BET1 encodes a Golgi-associated membrane protein involved in vesicular transport from the endoplasmic reticulum (ER) to the Golgi apparatus. While the role of BET1 in cancer development remains poorly understood, its function in glioblastoma multiforme (GBM) has not been systematically investigated. In this study, we found that 15 out of 33 cancer types showed significant differential BET1 expression between tumor and normal tissues. Furthermore, survival analysis identified BET1 as an independent prognostic factor in GBM. Additional analyses revealed correlations between BET1 expression and the infiltration of immune cells, such as Tregs and CD4 + T cells, in GBM. Moreover, BET1 knockdown in glioblastoma cells reduced their proliferation and migration capacities. This study provides a comprehensive analysis of BET1, thereby advancing our understanding of its oncogenic potential in GBM.

Death receptor 5 (DR5) can inhibit malignant proliferation via tumor necrosis factor‐related apoptosis‐inducing ligand (TRAIL)‐induced apoptosis in many cancers. Here we examined the expression and sublocalization of DR5 in gastric cancer, as well as its effects on clinical prognosis and cellular processes. Our analysis included a cohort of 240 gastric cancer patients. Bioinformatic analysis showed a significant correlation between DR5 and DNA replication, tumor mutation burden (TMB), and tumor stemness. Unlike death receptor 4 (DR4TRAIL‐R1), DR5 was expressed in the cytoplasm and nucleus, and was found to be positively correlated with lymphovascular invasion, lymph node metastasis, and TNM stage. Patients with positive DR5 had worse overall survival (OS) (P = 0.006). The multivariate Cox model showed that DR5 is an independent poor prognostic factor (hazard ratio = 1.693). Furthermore, knockdown of DR5 inhibited aggressive behaviors, including proliferation and metastasis in gastric cancer cells, and inhibited lung metastasis in vivo. In summary, nuclear localization of DR5 expression is a poor prognosis factor in gastric cancer and promotes growth, invasion, and metastasis of tumor cells in vitro and in vivo.

目的 探讨上皮细胞增殖(ECP)通路相关基因对老年非小细胞肺癌患者免疫治疗预后及疗效的提示作用.方法 2022年10月回顾性分析POPLAR及OAK临床研究中年龄≥70岁、接受免疫治疗的老年患者106例,依据突变基因情况将患者分为ECP通路相关基因突变(ECP突变组)25例和相关基因未突变(ECP未突变组)81例.主要研究终点为患者总生存时间(OS)和无进展生存时间(PFS).分别比较两组患者生存和疗效差异,并对各临床因素和通路涉及基因进行亚组分析.经Pyclone算法推算各患者主克隆及亚克隆分布并比较生存差异.结果 ECP突变组与ECP未突变组患者比较,mOS缩短(10.9个月比17.1个月,HR=1.84,95％CI:1.09～3.08,P＜0.05),mPFS 亦缩短(2.8 个月比 4.2 个月,HR=1.58,95％CI:1.00～2.51,P＜0.05).在 ECP 通路各基因中,RB1基因突变对全部患者预后作用显著,且在ECP突变组患者中,RB1负性预后作用显著,与ECP未突变组患者比较,mOS缩短(6.9个月比12.6个月,HR=3.14,95％CI:1.10～8.97,P=0.024).ECP通路基因处于主克隆突变患者10例,较亚克隆突变15例患者mPFS缩短,1.3个月比5.3个月(HR=3.23,95％CI:1.25～8.37,P=0.011).结论 接受免疫治疗的老年非小细胞肺癌患者ECP通路基因突变为负性预后因子,且突变位于主克隆对预后影响更强.

BACKGROUND:Neutrophil/lymphocyte ratio (NLR) is a vital index for systemic inflammation and a prognostic indicator for gastric cancer (GC). Despite the abundant literature on NLR's prognostic value for GC, the underlying factors mediating its impact on survival remain unclear. The objective of this study was to analyze the role of NLR in different prognostic models and subgroups, and investigate the mediating effects of immune infiltrates between NLR and survival. METHODS:A total of 924 patients who underwent D2 lymph node resection were enrolled in this study. According to the level of NLR, patients were divided into two groups, the high and low NLR groups. Clinical parameters, indexes related to immune infiltrates, and survival were compared between the two groups. Prognostic models, interaction analysis, and mediating effects analysis were performed to investigate the clinical association of NLR, immune infiltrates, and survival. RESULTS:The infiltration of CD3+ and CD8+ T cells was significantly different in the two NLR groups. The level of NLR was an independent prognostic predictor of GC. In addition, an interaction effect exists between NLR and MMR status on the prognosis of GC (p-interaction <0.01). Lastly, the mediating effect analysis revealed that the infiltration level of CD3+ T cells was the mediating factor between NLR and survival (p < 0.001). CONCLUSIONS:The level of NLR is an independent prognostic predictor of GC. The effect of NLR on prognosis is partly mediated by CD3+ T-cell infiltration.

Death receptor 5 (DR5) can inhibit malignant proliferation via tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in many cancers. Here we examined the expression and sublocalization of DR5 in gastric cancer, as well as its effects on clinical prognosis and cellular processes. Our analysis included a cohort of 240 gastric cancer patients. Bioinformatic analysis showed a significant correlation between DR5 and DNA replication, tumor mutation burden (TMB), and tumor stemness. Unlike death receptor 4 (DR4TRAIL-R1), DR5 was expressed in the cytoplasm and nucleus, and was found to be positively correlated with lymphovascular invasion, lymph node metastasis, and TNM stage. Patients with positive DR5 had worse overall survival (OS) (P = 0.006). The multivariate Cox model showed that DR5 is an independent poor prognostic factor (hazard ratio = 1.693). Furthermore, knockdown of DR5 inhibited aggressive behaviors, including proliferation and metastasis in gastric cancer cells, and inhibited lung metastasis in vivo. In summary, nuclear localization of DR5 expression is a poor prognosis factor in gastric cancer and promotes growth, invasion, and metastasis of tumor cells in vitro and in vivo.

非小细胞肺癌(NSCLC)的发病率和死亡率均位于恶性肿瘤的前列.节拍化疗的抗肿瘤机制主要为抑制肿瘤血管生成、调节免疫微环境和针对肿瘤细胞自身等.作为传统化疗的替代方案,节拍化疗在晚期NSCLC的治疗中展现出良好前景,多个临床试验探索了节拍化疗在晚期NSCLC治疗中的应用,方案包括单药或与化疗、抗血管生成治疗、靶向治疗及免疫治疗等的联合使用.现对节拍化疗的抗肿瘤作用机制及其在晚期NSCLC治疗中的临床应用进行综述,为NSCLC治疗方案的优化提供更多证据.

AbstractBackgroundVariants in the ATP binding cassette protein subfamily D member 1 (ABCD1) gene are known to cause X‐linked adrenoleukodystrophy (X‐ALD). This study focused on the characteristics of ABCD1 variants in Chinese X‐ALD families and elucidated the value of genetic approaches for X‐ALD.Methods68 male probands diagnosed as X‐ALD were screened for ABCD1 variants by the Sanger sequencing of polymerase chain reaction (PCR) products and multiplex ligation‐dependent probe amplification (MLPA) combined with long‐range PCR. Prenatal diagnosis was performed in 20 foetuses of 17 probands’ mothers. Descriptive statistics were used to summarise the gene variants and prenatal diagnosis characteristics and outcomes.ResultsThis study allowed the identification of 61 variants occurring in 68 families, including 58 single nucleotide variants or small deletion/insertion variants and 3 large deletions. Three probands with no variants detected by next‐generation sequencing were found to have variants by PCR‐sequencing. Prenatal diagnosis found that 10 of the 20 foetuses had no variants in ABCD1.ConclusionPCR primers that do not amplify the pseudogenes must be used for PCR‐sequencing. MLPA combined with long‐range PCR can detect large deletions and insertions, which are usually undetectable by PCR‐sequencing. Prenatal diagnosis could help to prevent the birth of infants with X‐ALD.

Background: Deoxyribonucleic acid (DNA) methyltransferase inhibitors, such as decitabine, have made great advances in cancer therapy as combinational drugs. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has an obvious anti-tumor effect; however, some gastric cancer (GC) cells are resistant to TRAIL-induced cell death. This study sought to explore the synergistic anti-tumor effect of TRAIL and decitabine, and the potential synergetic mechanism. Methods: The cell growth inhibition effect was monitored by the IncuCyte ZOOM Live-Cell Analysis System, and cell viability was determined by Cell Counting Kit- 8 assays. Apoptosis was detected by Annexin V/Propidium Iodide double staining. Death receptor 4 (DR4) was knocked down by ribonucleic acid (RNA) interference, and the effect of DR4 deletion on TRAIL sensitivity was analyzed. Methylationspecific polymerase chain reaction (PCR) was applied to determine the methylation status of DR4. The messenger RNA (mRNA) and protein expression levels were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. The expression of the DRs on the cell membrane surfaces was analyzed by flow cytometry. Results: The combined use of decitabine and TRAIL synergistically inhibited cell growth in 2 TRAILresistant cell lines. Further, decitabine augmented TRAIL-induced apoptosis in a caspase-dependent manner. The co-application of decitabine and TRAIL facilitated the activation of caspase-7, -8, -9, and poly ADPribose polymerase (PARP). Notably, decitabine increased the expression of DR4 at the transcriptional and post-transcriptional levels. DR4 expression on the cell membrane surfaces was also upregulated after decitabine exposure. The depletion of DR4 by specific inhibitors attenuated TRAIL-induced apoptosis and weakened the synergistic effects of decitabine and TRAIL. In addition, DR4 gene presented methylation status in SNU-1 cells. The low mRNA and protein expression of DR4 were also detected in SNU-1 cells. Conclusions: Decitabine enhances the effect of TRAIL by inhibiting the growth and inducing the apoptosis of GC cells. This is achieved by the epigenetic modification of decitabine, which upregulates DR4. Decitabine may act as a sensitizing agent of TRAIL. The combined use of decitabine and TRAIL may provide a novel idea for GC treatment.

In this report, we show that Epstein–Barr virus (EBV)-infected lymphoblastoid cell lines (LCL) express Fas and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor 2 and that LCL are lysed following engagement of these receptors by agonist Fas and TRAIL receptor-specific monoclonal antibodies (MAb). We also show that EBV-specific CD4+ T cells mediate bystander lysis of susceptible targets through both the Fas/Fas ligand (FasL) and the TRAIL pathways, but find that the dominant mechanism of lysis following cognate, HLA class II-restricted recognition of LCL is the perforin/granzyme pathway. Killing of LCL by EBV-specific CD4+ T cells was strongly inhibited by concanamycin A, an agent that elevates granule pH, resulting in accelerated destabilization and degradation of perforin. In contrast, blocking anti-FasL MAb showed only limited inhibition of LCL killing. Blocking anti-TRAIL MAb had no effect on lysis of LCL by EBV-specific CD4+ T cells. We further show that culture of EBV-specific CD4+ T cells in the presence of interleukin 4 markedly abrogates effector cytotoxic function against LCL through direct depletion of intracellular perforin, with no evidence of a Th1 to Th2 shift in patterns of cytokine expression.

Objective:Immunologic characteristics of differed between younger and older patients.This study aimed to screen potentially key genes related to tumor-infiltrated immune cells(TIICs)in senile patients with lung adenocarcinoma(LUAD).Methods:In this retrospective study, the gene expression data for the training set were extracted from the Cancer Genome Atlas(TCGA)database, and the GSE72094 data set from Gene Expression Database was selected as the validation set.The 91 LUAD patients aged ≥75 years and 14 matched normal samples were screened for analysis.The components of tumor infiltrated immune cells(TIICs)were estimated by the deconvolution algorithm.Then a weighted gene co-expression network analysis was conducted in the training set so as to identify key genes correlating to TIICs.The GSE72094 dataset was used for validation.Results:In elderly patients with LUAD, the high expressions of IKZF1 and PRKCB were related to autoimmune diseases and T cell receptor signaling pathway.And their gene encoding proteins could interact with various immunomodulatory factors, such as IL2RB, LCK, and CD5.In the high expression group of IKZF1 and PRKCB, the expression levels of immunological checkpoint genes such as PD-L1, PD-1 and CTLA-4 were significantly higher than those of the low expression group(all P<0.01). The results of the validation set showed that CD8 + T cells were significantly correlated with the expression of IKZF1( r=0.75, P<0.01)and PRKCB( r=0.65, P<0.01). Conclusions:The expressions of IKZF1 and PRKCB in the tumor tissues are related to tumor infiltrating CD8 T cells and expression of immune checkpoint genes in elderly patients with LUAD.

Objective:To explore the role of parental origin verification in chromosomal microarray analysis (CMA) on the determination of the clinical significance of copy number variations (CNVs).Methods:This retrospective study collected clinical information from 73 core families who underwent prenatal diagnosis at Peking University First Hospital from November 2017 to December 2019. Indications for prenatal diagnosis included ultrasound abnormality in 54 cases (including 12 with thickened nuchal translucency (≥2.5 mm), four with fetal growth restriction, seven with abnormal pregnancy history, and 31 with isolated ultrasound abnormality), NIPT indicated high-risk in four cases, advanced age in nine cases, abnormal pregnancy history alone in three cases, intrauterine death in two cases and one with maternal mental retardation. Genomic DNA of amniotic fluid sample, chorionic villi, cord blood, fetal tissues, and fetal heart blood were extracted using genomic DNA extraction kit. The CNVs of prenatal samples in 73 subjects were analyzed using array-based comparative genomic hybridization (array-CGH) analysis and single nucleotide polymorphism array (SNP-array). Peripheral blood DNA of the couples, and relevant families if necessary, were collected and analyzed in the same way. The results of parental origin detection in CMA were summarized.Results:A total of 76 CNVs were detected in these 73 samples, out of which nine were pathogenic and parental origin detection revealed that six were de novo, two were maternally, and one was paternally inherited; six CNVs were likely pathogenic, including three de novo, two maternally inherited and one paternally inherited; 20 CNVs were variants of uncertain significance, including five paternally inherited, three maternally inherited and 12 de novo; 41 CNVs were likely benign, among which 38 were inherited from parents with normal phenotype. Conclusions:Parental origin verification plays an important role in explaining the clinical significance of detected fetal CNVs and thereby can help to analyze its clinical effect and reproductive risk.

Objective:To investigate the expression changes of farnesoid X receptor (FXR) in the evolution of normal intestinal mucosa, colorectal adenoma (CRA) and colorectal cancer (CRC), and the correlation of FXR expression with clinicopathological features and prognosis of patients with colorectal tumors.Methods:The UALCAN website tool was used to analyze the expression level of FXR gene transcripts of CRC and normal colorectal tissues in The Cancer Genome Atlas (TCGA) database. The patients undergoing colonoscopy and treatment in the Aerospace Center Hospital from January 2019 to September 2020 were selected, and the immunohistochemistry was used to detect the expression of FXR protein in 100 CRA tissues, 47 CRC tissues and 11 normal colonic mucosal tissues from healthy people (healthy control). Combining with clinical data, the relationship between FXR protein expression and clinicopathological characteristics of patients with colorectal tumors was analyzed. According to the Kaplan-Meier Plotter online database, the median expression level of FXR gene transcripts in CRC patients was analyzed, and the patients were divided into FXR low-expression group and high-expression group, the relationship between the expression of FXR gene and prognosis of CRC patients was investigated.Results:The analysis of data from TCGA database showed that the expression level of FXR gene transcripts in CRC tissues was lower than that in normal colorectal tissues ( P < 0.01). Immunohistochemical examination of the collected tissues showed that the positive rate of FXR protein gradually decreased from the cecum to the rectum. The positive rates of FXR protein in healthy control, CRA patients and CRC patients were 90.9% (10/11), 24.0% (24/100), 6.3% (3/47), and the difference was statistically significant ( χ2 = 35.56, P < 0.01); the positive rate of FXR protein in cancer tissues from CRC patients was lower than that in normal tissues adjacent to cancer [6.3% (3/47) vs. 65.2% (15/23)], and the difference was statistically significant ( χ2 = 27.98, P < 0.01). There was no statistical difference in the positive rate of FXR among CRA patients with different gender, age, maximum diameter of adenoma, and aggression (all P > 0.05). There was also no statistical difference in the positive rate of FXR among CRC patients with different gender, age, tumor site, maximum diameter of tumor, degree of differentiation, TNM staging, and vascular tumor thrombus (all P > 0.05). According to the survival analysis of Kaplan-Meier Plotter online database, the recurrence-free survival of CRC patients with high expression of FXR was better than that of patients with low expression of FXR ( P = 0.003). Conclusions:The expression level of FXR gradually decreases in the intestinal tissues of healthy people, CRA patients and CRC patients. The prognosis of CRC patients with low FXR expression is poor.

Objective To determine changes in mitochondrial DNA (mtDNA) copy number in peripheral blood in Rett syndrome caused by methyl-CpG-binding protein-2 (MECP2) variants and explore the mechanism of mitochondrial dysfunction in Rett syndrome. Study design Female patients who were diagnosed with Rett syndrome and had an MECP2 variant (n = 142) were recruited in this study, along with the same number of age- and sex-matched healthy controls. MtDNA copy number was quantified by real-time quantitative polymerase chain reaction with TagMan probes. The differences in mtDNA copy number between the Rett syndrome group and the control group were analyzed using the independent-samples t test. Linear regression, biserial correlation analysis, and one-way ANOVA were applied for the correlations between mtDNA copy number and age, clinical severity, variant types, functional domains, and hot-spot variants. Results MtDNA copy number was found to be significantly increased in the patients with Rett syndrome with MECP2 gene variants compared with the control subjects. Age, clinical severity, variant types, functional domains, and hot-spot variants were not related to mtDNA copy number in patients with Rett syndrome. Conclusions MtDNA copy number is increased significantly in patients with Rett syndrome, suggesting that changes in mitochondrial function in Rett syndrome trigger a compensatory increase in mtDNA copy number and providing new possibilities for treating Rett syndrome, such as mitochondria-targeted therapies.

Objective:To summarize the characteristics of genetic variation and prenatal diagnosis in pedigrees with X-linked adrenoleukodystrophy (X-ALD) and elucidate the value of prenatal diagnosis in preventing the birth of children with X-ALD.Methods:Twenty pedigrees, clinically diagnosed with X-ALD in Peking University First Hospital from November 2012 and March 2019, were included in this retrospective study. Genomic DNA was extracted from peripheral blood and amniotic fluid or chorionic villi samples of probands and their families for detecting variants in ATP-binding cassette subfamily D member 1 ( ABCD1) gene using polymerase chain reaction (PCR)-Sanger sequencing. Linkage analysis was also performed on five microsatellite markers near ABCD1 gene to exclude maternal contamination. Characteristics of ABCD1 gene variants and prenatal diagnosis of X-ALD pedigrees were summarized by descriptive statistics. Results:Twenty ABCD1 gene variants were identified in the 20 pedigrees. The variants in three probands that were not detected by next-generation sequencing were identified by PCR-Sanger sequencing. Among the mothers of the 20 probands, 17 carried ABCD1 variants and three did not. We performed 24 prenatal diagnoses on 20 pregnancies (24 fetuses) and identified eight fetuses with variants who were finally terminated. The 16 cases without variants were born alive. The validation results obtained after termination or delivery were consistent with those performed prenatally. Conclusions:No hotspot variants in ABCD1 gene are detected in these X-ALD patients and most variants are maternally inherited. PCR-Sanger sequencing is an effective method for detecting ABCD1 variants. Prenatal diagnosis for mothers who had a body with X-ALD could prevent another one from birth.

Objective:To study the value of chromosome microarray analysis (CMA) application in children with developmental delay (DD), intellectual disability (ID), autistic spectrum disorder (ASD) and multiple congenital anomalies (MCA).Methods:Genomic DNA was extracted from peripheral blood samples. Array-based comparative genomic hybridization (array-CGH) analysis and single nucleotide polymorphism array (SNP-array) were performed in 1 320 children with DD/ID, ASD, with or without epilepsy and MCA who were admitted to Peking University First Hospital from 2014 to 2019. The results of genetic etiology test of CMA in children with mental retardation or global DD was summarized.Results:Of 1 320 samples, there were 10 cases of aneuploid abnormality, 6 cases of uniparental disomy and one case of mosaicism, respectively. Pathogenic copy number variations (CNVs) were found in 320 cases and pathogenic CNVs were detected in 23 cases, with a combined detection rate of 26% (343/1 320). CNVs of uncertain clinical significance occurred in 107 cases, accounting for 8.1% (107/1 320). There were 25 cases of possible benign CNVs, accounting for 2% (25/1 320), while benign CNVs were reported in 20 cases, accounting for 1.5% (20/1 320). The detection rate of MCA with DD/ID was 39.8% (130/327).Conclusions:CMA has the advantages of high resolution and covering the whole genome. It can detect the chromosomal abnormalities, microdeletions and duplications seen under the microscope, thus the genetic etiology of children with mental retardation or global DD can be diagnosed.

目的 检测肿瘤坏死因子相关凋亡诱导配体(TRAIL)对胃癌细胞的杀伤作用及其受体在胃癌细胞中的表达情况,评估TRAIL信号在胃癌治疗中的可行性.方法 研究选取11株胃癌细胞进行实验,采用实时荧光定量PCR方法检测胃癌细胞中TRAIL相关受体(DR4、DR5、DcR1、DcR2)mRNA表达.采用Cell Counting Kit-8(CCK-8)法检测TRAIL抑制胃癌细胞生长,Annexin V/PI双染色法测定TRAIL诱导细胞凋亡,Western blot检测TRAIL介导Caspase裂解.结果 死亡受体DR4、DR5在11株胃癌细胞内普遍高表达,表达水平显著高于诱骗受体DcR1、DcR2.TRAIL对9株胃癌细胞有不同程度的生长抑制作用,SNU-16、NUGC3、NCI-N87和SNU-1灵敏度最高,抑制作用呈时间和剂量依赖性.TRAIL通过诱导细胞凋亡发挥肿瘤杀伤作用,低浓度TRAIL(200 ng/ml)作用24 h后50％以上细胞发生凋亡.Caspase-3、-8、-9和PARP的裂解水平与凋亡程度相关.结论 TRAIL对胃癌细胞具有不同程度的生长抑制和凋亡诱导作用,在胃癌中具有潜在应用价值.

目的 通过回顾电子结肠镜检出结肠憩室患者的资料,分析结肠憩室发病特点及其与伴发疾病的相关性.方法 回顾性分析2014年6月-2019年5月该院13638例行电子结肠镜检查的内镜资料,采用SPSS 19.0统计软件分析结肠憩室患者检出情况及内镜下组织表现,以及其与伴发疾病的相关性.结果 共发现结肠憩室379例,检出率为2.78％,呈逐年升高趋势,由1.79％增长至3.35％,第5年较第1年检出率明显提高(P<0.05).结肠憩室发病与结肠息肉、结肠癌、结肠脂肪瘤、结肠黏膜黑变病和肠道手术史呈正相关(P<0.05),与缺血性结肠炎无明显相关性(P>0.05).结论 5年间电子结肠镜下结肠憩室检出率明显升高,结肠憩室检出率与结肠息肉、结肠癌、结肠脂肪瘤、结肠黑变病及肠道手术史均有相关性.

本文总结了1例因穿刺部位选择不当导致桡神经损伤的护理经验,包括药物治疗、物理治疗、心理干预以及预防措施等.

本文主要总结了1例宫颈炎症性肌纤维母细胞肿瘤(IMT)患者的围手术期护理经验,包括术前的入院介绍、护理评估、疾病讲解以及术前准备,术后的体位摆放、饮食指导、管道管理、疼痛干预、并发症防治等.

目的 评估2014年《中国早期胃癌筛查及内镜诊治共识意见》关于胃癌高危人群筛查在不同地区的适用性及有效性.方法 选取2018年1月至2018年6月就诊于安阳市人民医院和航天中心医院消化内科的患者,通过问卷调查方式采集胃癌相关高危因素信息,根据《共识意见》分为高危组及低危组,经胃镜及病理检查确认,比较两组患者胃癌、癌前疾病及癌前病变的检出情况,并分析胃癌高危因素.结果 384例患者根据《共识意见》分为胃癌高危组265例(69.0％)、低危组119例(31.0％).高危组患者胃癌、癌前病变检出率均为9.4％(25/265),显著高于低危组胃癌(1.7％,2/119)和癌前病变检出率(3.4％,4/119)(P<0.01),《共识意见》对胃癌的敏感性为92.6％,特异性为32.8％;高危组患者问卷调查中危险因素符合项数主要体现为2～3项,其中胃癌前疾病史及不良饮食习惯是胃癌发病的独立危险因素.结论 2014年《中国早期胃癌筛查及内镜诊治共识意见》在不同地区医院内筛查胃癌高危人群的适用性相同,其敏感性高而特异性及总符合率较低.与其他高危因素相比,既往癌前疾病史、吃饭速度快及饮食不规律与胃部疾病相关性更高.