As a tumor-specific antigen highly expressed in various types of tumors, MACE-A does not exist in normal adult tissues, except for testis and placenta. Therefore MAGE-A antigens are regarded. tumor specific antigen,and have significant significance for cancer immunotherapy.

Objective To compare the risk factor of chilldren with autism and ordinary children during perinatal period. Methods One hundred and fourty children with autism and 82 ordinary children were reviewed by self-written general circumstance questionnaire and risk factor questionnaire. Results Viral influenza during pregnancy (x2 =15.29) ,bom suffocate( x2 =6. 04) , premature delivery (x2 =6. 48) , dystocia (x2 =2. 83) and artificial feeding ( x2 = 6. 02 ) were risk factors for children autism (P < 0. 05 ). Conclusion Childeren autism is associated with risk factors in rinatal period. Early dectecion and early prevention and treatment may improve the outcome.

Objective To evaluate the relationship between the anxiety condition and educational background of the autistic children's parents. Methods Questionnaires for the self-evaluation of anxiety were collected from the parents of 140 children with autism. Results The autistic children's mothers had significantly higher score of anxiety than the fathers (42. 73 ±8. 25) (t =6. 783,P ＜0. 05). The autistic boy's parents had significantly higher anxiety pressure than autistic girl's parents ( 51.38 ± 11.24 vs. 43.23 ± 6. 12) ( t = 4. 894,P ＜0. 05). The anxiety intensity of the autistic children's parents was negatively correlated with the parents'educational background ( F = 10. 788, P ＜ 0. 05 ). Conclusion The autistic children' s parents had certain anxiety,which is correlated with the their educational background and genders of the autistic children. It is necessary to interfere the negative mood to facilitate the treatment of the autistic children.

Background and purpose: Protein kinase P1k3 could increase the transcriptional activity of p53. However, the effect of P1k3 on the transcriptional activity of p73 is still unknown. Our study was to investigate the effect of P1k3 on the transcriptional activity of p73. Methods: Luciferase reporter assay, RT-PCR and colony formation assay were adopted to study the effect of P1k3 and kinase-deficient P1k3 (K52R) on the transcriptional activity of p73 in p53-deficient human lung carcinoma H1299 cells. Results: Luciferase reporter assay showed that p73 increased the luciferase activities induced by p21~(WAF1) and Bax promoters (P<0.05). After co-transfection with p73 and P1k3, the luciferase activities induced by p21~(WAF1) and Bax promotors were significantly decreased in a dose-dependent manner as compared with the group that transfected p73 only (P<0.05). However, kinase-deficient Plk3 (K52R) had no significant effect on the luciferase activities induced by p21~(WAF1) and Bax promoters (P>0.05). RT-PCR showed that p73 increased the mRNA expressions of p21~(WAF1) and BAX (P<0.05). P1k3 decreased the expressions of p21~(WAF1) and Bax induced by p73 (P<0.05). Kinase-deficient P1k3 (K52R) had no significant effect on the expressions of p21~(WAF1) and Bax induced by p73 (P>0.05). Colony formation assay revealed that p73 decreased the colony formation of H1299 cells (P<0.05). P1k3 decreased the inhibitory effect of p73 on the colony formation of H1299 cells (P<0.05). Kinase-deficient P1k3 (K52R) had no significant effect on the inhibitory effect of p73 on the colony formation of H1299 cells (P>0.05).Conclusion: P1k3 can inhibit the transcriptional activity of p73, where as kinase-deficient P1k3 has no effect on the transcriptional activity of p73.

Objective:This work aims to detect the levels of miR-200c/141 methylation and miR-200c/141 in gastric cancer tissue and investigate the relationship between miR-200c/141 expression and clinical parameters. Methods:The methylation status of miR-200c/141 CpG island and miR-200c/141 in gastric cancer tissue specimens was evaluated by qRT-PCR or BS-MSP method. We analyzed the relationship among the methylation status of miR-200c/141 CpG island, expression level of miR-200c or miR-141, and clinical parame-ters. Results:The status of miR-200c/141 CpG island methylation in gastric cancer tissue was significantly higher compared with that in paracarcinoma tissue. MiR-200c and miR-141 were markedly decreased in gastric cancer tissue compared with those in adjacent tis-sue. MiR-200c/141 CpG island methylation was negatively related with the expression of miR-200c and miR-141 in gastric cancer speci-mens. Conclusion:The upregulation of miR-200c/141 CpG methylation inhibits miR-200c/141 expression in gastric cancer tissue.

Objective:To study the correlation of C(-938)A single nucleotide polymorphism (SNP) in the promoter of anti-apoptosis gene Bcl-2 with the clinical biological parameters of breast cancer patients in Hebei Province. Methods:Three genotypes(AA, AC, CC) of Bcl-2 C(-938)A from 113 samples of breast cancer patients were analyzed by using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method, and the results were associated with clinical biological parameters. The distribution of genotype frequency was compared between different groups. Results:When stratified for axillary lymph node metastases, the frequency of AA genotype were 26.8%, 47.8% and 52.6% and the distribution of AC+CC genotypes were 73.2%, 52.2% and 47.4% in negative group, 1-3 metastasis group, and ≥4 metastasis group. The difference between the two groups was significant (χ~2=6.337, P=0.042). Compared with the AC+CC genotypes, the OR value of AA genotype in ≥4 metastasis group was 3.041 (95%CI=1.072-8.626). The frequency of AA genotype were 30.9% and 69.1% in gradeⅠ-Ⅱ group and grade Ⅲ group, and the frequency of AC+CC genotypes were 57.9% and 42.1%. The difference between the two groups was significant (χ~2=5.055; P=0.025). Compared with the AC+CC genotypes, the OR value of AA genotype in differentiated tumors(grade Ⅲ)was 3.082 (95%CI=1.122-8.465). Stratified for estrogen receptor (ER), progesterone receptor (PR) and C-erbB2, there was no difference between the distribution of AA genotype and AC+CC genotypes (χ~2=3.005, χ~2=1.504, χ~2=1.163, P>0.05). Conclusion:The AA genotype of Bcl-2 gene C(-938)A maybe correlated with high lymph node metastasis rate and poor differentiation.

Objective: To investigate the expressions of programmed death ligand 1（PD-L1）in triple-negative breast cancer (TNBC) and its correlation with angiogenesis. Methods: 120 cases of TNBC patients who underwent surgery in the Fourth Hospital of Hebei Medical University from March 1, 2011 to June 1, 2012 were collected. The tumor tissues of patients were surgically resected and confirmed by pathology. PD-L1 protein expression in TNBC tissues of 120 patients was detected by tissue microarray combined with immunohistochemistry, and its relationship with various clinical indicators was analyzed. Blood vessels and lymphatic vessels were labeled withCD34andD2-40todetectmicrovesseldensity(MVD)andlymphaticvesseldensity(LVD)inTNBC.Results:Thepositiveexpression rate of PD-L1 in the tumor cells and interstitial infiltrating lymphocytes fromTNBC was 56.7% (68/120); No correlation was found between PD-L1 protein expression and the gender, age, histological grade, clinical stage, or tumor size of patients with TNBC (P>0.05), but related to the lymph node metastasis (P<0.05) and vascular thrombus (P<0.05). TNBC with high PD-L1 expression exhibited high incidence of lymph node metastasis and formation of vascular thrombus, and the expression of PD-L1 was positively correlated with MVD (r=0.500, P=0.02) as well as LVD (r=0.662, P=0.01). Log-Rank test showed that the survival time of TNBC patients with positive PD-L1 protein expression was significantly shorter than that of patients with negative expression (P<0.05). Cox multivariate analysis suggested that PD-L1 protein expression could be an independent prognostic factor for TNBC overall survival. Conclusion: PD-L1 plays an important role in TNBC angiogenesis and lymphangiogenesis, and is closely related to TNBC invasion and metastasis; blocking PD1/PD-L1 signal pathway is expected to be an effective new strategy for TNBC treatment.

Objective: To investigate the expression of ciRS-7 in esophageal squamous cell carcinoma (ESCC) and its effect on the cellular proliferation, migration and invasion. Methods: The cancer tissues and paired adjacent normal tissues from 60 ESCC patients treated in the Fourth Hospital of Hebei Medical University between May, 2016 andApril, 2017 were selected for this study. The expressions of ciRS-7 were detected by qRT-PCR. After over-expressing or silencing of ciRS-7, the proliferation of ESCC cell line TE1 was measured by CCK-8 assay; and the migration and invasion were tested by wound healing assay and Transwell invasion assay，respectively. Finally, the effect was validated via animal experiment. Results: CiRS-7 was highly expressed in ESCC tissues (P<0.05), and its expression level was closely related to pathological grade and lymph node metastasis (P<0.05). Over-expression of ciRS-7 significantly increased the proliferation, migration and invasion (all P<0.05) of TE1 cells; while silencing of ciRS-7 remarkably suppressed the proliferation, migration and invasion (all P<0.05). Conclusion: CiRS-7 was up-regulated in ESCC and could enhance ESCC cell proliferation, migration and invasion, suggesting that ciRS-7 could be used as a potential target for the diagnosis and treatment of ESCC.

[Abstract] Objective: To investigate the expression of long non-coding RNA (lncRNA) DiGeorge syndrome critical region gene 5 (DGCR5) in esophageal squamous cell carcinoma (ESCC) tissues, and to analyze its relationship with clinicopathological features and prognosis of ESCC patients. Methods: The expression of DGCR5 in ESCC data set from TCGA database was analyzed by bioinformatics method. Sixty pairs of ESCC tissues and para-cancerous tissues resected at the Fourth Hospital of Hebei Medical University from August 2016 to March 2017 were collected for this study. The expression of DGCR5 in ESCC tissues was detected by qPCR. The correlation between the expression of DGCR5 and the clinicopathological features and prognosis of ESCC patients was analyzed. Results: TCGAdatabase analysis showed that the expression of DGCR5 in ESCC tissues was significantly higher than that in normal esophageal tissues (P<0.01). The expression of DGCR5 in ESCC tissues was significantly higher than that in para-cancerous tissues (P<0.01). The expression level of DGCR5 was significantly correlated with TNM staging and lymph node metastasis in ESCC patients (all P<0.05). Kaplan-Meier univariate analysis showed that the 2-year survival rate of ESCC patients with high DGCR5 expression was significantly lower than that of patients with low expression (P<0.05). Conclusion: DGCR5 is highly expressed in ESCC tissues and is closely related to TNM staging, lymph node metastasis and poor prognosis, which may serve as a molecular marker for early diagnosis and prognosis prediction of ESCC.

Objective: To detect the expression of miR-133a-3p in gastric cancer (GC) tissues and plasma of GC patients, and to investigate its effect on the proliferation of GC cells as well as its correlation toprognosis of GC patients. Methods: 52 cases of cancertissues (non-necrosis part) and corresponding adjacent tissues as well as the pre-operative peripheral blood samples from GC patients, who underwent surgery at Department of General Surgery, the Forth Hospital of Hebei Medical University(Shijiazhuang, China) between May 2012 and May 2013, were collected for this study. The plasma sample (n=35) from healthy donors were obtained during their physical examination. RT-qPCR was adopted to detect the expression of miR-133a-3p in gastric cancer tissues, adjacent tissuesand plasma samples of GC patients and healthy volunteers. The relationships between miR-133a-3p expression and the median DFS as well as clinicopathological parameters were also analyzed. CCK-8 assay was adopted to detect the effect of miR-133a-3p silence or over-expression on proliferation of gastric cancer SGC7901 cells. Results: miR-133a-3p was dramatically decreased in gastric cancer tissues (P<0.01), and its expression was associated with TNM stage, tumor infiltration (T), lynphonode metastasis (N), and vascular tumor thrombus (all P<0.01); miR-133a-3p was significantly increased in the plasma of GC patients (P<0.01), and its expression was associated with TNM stage, lynphonode metastasis (N), and vascular tumor thrombus (all P<0.05). miR-133a-3p expression was positively correlated with serum CA199 level of GC patients (P<0.01). The median DFS of patients with high miR-133a-3pexpression in cancer tissues was significantly longer than that of the patients with low expression(20.8 vs 14.8 months, P<0.05); The median DFS of patients with high plasma miR-133a-3p expression was significantly shorter than that of the patients with low expression (14.4 vs 20.3 months, P<0.05). Over-expression of miR-133a-3p could significantly inhibit the proliferation of gastric cancer SGC7901 cells, while miR-133a-3p silence could significantly promote the proliferation (all P<0.05). Conclusion: miR-133a-3p could significantlyinhibit the proliferation of SGC7901 cells; miR-133a-3p aberrantlyexpressed in gastric cancer tissues and plasma, and obviously correlated with prognosis of gastric cancer patients, which may be used as a potential clinical bio-maker for early diagnosis and treatment as well as the prognosis prediction of gastric cancer.