS1 fusion gene mutation was associated with age， gender， smoking history， pathological types and clinical stage （P＜0.05）. Three patients were identified with EGFR mutation from 54 patients who harboring ROS1 fusion genes mutation, including 2 cases of EGFR19 exon deletion mutation （19-del）， and 1 case of EGFR L858R mutations. The 3 double mutative cases were of ROS1 variant 2 （R2）. Conclusion ROS1 fusion gene mutative rate of NSCLC patients in Northwest China is 1.5％. ROS1 fusion gene and EGFR mutations can coexist in NSCLC.

Exosomes are a extracellular vesicles， which contain a large number of bioactive substances within lipid bilayer membrane. Researches have indicated that exosomes of non-small cell lung cancer（NSCLC） can change tumor sensitivity to chemotherapy drugs and participate in the regulation of tumor cells and microenvironment. The study of exosomes has unique value in lung cancer research， including molecular mechanism of drug resistance， early diagnosis of tumor development and new drug carriers design. This paper carries out a review on the progression of NSCLC drug resistance and exosomes inrecent years.

Much substantial evidence suggests that financial toxicity has become an issue in the era of molecular and immune therapy of cancer treatment. Some independent factors related to financial toxicity including illness status， patients’ general health， age， race， income， health insurance. Financial problem can lead to lower quality of life， poor medical care， treatment nonadherence， impaired working ability and thus increase the mortality. Therefore， the interventions should be done in multiple levels and requires all parts of populaion involved. At the same time， we need more evidence-based research and statistics for guidance.