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 dete...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.展开更多
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 stag...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 or<sup>14</sup>C 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,Area<sub>1</sub>:748±572,302±202 μm<sup>2</sup>,Area<sub>2</sub>:3050±1661,1681±1990 μm<sup>2</sup>,all P【0.05;Ellipseb:79±23,58±15 μm,Ratio<sub>1</sub>:22%±5%,13%±4%,Ratio<sub>2</sub>: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 展开更多
目的通过检测慢性胃炎、肠化生、不典型增生和胃癌组织中幽门螺杆菌(Hp)感染、蛋白激酶C(PKC)水平、细胞增殖水平以及p53突变基因表达状态探讨Hp感染在胃癌发生中的作用及其作用机制。方法采用病例对照研究,病例来源于中山医院,经内镜...目的通过检测慢性胃炎、肠化生、不典型增生和胃癌组织中幽门螺杆菌(Hp)感染、蛋白激酶C(PKC)水平、细胞增殖水平以及p53突变基因表达状态探讨Hp感染在胃癌发生中的作用及其作用机制。方法采用病例对照研究,病例来源于中山医院,经内镜和病理检查证实。Hp感染采用快速尿素酶和病理Gimsa染色检测。PKC的检测采用免疫组化EnVision^(TM)法,增殖细胞核抗原(PCNA)、突变型p53基因表达的检测采用免疫组织化学方法。结果①总的Hp感染的检出率为76.2％(138/181)。在慢性胃炎肠化生组、不典型增生组、胃癌组分别为62.0％(31/50),88.6％(39/44),78.3％(68/87),均明显高于单纯慢性胃炎对照组52.6％(20/38,P<0.05)。②PCNA增殖指数在三组病例中均处于高水平,且Hp阳性组均高于Hp阴性组。③突变型p53基因表达在肠上皮化生、不典型增生和胃癌组阳性率分别为36.0％(18/50),54.6％(24/44),57.2％(48/84)。不典型增生和胃癌组均明显高于肠上皮化生组。在肠化生组,Hp阳性病例的P53表达率明显高于Hp阴性病例(48.5％ vs15.8％,P=0.020)。但在不典型增生和胃癌组,Hp阳性与Hp阴性病例的P53突变蛋白表达率无明显差别(53.9％ vs60.0％,P=0.794;53.8％ vs 68.4％,P=0.258)。P53表达与PCNA增殖指数有明显的相关性。④PKC在慢性胃炎伴肠化生、不典型增生和胃癌组阳性表达的比例呈递增趋势,分别为16.0％,28.5％,41.8％,对照组的阳性表达率不足5％。Hp阳性组PKC表达阳性率(47/130,36.2％)高于Hp阴性组(6/41,14.6％.P=(0.010)。PKC表达组,其P53表达的阳性率和阳性表达程度均高于PKC无表达的病例,在肠化生组统计学检验差异有显著性(75.0％ vs 28.6％,P=0.012),不典型增生(66.7％ vs 50.0％,P=0.430)和胃癌(63.6％ vs 52.2％,P=0.310)统计学检验差异无显著性。结论在从慢性胃炎到肠上皮化生、不典型增生、胃癌的发生过程中,存在PKC表达水平的增高、P展开更多
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.
基金the Natural Science Foundation of the Educational Committee of Jiangsu Province,No.125FA9608.
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 or<sup>14</sup>C 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,Area<sub>1</sub>:748±572,302±202 μm<sup>2</sup>,Area<sub>2</sub>:3050±1661,1681±1990 μm<sup>2</sup>,all P【0.05;Ellipseb:79±23,58±15 μm,Ratio<sub>1</sub>:22%±5%,13%±4%,Ratio<sub>2</sub>: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
文摘目的通过检测慢性胃炎、肠化生、不典型增生和胃癌组织中幽门螺杆菌(Hp)感染、蛋白激酶C(PKC)水平、细胞增殖水平以及p53突变基因表达状态探讨Hp感染在胃癌发生中的作用及其作用机制。方法采用病例对照研究,病例来源于中山医院,经内镜和病理检查证实。Hp感染采用快速尿素酶和病理Gimsa染色检测。PKC的检测采用免疫组化EnVision^(TM)法,增殖细胞核抗原(PCNA)、突变型p53基因表达的检测采用免疫组织化学方法。结果①总的Hp感染的检出率为76.2％(138/181)。在慢性胃炎肠化生组、不典型增生组、胃癌组分别为62.0％(31/50),88.6％(39/44),78.3％(68/87),均明显高于单纯慢性胃炎对照组52.6％(20/38,P<0.05)。②PCNA增殖指数在三组病例中均处于高水平,且Hp阳性组均高于Hp阴性组。③突变型p53基因表达在肠上皮化生、不典型增生和胃癌组阳性率分别为36.0％(18/50),54.6％(24/44),57.2％(48/84)。不典型增生和胃癌组均明显高于肠上皮化生组。在肠化生组,Hp阳性病例的P53表达率明显高于Hp阴性病例(48.5％ vs15.8％,P=0.020)。但在不典型增生和胃癌组,Hp阳性与Hp阴性病例的P53突变蛋白表达率无明显差别(53.9％ vs60.0％,P=0.794;53.8％ vs 68.4％,P=0.258)。P53表达与PCNA增殖指数有明显的相关性。④PKC在慢性胃炎伴肠化生、不典型增生和胃癌组阳性表达的比例呈递增趋势,分别为16.0％,28.5％,41.8％,对照组的阳性表达率不足5％。Hp阳性组PKC表达阳性率(47/130,36.2％)高于Hp阴性组(6/41,14.6％.P=(0.010)。PKC表达组,其P53表达的阳性率和阳性表达程度均高于PKC无表达的病例,在肠化生组统计学检验差异有显著性(75.0％ vs 28.6％,P=0.012),不典型增生(66.7％ vs 50.0％,P=0.430)和胃癌(63.6％ vs 52.2％,P=0.310)统计学检验差异无显著性。结论在从慢性胃炎到肠上皮化生、不典型增生、胃癌的发生过程中,存在PKC表达水平的增高、P
