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| 1 | Function of apoptosis and expression of the proteins Bcl-2,p53 and C-myc in the development of gastric cancer显示文摘INTRODUCTIONIn China ,the incidence and mortality of gastric cancer rank the second among all cancers. Recent development of cancer [1-20].The aim of this study was investigat the insight of apoptosis and bcl-2, p53 and C-myc protein expression in the development of gastric cancer . | An Gao Xu Shao Guang Li Ji Hong Liu Ai Hua Gan Research Laboratory of Digestive Disease,Huizhou Central People’s Hospital,Huizhou 516001,Guangdong Province,ChinaDr.An Gao Xu graduated from Guangdong Medical College in 1984.He is an associate physician-in-chief,specializing in the research and treatment of gastrointestinal and liver tumors.He has published 24 papers and 1 book. | 2001 | World Journal of Gastroenterology2001，7，3： | 91 |
| 2 | Effect of phosphorylation of MAPK and Stat3 and expression of c-fos and c-jun proteins on hepatocarcinogenesis and their clinical significance显示文摘AIM To study the effect of phosphorylation ofMAPK and Stat3 and the expression of c-fos andc-jun proteins on hepatocellular carcinogenesisand their clinical significance.METHODS SP immunohistochemistry was usedto detect the expression of p42/44MAPK, p-Stat3,c-fos and c-jun proteins in 55 hepatocellularcarcinomas (HCC) and their surrounding livertissues.RESULTS The positive rates and expressionlevels of p42/44MAPK, p-Stat3, c-fos and c-junproteins in HCCs were significantly higher thanthose in pericarcinomatous liver tissues (PCLT).A positive correlation was observed between theexpression of p42/44MAPK and c-fos proteins, andbetween p-Stat3 and c-jun, but there was nosignificant correlation between p42/44MAPK and p-Stat3 in HCCs and their surrounding livertissues.CONCLUSION The abnormalities of Ras/Rat/MAPK and JAKs/ Stat3 cascade reaction maycontribute to malignant transformation ofhepatocytes. Hepatocytes which are positive forp42/ 44MAPK, c-fos or c-jun proteins may bepotential malignant pre-cancerous cells.Activation of MAPK and Stat3 proteins may be anearly event in hepatocellular carcinogenesis. | De Yun Feng Hui Zheng Yi Tan Rui Xue Cheng Department of Pathology, Hunan Medical University, Changsha 410078, Hunan Province, China New England Biolab, MA, USA | 2001 | World Journal of Gastroenterology2001，7，1： | 75 |
| 3 | Multiple genetic alterations and behavior of cellular biology in gastric cancer and other gastric mucosal lesions:H.pylori infection,histological types and staging显示文摘AIM To investigate the expression of multiplegenes and the behavior of cellular biology ingastric cancer(GC)and other gastric mucosallesions and their relations to Helicobacter pylori(H.pylori)infection,tumor staging andhistological subtypes.METHODS Three hundred and twenty-sevenspecimens of gastric mucosa obtained viaendoscopy or surgical resection,and ABCimmunohistochemical staining were used todetect the expression of p53,p16,Bcl-2 andCOX-2 proteins.H.pylori was determined byrapid urea test combined with pathologicalstaining or14C urea breath test.Cellular image analysis was performed in 66 patients withintestinal metaplasia(IM)and/or dysplasia(Dys).In 30 of them,both cancer and theparacancerous tissues were obtained at the timeof surgery.Histological pattern,tumor staging,lymph node metastasis,grading ofdifferentiation and other clinical data werestudied in the medical records.RESULTS p16 expression of IM or Dys wassignificantly lower in positive H.pylori chronicatrophic gastritis(CAG)than those withnegative H.pylori(CAG:54.8% vs 88.0%,IM:34.4% vs 69.6%,Dys:23.8% vs 53.6%,allP<0.05),Bcl-2 or COX-2 expression of IM orDys in positive H.pylori cases was significantlyhigher than that without H.pylori(Bcl-2:68.8%vs23.9%,90.5% vs 60.7%;COX-2:50.0% vs10.8%,61.8% vs 17.8%;all P<0.05).Themean number of most parameters of cellularimage analysis in positive H.pylori group wassignificantly higher than that in negative H.pylori group(Ellipser:53±14,40±12μm,Area1:748±572,302±202 μm2,Area2:3050±1661,1681±1990 μm2,all P<0.05;Ellipseb:79±23,58±15 μm,Ratio1:22%±5%,13%±4%,Ratio2:79%±17%,53%±20%,all P<0.01).There was significant correlation between Bcl-2and histologic pattern of gastric carcinoma,andbetween COX-2 and tumor staging or lymph nodemetastasis(Bcl-2:75.0% vs 16.7%;COX-2:76.0% vs 20.0%,79.2% vs 16.7%;allP<0.05).CONCLUSION p1l6, Bcl-2, and COX-2 but not p53 gene may play a role in the early genesis/ progression of gastric carcinoma and are associated with H. pylori infection. p53 gene is relatively late event in gastric tumorigenesis and mainly relates to its progression. There is more cellular-biological behavior of malignant tumor in gastric mucosal lesions with H. pylori infection. Aberrant Bcl-2 protein expression appears to be preferentially associated with the intestinal type cancer. COX-2 seems to be related to tumor staging and lymph node metastasis. | Heng Jun Gao Lian Zhen Yu Jian Feng Bai Yan Shen Peng Gu Sun Han Lin Zhao Kun Miu Xiu Zhen Lü Xiao Yong Zhang Zhi Quan Zhao | 2000 | World Journal of Gastroenterology2000，6，6： | 52 |
| 4 | Apoptosis,proliferation and p53 gene expression of H.pylori associated gastric epithelial lesions显示文摘AIM: To study the relationship between Helicobacter pylori (H. Pylori) and gastric carcinoma and its possible pathogenesis by H. Pylori.METHODS: DNEL technique and immunohistochemical technique were used to study the state of apoptosis,proliferation and p53 gene expression. A total of 100 gastric mucosal biopsy specimens, including 20 normal mucosa, 30H. Pylori-negative and 30 H. Pylorf-positive gastric precancerous lesions along with 20 gastric carcinomas were studied.RESULTS: There were several apoptotic cells in the superficial epithelium and a few proliferative cells within the neck of gastric glands, and no p53 protein expression in normal mucosa. In gastric carcinoma, there were few apoptotic cells, while there were a large number of proliferative cells, and expression of p53 protein significantly was increased. In the phase of metaplasia, the apoptotic index (Al, 4.36% ± 1.95%), proliferative index (PI, 19.11% ± 6.79%) and positivity of p53 expression (46.7%) in H. Pylori-positive group were higher than those in normal mucosa (P< 0.01). Al in H. Pylori-positive group was higher than that in H. Pylori-negative group (3.81% ±1.76%), PI in H. Pylori-positive group was higher than that in H. Pylori-negative group (12.25% ±5.63%, P<0.01 ). In the phase of dysplasia, Al (2.31% ± 1.10%) in H. Pylori-positive group was lower (3.05% ± 1.29%) than that in H. Pylori-negative group, but PI (33.89% ± 11.65%)wassignificantly higher(22.09± 8018%, P< 0.01). In phases of metaplasia, dysplasia and gastric cancer in the H. Pylori-positive group, Als had an evidently graduall decreasing trend (P < 0.01 ), while Pis had an evidently gradual increasing trend (P< 0.05 or P< 0.01), and there was also a trend of gradual increase in the expression of p53 gene.CONCLUSION: In the course of the formation of gastric carcinoma, proliferation of gastric mucosa can be greatly increased by H. Pylori, and H. Pylori can induce apoptosis in the phase of metaplasia but in the phase of dysplasia H.pylori can inhibit cellular apoptosis. And H. Pylori infection can strengthen the expression of mutated p53 gene. | Zhong Zhang~1 Yuan Yuan Hua Gao Ming Dong Lan Wang Yue-Hua Gong 1 Department of Pathology,Shenyang Medical College,Shenyang 110031 Liaoning Province,China | 2001 | World Journal of Gastroenterology2001，7，6： | 46 |
| 5 | Research of Helicobacter pylori infection in precancerous gastric lesions显示文摘INTRODUCTION Helicobacter pylori(Hp)infection has beenconsidered to play significant roles in pathogenesisof peptic ulcer.Additionally Hp is associated withthe development of gastric epithelial hyperplasiaand lymphoid malignancies.The InternationalAgency for Research on Cancer has classified lip asa class Ⅰ carcinogen and a definite cause of gastriccancer in humans.Hp infection first causes chronicactive gastritis and may slowly lead to infection ofwhole stomach.In the late stages of infection,mucosal atrophy and intestinal metaplasia(IM), | Xiao Qiang Zhuang San Ren Lin | 2000 | World Journal of Gastroenterology2000，6，3： | 24 |
| 6 | Narrow-band imaging with magnifying endoscopy is accurate for detecting gastric intestinal metaplasia显示文摘AIM:To investigate the predictive value of narrowband imaging with magnifying endoscopy (NBI-ME) for identifying gastric intestinal metaplasia (GIM) in unselected patients. METHODS:We prospectively evaluated consecutive patients undergoing upper endoscopy for various indications, such as epigastric discomfort/pain, anaemia, gastro-oesophageal reflux disease, suspicion of peptic ulcer disease, or chronic liver diseases. Patients underwent NBI-ME, which was performed by three blinded, experienced endoscopists. In addition, five biopsies (2 antrum, 1 angulus, and 2 corpus) were taken and examined by two pathologists unaware of the endoscopic findings to determine the presence or absence of GIM. The correlation between light blue crest (LBC) appearance and histology was measured. Moreover, we quantified the degree of LBC appearance as less than 20% (+), 20%-80% (++) and more than 80% (+++) of an image field, and the semiquantitative evaluation of LBC appearance was correlated with IM percentage from the histological findings. RESULTS:We enrolled 100 (58 F/42 M) patients who were mainly referred for gastro-esophageal reflux disease/dyspepsia (46%), cancer screening/anaemia (34%), chronic liver disease (9%), and suspected celiac disease (6%); the remaining patients were referred for other indications. The prevalence of Helicobacter pylori (H. pylori ) infection detected from the biopsies was 31%, while 67% of the patients used proton pump inhibitors. LBCs were found in the antrum of 33 patients (33%); 20 of the cases were classified as LBC+, 9 as LBC++, and 4 as LBC+++. LBCs were found in the gastric body of 6 patients (6%), with 5 of them also having LBCs in the antrum. The correlation between the appearance of LBCs and histological GIM was good, with a sensitivity of 80% (95%CI:67-92), a specificity of 96% (95%CI:93-99), a positive predictive value of 84% (95%CI:73-96), a negative predictive value of 95% (95%CI:92-98), and an accuracy of 93% (95%CI:90-97). The NBI-ME examination overlooked GIM in 8 cases, but the GIM was less than 5% in 7 of the cases. Moreover, in the 6 false positive cases, the histological examination showed the presence of reactive gastropathy (4 cases) or H. pylori active chronic gastritis (2 cases). The semiquantitative correlation between the rate of LBC appearance and the percentage of GIM was 79% (P < 0.01). CONCLUSION:NBI-ME achieved good sensitivity and specificity in recognising GIM in an unselected population. In routine clinical practice, this technique can reliably target gastric biopsies. | Edoardo Savarino Marina Corbo Pietro Dulbecco Lorenzo Gemignani Elisa Giambruno Luca Mastracci Federica Grillo Vincenzo Savarino | 2013 | World Journal of Gastroenterology2013，19，17： | 23 |
| 7 | Identifying high-risk individuals for gastric cancer surveillance from western and eastern perspectives: Lessons to learn and possibility to develop an integrated approach for daily practice显示文摘Current evidence shows that individuals with gastric dysplasia, severe and extensive gastric atrophy, extensive gastric intestinal metaplasia and the incomplete subtype of intestinal metaplasia are at high risk for gastric cancer(GC) development. There are several approaches to identifying these subjects,including noninvasive methods, esophagogastroduodenoscopy and histology.The main approach in Western countries is histology-based while that in Eastern countries with a high prevalence of GC is endoscopy-based. Regarding asymptomatic individuals, the key issues in selecting applicable approaches are the ability to reduce GC mortality and the cost-effectiveness of the approach. At present, population-based screening programs have only been applied in a few Asian countries with a high risk of GC. Pre-endoscopic risk assessment based on demographic and clinical features, such as ethnicity, age, gender, smoking and Helicobacter pylori status, is helpful for identifying subjects with high pre-test probability for a possibly cost-effective approach, especially in intermediate-and low-risk countries. Regarding symptomatic patients with indications for esophagogastroduodenoscopy, the importance of opportunistic screening should be emphasized. The combination of endoscopic and histological approaches should always be considered as endoscopy provides a real-time assessment of the patient’s risk level. In addition, imaging enhanced endoscopy(IEE) has been shown to facilitate targeted biopsies resulting in better correlation between endoscopic and histological findings. Currently, the use of IEE is recommended for endoscopic examinations, and the Operative Link for Gastric Intestinal Metaplasia or Operative Link on Gastritis Assessment grading systems are recommended for histological examinations whenever available. However,resource limitations are an important barrier in many regions worldwide. Thus,for an approach to be applicable in real-life practice, it should be not only evidence-based but also resource-sensitive. In this review, we discuss the current understanding and approaches to identifying high-risk individuals from western and eastern perspectives, as well as the possibility of an integrated, resourcesensitive approach. | Duc Trong Quach Toru Hiyama Takuji Gotoda | 2019 | World Journal of Gastroenterology2019，25，27： | 18 |
| 8 | Study on the risk factors of lymphatic metastasis and the indications of less invasive operations in early gastric cancer显示文摘INTRODUCTIONThe principle of surgical treatment for gastric cancer is theradical resectioning although the suitable resetting range fordifferent cases of gastric cancer is still being arguedupon.However,the diagnostic accuracy of | Jiang BJ Sun RX Lin H Gao YF | 2000 | World Journal of Gastroenterology2000，6，4： | 15 |
| 9 | A preliminary study on ras protein expression in human esophageal cancer and precancerous lesions显示文摘INTRODUCTIONThe esophageal carcinoma is a common malignanttumor in Linzhou City (Linxian) of Henan Provincein northern China.Although the etiology andnatural history of csophageal carcinoma are notclear,a substantial amount of evidence has beenprovided to suggest that the development of humanesophageal squamous cell carcinomas (SCC) is amultistage progressive process.An | Jian Li Chang Wei Feng Zhi Guo Zhao Qi Zhou Li Dong Wang | 2000 | World Journal of Gastroenterology2000，6，2： | 15 |
| 10 | Changes of p53 and Waf1p21 and cell proliferation in esophageal carcinogenesis显示文摘Changesofp53andWaf1p21andcelproliferationinesophagealcarcinogenesisWANGLiDong1,YANGWanCai1,ZHOUQi1,XINGYing1,JIAYunYing2a... | WANG Li Dong 1, YANG Wan Cai 1, ZHOU Qi 1, XING Ying 1,JIA Yun Ying 2 and ZHAO Xin 1 | 1997 | World Journal of Gastroenterology1997，3，2： | 15 |
| 11 | Expression of p-STAT3 and vascular endothelial growth factor in MNNG-induced precancerous lesions and gastric tumors in rats显示文摘AIM: To investigate the dynamic expression of p-signal transducer and activator of transcription 3(STAT3) and vascular endothelial growth factor(VEGF) in the formation of gastric tumors induced by drinking water containing N-methyl-N'-nitro-N-nitrosoguanidine(MNNG) in Wistar rats.METHODS: One hundred and twenty Wistar rats were randomly divided into two groups(60 in each group): Control group and Model group. The rats in each group were then randomly divided into three groups(20 in each group): C/M15, C/M25 and C/M40(15, 25 and 40 represent the number of feeding weeks from termination). Rats in the control group received normal drinking water and rats in the model group received drinking water containing 100 μg/m L MNNG. Stomach tissues were collected at the end of the 15 th, 25 th and 40 th week, respectively, for microscopic measurement using hematoxylin and eosin staining. The expression of p-STAT3 and VEGF in different pathological types of gastric tissue, including normal, inflammation, atrophy, hyperplasia and gastric stromal tumor, was observed by immunohistochemistry and Western blot, and the corelation between p-STAT3 and VEGF was analyzed. RESULTS:(1) The expression of p-STAT3 in tissue with gastritis, atrophy, dysplasia and gastric stromal tumor were significantly increased in the model group compared with the control group(2.5 ± 1.0, 2.75 ±0.36, 6.2 ± 0.45, 5.67 ± 0.55 vs 0.75 ± 0.36, P = 0.026, 0.035, 0.001, 0.002, respectively); the expression of p-STAT3 in tissue with dysplasia was higher than that in samples with gastritis or atrophy(6.2 ± 0.45 vs 2.5 ± 1.0, P = 0.006; 6.2 ± 0.45 vs 2.75 ± 0.36, P = 0.005, respectively); however, the expression of p-STAT3 in gastritis and atrophy was not significantly different(P > 0.05);(2) the expression of VEGF in tissue with gastritis, atrophy, dysplasia and gastric stromal tumor was significantly increased in the model group compared with normal gastric mucosa; and the expression of VEGF in tissue with dysplasia was higher than that in tissue with inflammation and atrophy(10.8 ± 1.96 vs 7.62 ± 0.25, P = 0.029; 10.8 ± 1.96 vs 6.26 ± 0.76, P = 0.033, respectively); similarly, the expression of VEGF in tissue with gastritis and atrophy was not significantly different(P > 0.05); and(3) the expression of VEGF was positively correlated with p-STAT3. CONCLUSION: p-STAT3 plays an important role in gastric cancer formation by regulating the expression of VEGF to promote the progression of gastric tumor from gastritis. | Xiao-Yan Wang Lou-Lei Wang Xuan Zheng Li-Na Meng Bin Lyu Hai-Feng Jin | 2016 | World Journal of Gastrointestinal Oncology2016，8，3： | 14 |
| 12 | Latest developments in precancerous lesions of hepatocellular carcinoma显示文摘Hepatocarcinogenesis in human chronic liver diseases is a multi-step process in which hepatic precancerous lesions progress into early hepatocellular carcinoma(HCC) and progressed HCC, and the close surveillance and treatment of these lesions will help improve the survival rates of patients with HCC. The rapid development and extensive application of imaging technology have facilitated the discovery of nodular lesions of ambiguous significance, such as dysplastic nodules. Further investigations showed that these nodules may be hepatic precancerous lesions, and they often appear in patients with liver cirrhosis. Although the morphology of these nodules is not sufficient to support a diagnosis of malignant tumor, these nodules are closely correlated with the occurrence of HCC, as indicated by long-term follow-up studies. In recent years, the rapid development and wide application of pathology, molecular genetics and imaging technology have elucidated the characteristics of precancerous lesions. Based on our extensive review of the relevant literature, this article focuses on evidence indicating that high-grade dysplastic nodules are more likely to transform into HCC than low-grade dysplastic nodules based on clinical, pathological, molecular genetic and radiological assessments. In addition, evidence supporting the precancerous nature of large cell change in hepatitis B virus-related HCC is discussed. | Zhao-Shan Niu Xiao-Jun Niu Wen-Hong Wang Jing Zhao | 2016 | World Journal of Gastroenterology2016，22，12： | 13 |
| 13 | Expression and significance of Musashi-1 in gastric cancer and precancerous lesions显示文摘AIM:To investigate expression of stem cell marker Musashi-1(Msi-1)in relationship to tumorigenesis and progression of intestinal-type gastric cancer(GC).METHODS:Endoscopic biopsy specimens and surgical specimens were obtained,including 54 cases of intestinal-type GC,41 high-grade intraepithelial neoplasia,57low-grade intraepithelial neoplasia,31 intestinal metaplasia,and 36 normal gastric mucosa.Specimens were fixed in 10%paraformaldehyde,conventionally dehydrated,embedded in paraffin,and sliced in 4-μm-thick serial sections.Two-step immunohistochemical staining was used to detect Msi-1 and proliferating cell nuclear antigen(PCNA)expression.Correlation analysis was conducted between Msi-1 and PCNA expression.The relationship between Msi-1 expression and clinicopathological parameters of GC was analyzed statistically.RESULTS:There were significant differences in Msi-1and PCNA expression in different pathological tissues(χ2=15.37,P<0.01;χ2=115.36,P<0.01).Msi-1and PCNA-positive cells were restricted to the isthmus of normal gastric glands.Expression levels of Msi-1and PCNA in intestinal metaplasia were significantly higher than in normal mucosa(U=392.0,P<0.05;U=40.50,P<0.01),whereas there was no significant difference compared to low or high-grade intraepithelial neoplasia.Msi-1 and PCNA expression in intestinaltype GC was higher than in high-grade intraepithelial neoplasia(U=798.0,P<0.05;U=688.0,P<0.01).There was a significantly positive correlation between Msi-1 and PCNA expression(rs=0.20,P<0.01).Msi-1expression in GC tissues was correlated with their lymph node metastasis and tumor node metastasis stage(χ2=12.62,P<0.01;χ2=11.24,P<0.05),but not with depth of invasion and the presence of distant metastasis.CONCLUSION:Msi-1-positive cells may play a key role in the early events of gastric carcinogenesis and may be involved in invasion and metastasis of GC. | Rong-Guang Kuang Yan Kuang Qing-Feng Luo Cheng-Jun Zhou Rui Ji Jian-Wen Wang | 2013 | World Journal of Gastroenterology2013，19，39： | 12 |
| 14 | Factors affecting occurrence of gastric varioliform lesions: A case-control study显示文摘AIM: To investigate the factors influencing the occurrence of gastric varioliform lesions(GVLs) and their possible link with gastric cancer.METHODS: A 1:1 matched case-control study was performed to retrospectively analyze data from 1638 chronic gastritis patients who had undergone gastroscopy at one of two Chinese hospitals between 2009 and 2014. Patients with GVLs(cases) were compared to those without such lesions(controls). Endoscopic and pathological findings were recorded, along with interview information on Helicobacter pylori(H. pylori) infection, medical, drug and family histories, lifestyle and eating habits. The association between each factor and the occurrence of GVLs was estimated, and then multivariate conditional logistic regression was used to evaluate the independent factors.RESULTS: The frequency and severity of glandular atrophy, intestinal metaplasia(IM) and low-grade intraepithelial neoplasia were significantly increased in the GVL group(P < 0.01). Overall analysis showed that H. pylori infection [3.051(2.157, 4.317), P <0.001], allergic respiratory diseases [3.636(2.183, 6.055), P < 0.001], work-related stress [2.019(1.568, 2.600), P < 0.001], irregular meals [2.300(1.462, 3.619), P < 0.001], high intake of spicy food [1.754(1.227, 2.507), P = 0.002] and high intake of fresh fruit [0.231(0.101, 0.529), P = 0.001] were significantly correlated with the occurrence of GVLs(positively, except for the latter). Stratified analyses indicated that pickled food consumption in patients over 50 years old [7.224(2.360, 22.115), P = 0.001] and excessive smoking in men [2.013(1.282, 3.163), P = 0.002] were also positively correlated, and that, for antral GVLs, vegetable consumption [0.491(0.311, 0.776), P = 0.002] was negatively correlated. CONCLUSION: Seven risk factors and two protective factors are determined for GVLs, which were found to be associated with premalignant abnormalities. | Tian-Hui Zou Ru-Hua Zheng Qin-Yan Gao Xuan Kong Xiao-Yu Chen Zhi-Zheng Ge Ying-Xuan Chen Xiao-Ping Zou Jing-Yuan Fang | 2016 | World Journal of Gastroenterology2016，22，22： | 9 |
| 15 | Signal transducer and activator of transcription 3 promotes the Warburg effect possibly by inducing pyruvate kinase M2 phosphorylation in liver precancerous lesions显示文摘BACKGROUND Study shows that signal transducer and activator of transcription 3(STAT3) can increase the Warburg effect by stimulating hexokinase 2 in breast cancer and upregulate lactate dehydrogenase A and pyruvate dehydrogenase kinase 1 in myeloma. STAT3 and pyruvate kinase M2(PKM2) can also be activated and enhance the Warburg effect in hepatocellular carcinoma. Precancerous lesions are critical to human and rodent hepatocarcinogenesis. However, the underlying molecular mechanism for the development of liver precancerous lesions remains unknown. We hypothesized that STAT3 promotes the Warburg effect possibly by upregulating p-PKM2 in liver precancerous lesions in rats.AIM To investigate the mechanism of the Warburg effect in liver precancerous lesions in rats.METHODS A model of liver precancerous lesions was established by a modified Solt-Farber method. The liver pathological changes were observed by HE staining and immunohistochemistry. The transformation of WB-F344 cells induced with Nmethyl-N'-nitro-N-nitrosoguanidine and hydrogen peroxide was evaluated by the soft agar assay and aneuploidy. The levels of glucose and lactate in the tissue and culture medium were detected with a spectrophotometer. The protein levels of glutathione S-transferase-π, proliferating cell nuclear antigen(PCNA), STAT3,and PKM2 were examined by Western blot and immunofluorescence.RESULTS We found that the Warburg effect was increased in liver precancerous lesions in rats. PKM2 and p-STAT3 were upregulated in activated oval cells in liverprecancerous lesions in rats. The Warburg effect, p-PKM2, and p-STAT3 expression were also increased in transformed WB-F344 cells. STAT3 activation promoted the clonal formation rate, aneuploidy, alpha-fetoprotein expression,PCNA expression, G1/S phase transition, the Warburg effect, PKM2 phosphorylation, and nuclear translocation in transformed WB-F344 cells.Moreover, the Warburg effect was inhibited by stattic, a specific inhibitor of STAT3, and further reduced in transformed WB-F344 cells after the intervention for PKM2.CONCLUSION The Warburg effect is initiated in liver precancerous lesions in rats. STAT3 activation promotes the Warburg effect by enhancing the phosphorylation of PKM2 in transformed WB-F344 cells. | Yang-Hui Bi Wen-Qi Han Ruo-Fei Li Yun-Jiao Wang Zun-Shu Du Xue-Jiang Wang Ying Jiang | 2019 | World Journal of Gastroenterology2019，25，16： | 8 |
| 16 | Experimental study on model establishment,mechanism of production,and reverse therapy of gastric mucosal precancerous lesions显示文摘Experimentalstudyonmodelestablishment,mechanismofproduction,andreversetherapyofgastricmucosalprecancerouslesionsinrats￥LiChun... | 李春启 刘为纹 房殿春 | 1994 | Journal of Medical Colleges of PLA(China)1994，9，2： | 8 |
| 17 | Role of gene polymorphisms in gastric cancer and its precursor lesions:Current knowledge and perspectives in Latin American countries显示文摘Latin America shows one of the highest incidence rates of gastric cancer in the world,with variations in mortality rates among nations or even within countries belonging to this region.Gastric cancer is the result of a multifactorial complex process,for which a multistep model of carcinogenesis is currently accepted.Additionally to the infection with Helicobacter pylori,that plays a major role,environmental factors as well as genetic susceptibility factors are significant players at different stages in the gastric cancer process.The differences in population origin,demographic structure,socio-economic development,and the impact of globalization lifestyles experienced in Latin America in the last decades,all together offer opportunities for studying in this context the influence of genetic polymorphisms in the susceptibility to gastric cancer.The aim of this article is to discuss current trends on gastric cancer in Latin American countries and to review the available published information about studies of association of gene polymorphisms involved in gastric cancer susceptibility from this region of the world.A total of 40 genes or genomic regions and69 genetic variants,58%representing markers involved in inflammatory response,have been used in a number of studies in which predominates a low number of individuals(cases and controls)included.Polymorphisms of IL-1B(-511 C/T,14 studies;-31 T/C,10 studies)and IL-1RN(variable number of tandem repeats,17 studies)are the most represented ones in the reviewed studies.Other genetic variants recently evaluated in large metaanalyses and associated with gastric cancer risk were also analyzed in a few studies[e.g.,prostate stem cell antigen(PSCA),CDH1,Survivin].Further and better analysis centered in gene polymorphisms linked to other covariates,epidemiological studies and the information provided by meta-analyses and genome-wide association studies should help to improve our understanding of gastric cancer etiology in order to develop appropriate health programs in Latin America. | Miguel Angel Chiurillo | 2014 | World Journal of Gastroenterology2014，20，16： | 6 |
| 18 | Gastric precancerous lesions are associated with gene variants in Helicobacter pylori -susceptible ethnic Malays显示文摘AIM: To identify genes associated with gastric pre-cancerous lesions in Helicobacter pylori (H. pylori )susceptible ethnic Malays. METHODS: Twenty-three Malay subjects with H. pylori infection and gastric precancerous lesions identified during endoscopy were included as 'cases'. Thirtyseven Malay subjects who were H. pylori negative and had no precancerous lesions were included as 'controls'. Venous blood was collected for genotyping with Affymetrix 50K Xba1 kit. Genotypes with call rates < 90% for autosomal single nucleotide polymorphisms (SNPs) were excluded. For each precancerous lesion, associated SNPs were identified from Manhattan plots, and only SNPs with a χ2 P value < 0.05 and Hardy Weinberg Equilibrium P value > 0.5 was considered as significant markers. RESULTS: Of the 23 H. pylori -positive subjects recruited, one sample was excluded from further analysis due to a low genotyping call rate. Of the 22 H. pylori positive samples, atrophic gastritis only was present in 50.0%, complete intestinal metaplasia was present in 18.25%, both incomplete intestinal metaplasia and dysplasia was present in 22.7%, and dysplasia only was present in 9.1%. SNPs rs9315542 (UFM1 gene), rs6878265 (THBS4 gene), rs1042194 (CYP2C19 gene) and rs10505799 (MGST1 gene) were significantly associated with atrophic gastritis, complete intestinal metaplasia, incomplete metaplasia with foci of dysplasia and dysplasia, respectively. Allele frequencies in 'cases' vs 'controls' for rs9315542, rs6878265, rs1042194 and rs10505799 were 0.4 vs 0.06, 0.6 vs 0.01, 0.6 vs 0.01 and 0.5 vs 0.02, respectively. CONCLUSION: Genetic variants possibly related to gastric precancerous lesions in ethnic Malays susceptible to H. pylori infection were identified for testing in subsequent trials. | Sathiya Maran Yeong Yeh Lee Shuhua Xu Nur-Shafawati Rajab Norhazrini Hasan Syed Hassan Syed Abdul Aziz Noorizan Abdul Majid Bin Alwi Zilfalil | 2013 | World Journal of Gastroenterology2013，19，23： | 5 |
| 19 | Abnormal Change of p53 Gene in Gastric and PrecancerousLesions and APC Gene Deletion in Gastric Carcinoma and Near Tissues显示文摘p53 gene mutation (exon4, 5, 6, 7, 8 and intron6) in gastric cancer and precancerous lesions and p53 gene (exon4 and ontron6), APC gene deletion in gastric carcinomas were studied by PCR/SSCP and PCR/RFLP- Results showed mutation rate of p53 in metaplasia, dysplasia and gastric carcinoma was 37. 5 % (3/8), 42. 11 % (8/19), 53. 33 (16/30) respectively- There was significant dif-ference among groups of metaplasia, dysplasia, cancer and normal controls. Noexon8 mutation was found in metaplasia and dysplasia, but 4 cases were found to have exon8 mutation in cancer group. It is suggested that exon8 mutation occurs at the late stage of gastric cancer, but exon 5, 6, 7 mutation occur in the course ofprecancerous lesion to cancer. Loss of heterozygosity (LOH) of exon4, intron6,APC was 47,37 % (9/19), 8. 73% (2/23), 16. 67 % (3/18) respectively. LOH of exon4 had something to do with poor differentiation, lymph node metastasis,depth of invasion- LOH of exon4 may be one of prognostic marker of gastric cancer. We are led to conclude that p53 gene mutation is an early event and perhaps work together with ras oncogene in gastric | 郝莹 张锦坤 易粹琼 钱伟 | 1997 | Journal of Huazhong University of Science and Technology(Medical Sciences)1997，17，2： | 5 |
| 20 | Effect of transplantation of BMMSCs on pathological change of gastric precancerous lesions of rats显示文摘Objective:To build the rat model of gastric precancerous lesions and discuss the effect of transplantation of mesenchymal stem cells(BMMSCs) on the pathological change.Methods:The rat model of gastric precancerous lesions was built using N-methyl-N-nitro-N-nitrosoguanidine.After the intravenous transplantation of BMMSCs,the migration and colonization location was then observed,as well as its effect on the related factors of gastric precancerous lesions,including VEGF,IL-10 and IFN-γ.Results:BMMSCs were mainly colonized in the gastric body and gastric antrum,which could be differentiated into the epithelial and interstitial cells.The expression of VEGF in the transplantation group and non-transplantation group was significantly higher than that in the control group(P<0.05);while the expression of VEGF in the transplantation group was significantly higher than that in the non-transplantation group(t=3.88,P<0.001).The expression of serum IL-10 and IFN- y in the transplantation group and non-transplantation group was significantly higher than that in the control group(P<0.05).while the expression of IL-10 and IFN-γ in the transplantation group was significantly lower than that in the non-transplantation group(t=3.03,P=0.004;t=3.80.P<0.001).Conclusions:BMMSCs can be directionally differentiated into the epithelial and interstitial cells and can also regulate the related growth factors and inflammatory factors to reduce the injury of inflammation,relieve or reverse the process of gastric precancerous lesions. | Zhen-Lv Lin Guang-Wei Zheng Lin Zhang Jian-Tao Zheng Hui Chen | 2015 | Asian Pacific Journal of Tropical Medicine2015，8，12： | 5 |
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