胃癌染色体17p微卫星不稳定性及突变型p53蛋白的表达

目的研究微卫星不稳定性（ＭＳＩ）及突变型ｐ５３基因在胃癌发生中的作用。方法采用ＰＣＲ为基础的方法及免疫组织化学技术检测了５０例手术切除胃癌标本染色体１７ｐ的ＭＳＩ及突变型ｐ５３蛋白的表达。结果胃癌ＭＳＩ总阳性率为３４％（１７／５０），突变型ｐ５３蛋白表达阳性率为３６％，其中高－中分化腺癌ＭＳＩ阳性率（６６．７％）显著高于低分化腺癌（１９．４％，Ｐ＜０．０１）；肠型胃癌ＭＳＩ阳性率（５５．６％）显著高于胃型胃癌（２０％，Ｐ＜０．０５）。ＭＳＩ与胃癌部位、大小、浸润、分期及突变型ｐ５３蛋白的表达无显著相关性。结论研究提示，ＭＳＩ在胃癌的发生中心能起重要作用，其作用机制可能不同于由突变型ｐ５３基因介导的致癌机制。     

人胃癌组织中金属蛋白酶类基因的过度表达

目的探讨组织金属蛋白酶家族成员在人胃癌组织中的表达．方法应用免疫组织化学（ＳＰ法）和原位杂交（ｃＤＮＡｍＲＮＡ）技术对４１例人胃癌１７例癌旁组织中的金属蛋白酶ＭＭＰ２，ＭＭＰ９及ＭＴＭＭＰ基因表达进行检测．结果ＭＭＰ２及ＭＴＭＭＰ蛋白在胃癌及癌旁组织阳性率分别为７３１％（３０／４１），６５８％（２７／４１）和２２５％（４／１７），４１１％（７／１７）．胃癌及癌旁组织ＭＭＰ２，ＭＭＰ９及ＭＭＰＭＴｍＲＮＡ阳性率分别为７０７％（２９／４１），５１２％（２１／４１），５６０％（２３／４１）和２３５％（４／１７），２３５％（４／１７），３５２％（６／１７）．一致性检验显示基因的免疫组化和原位杂交检验结果的关系密切（Ｐ＜００５）．结论ＭＭＰｓ基因的过度表达参与了胃癌的发生发展过程，ＭＭＰｓ的免疫组化是检测胃癌组织侵袭、转移倾向的可靠方法．     

胃癌及消化性溃疡患者胃窦粘膜胃肠激素的变化

目的探讨胃癌及消化性溃疡（ＰＵ）患者胃窦粘膜胃肠激素变化的意义．方法内镜及活检确诊的浅表性胃炎（ＣＳＧ）１０例，胃溃疡（ＧＵ）１５例，十二指肠溃疡（ＤＵ）１２例，胃癌（ＧＣ）６例．胃镜下取胃窦粘膜，用ＲＩＡ法测定胃泌素（Ｇａｓ）、生长抑素（ＳＳ）、Ｐ物质（ＳＰ）的含量，各组间进行比较．结果胃窦粘膜ＳＳ含量在ＧＵ，ＤＵ，ＣＳＧ，ＧＣ组分别为２５１ｐｇ／ｍｇ±１９４ｐｇ／ｍｇ（以下同），４７０±１７９，５３２±２１１及１２９３±５２３。其中ＧＵ组低于其余各组（Ｐ＜００５），而ＧＣ时则显著升高（Ｐ＜００１）．ＳＰ含量在ＤＵ组显著降低，与ＧＵ，ＣＳＧ，ＧＣ比较分别为４７９±１５７ｖｓ７６５±４１５，７８９±３９０及８０１±３４６，Ｐ＜００５；ＧＣ患者Ｇａｓ水平显著高于ＣＳＧ组，为４６４５±２９４４，ｖｓ２７６８±１５７２，Ｐ＜００１．结论胃粘膜中Ｇａｓ，ＳＳ，ＳＰ含量的变化可能在ＰＵ及胃癌的发病机理中起重要作用．     

胃癌微卫星不稳定性研究

为了研究微卫星不稳定性（ＭＳＩ）在胃癌发生中的作用，使用ＰＣＲ为基础的方法检测５０例胃癌活检标本的ＭＳＩ。结果发现：胃癌ＭＳＩ阳性率为３４％（１７／５０），其中两个位点ＭＳＩ均阳性者占ＭＳＩ阳性病例的５８．８％（１０／１７），３例早期胃癌ＭＳＩ均阳性，进展期胃癌ＭＳＩ阳性率为２９．８％（１４／４７）。中—高分化腺癌ＭＳＩ阳性率（６０％）显著高于低分化腺癌（１９．４％）（Ｐ＜０．０５）。ＭＳＩ与胃癌部位、大小、Ｌａｕｒｅｎｓ分型、淋巴结转移、浆膜浸润及分期无明显相关。以上结果提示，ＭＳＩ在胃癌的发生中可能起重要作用，是胃癌的一种早期分子标志。检测ＭＳＩ可能成为胃癌高危人群的筛选、胃癌早期诊断的有用指标     

p53 C-myc和P-gp蛋白在胃癌细胞中表达

目的研究胃癌组织中ｐ５３和Ｃｍｙｃ的表达与多药耐药性（ＭＤＲ）的关系．方法应用ＬＳＡＢ免疫组织化学方法研究６７例（男４１例，女２６例，平均年龄４６±１５８岁）胃癌标本中ｐ５３，Ｃｍｙｃ和Ｐｇｐ的表达．结果本组胃癌中ｐ５３阳性３２例（４７８％），Ｃｍｙｃ阳性３７例（５５２％），Ｐｇｐ阳性３９例（５８２％）．淋巴结转移阳性胃癌ｐ５３阳性率（５６９％）和Ｃｍｙｃ阳性率（６４７％）显著高于淋巴结转移阴性的胃癌（Ｐ＜００５）．ｐ５３的异常表达与ｍｄｒ１基因表达呈显著正相关（ｒ＝０６３，Ｐ＜００５），而Ｃｍｙｃ和ｍｄｒ１的表达无明显相关．结论ｐ５３异常表达可增加ｍｄｒ１基因的表达，从而使胃癌细胞获得ＭＤＲ表型     

胃食管癌患者血浆和癌组织中表皮生长因子和生长抑素的含量

目的研究表皮生长因子（ＥＧＦ）和生长抑素（ＳＳ）与胃食管癌的关系．方法本组９５例，年龄７８岁～２４岁，男６３例，女３２例；胃癌４３例，食管癌２２例，正常对照组３０例．血浆及粘膜中ＥＧＦ和ＳＳ测定采用ＲＩＡ法测定．结果①血浆（μｇ／Ｌ）和癌组织（μｇ／ｇ）ＥＧＦ含量在胃癌（３２８５±９４６和１３５３３±３８４１）和食管癌（２８６１±１０５１和１５０７０±２９５５）显著高于正常人（１０４７±４６和５１０１±１７７０，Ｐ＜００１）．②血浆（ｎｇ／Ｌ）和癌组织（ｎｇ／ｇ）ＳＳ的含量在胃癌（１１２４±５１１和１３０１８±３７７３）和食管癌（１７８７±５３１和４４４１±１３２６）显著低于正常人（２８４１±６７７和２１７４６±５０８７，Ｐ＜００１）．结论胃食管癌患者存在ＥＧＦ和ＳＳ分泌异常，可能与癌肿形成有关．     

胃癌组织5q微卫星不稳定性与APC/MCC基因杂合性缺失的研究

目的探讨５ｑ微卫星不稳定性（ＭＳＩ）与ＡＰＣ／ＭＣＣ基因杂合缺失（ＬＯＨ）的关系。方法应用ＰＣＲ－ＳＳＬＰ及ＰＣＲ－ＲＦＬＰ技术分析５２例手术切除胃癌组织中ＭＳＩ及ＡＰＣ／ＭＭＣ基因ＬＯＨ。结果５ｑＭＳＩ检出率为３４．０％（１６／４７）,ＡＰＣ／ＭＣＣ基因ＬＯＨ率为３１．４％（１１／３５）。早期胃癌５ｑＭＳＩ阳性率为６６．７％（２／３）,ＡＰＣ／ＭＣＣＬＯＨ率为５０％（１／２）;进展期分别为３１．８（１４／４４）,３０．３％（１０／３３）。两组间无显著差别（Ｐ＞０．０５）。ＭＳＩ及杂合缺失与肿瘤大小、浸润深度、淋巴结转移及临床分期无关。粘液（印戒）细胞癌ＡＰＣ／ＭＣＣＬＯＨ率（５５．６％）显著高于高、中分化管状腺癌（Ｐ＜０．０５）。胃、肠两型胃癌５ｑＭＳＩ及ＡＰＣ／ＭＣＣＬＯＨ差异无显著性及５ｑＭＳＩ与ＡＰＣ／ＭＣＣＬＯＨ无相关性（Ｐ＞０．０５）。结论染色体５ｑＭＳＩ有ＡＰＣ／ＭＣＣ基因ＬＯＨ在两型胃癌的早期发生及发展中起一定作用。染色体５ｑ可能是胃癌的易感部位。     

自由基在实验性胃癌及癌前病变发生中的作用

目的探讨自由基在胃癌及其癌前病变发生中的作用．方法将１００只Ｗｉｓｔａｒ大鼠分为２组，实验组（７０只），给予１００ｍｇ／Ｌ甲基硝基亚硝基胍（ＭＮＮＧ）水溶液自由饮用３０ｗｋ，对照组（３０只）饮用自来水．选５个时相点，动态观察ＭＮＮＧ诱发实验性胃癌及其癌前病变过程中大鼠体内丙二醛（ＭＤＡ）、脂质过氧化物（ＬＰＯ）、谷胱甘肽过氧化物酶（ＧＳＨＰＸ）及超氧化物歧化酶（ＳＯＤ）等的变化情况．结果在实验组，ＭＤＡ平均含量在５２ｗｋ非常显著地大于０ｗｋ（Ｐ＜００１），并显著地大于１６ｗｋ以前（Ｐ＜００５）．胃癌组织ＭＤＡ含量显著高于胃癌癌前病变组织（Ｐ＜００５）．癌组织ＬＰＯ的含量显著高于癌前病变组织（Ｐ＜００５）．实验组，总ＳＯＤ和ＣｕＺｎＳＯＤ活性在５２ｗｋ明显低于１６ｗｋ之前（分别为Ｐ＜００５和Ｐ＜００１）．癌组织ＣｕＺｎＳＯＤ含量非常显著地小于正常胃粘膜（Ｐ＜００１），亦明显低于胃粘膜异型增生和肠上皮化生（Ｐ＜００５）．在３０ｗｋ和５２ｗｋＧＳＨＰＸ活性显著低于１６ｗｋ以前．结论自由基在实验性胃癌及其癌前病变发生中具有一定作用，自由基清除剂可能对胃癌的综合防治具有积极意义     

原发性肝癌雌激素受体表达及内分泌治疗

目的研究原发性肝癌雌激素受体（ＥＲ）的表达及内分泌治疗的临床价值．方法应用Ｌｅｅ氏荧光配体细胞化学法检测４１例手术病理确诊的原发性肝癌ＥＲ的表达．本组男３８例，女３例，年龄２５岁～７２岁．同时检测肝癌的组织类型、分化程度、肿瘤大小、血清ＡＦＰ及ＣＥＡ．６例ＥＲ阳性者采用他莫昔芬治疗（每次２０ｍｇ，２次／ｄ，长期服用）并观察疗效．结果肝癌组织ＥＲ阳性２０／４１例，阳性率４８８％．ＥＲ阳性率与患者年龄、性别、ＡＦＰ、ＣＥＡ含量及组织类型（梁状型ＥＲ阳性４５０％，腺样型３３３％，实体型７１４％，硬化型６６７％，透明细胞型２５０％；Ｐ＞００５）无明显关系，与肿瘤体积（≥１０ｃｍ，ＥＲ阳性率７５０％；＜１０ｃｍ，ＥＲ阳性２３８％；Ｐ＜００１）和分化程度（分化好２６例，ＥＲ阳性３４６％；分化差１５例，ＥＲ阳性７３３％；Ｐ＜００５）有显著关系．本组ＥＲ阳性病例中６例经他莫昔芬内分泌治疗有效５／６（８３３％），其中４例ＡＦＰ下降．结论ＥＲ阳性肝细胞癌患者进行内分泌治疗有一定疗效     

梗阻性黄疸内毒素血症与细胞免疫功能的关系

目的研究梗阻性黄疸免疫功能及其与内毒素血症的相关性．方法检测２８例梗阻性黄疸患者及２０例健康对照者血清内毒素，Ｔ淋巴细胞亚群及血清ＳＩＬ２Ｒ的水平．结果梗阻性黄疸患者血清内毒素和ＳＩＬ２Ｒ水平较对照组明显升高（４７０ｎｇ／Ｌ±１１３ｎｇ／Ｌ和７２５ｋＵ／Ｌ±２０１ｋＵ／Ｌｖｓ２８４ｎｇ／Ｌ±１０３ｎｇ／Ｌ和３２４ｋＵ／Ｌ±１１６ｋＵ／Ｌ，Ｐ＜００１），Ｔ淋巴细胞亚群ＣＤ３，ＣＤ４，ＣＤ４／ＣＤ８明显降低（５０４％±３３％和２９９％±３８％ｖｓ６３８％±４４％和３８３％±２８％，Ｐ＜００１；１２２±０３２ｖｓ１４３±０３７，Ｐ＜００５），同时亦发现梗阻性黄疸内毒素血症组较非内毒素血症组ＣＤ３，ＣＤ４水平明显减低，ＳＩＬ２Ｒ水平明显升高（４７４％±５１％和２７６％±５２％和８６７ｋＵ／Ｌ±２３１ｋＵ／Ｌｖｓ５２３％±５２％和３１２％±４３％和６７４ｋＵ／Ｌ±１８９ｋＵ／Ｌ，Ｐ＜００５）．相关分析显示血清内毒素水平与血清ＳＩＬ２Ｒ水平呈显著正相关（ｒ＝０８５１７，Ｐ＜００１）．结论梗阻性黄疸时内毒素血症与免疫功能状态密切相关．     

Expression, deletion [was deleton] and mutation of p16 gene in human gastric cancer

AIM: To investigate the relationship between the expression of p16 gene and the gastric carcinogenesis, depth of invasion and lymph node metastases, and to evaluate the deletion and mutation of exon 2 in p16 gene in gastric carcinoma. METHODS: The expression of p16 protein was examined by streptavidin-peroxidase conjugated method (S-P);the deletion and mutation of p16 gene were respectively examined by polymerase chain reaction (PCR) and polymerase chain reaction single-strand conformation polymorphism analysis (PCR-SSCP) in gastric carcinoma. RESULTS: Expression of p16 protein was detected in 96.25% (77/80) of the normal gastric mucosa, in 92.00% (45/50) of the dysplastic gastric mucosa and in 47.54% (58/122) of the gastric carcinoma. The positive rate of p16 protein expression in gastric carcinoma was significantly lower than that in normal gastric mucosa and dysplastic gastric mucosa (P < 0.05). The positive rate of p16 protein expression in mucoid carcinoma 10.00% (1/10) was significantly lower than that in poorly differentiated carcinoma 51.22% (21/41), undifferentiated carcinoma 57.69% (15/26) and signet ring cell carcinoma 62.50% (10/16) (P < 0.05). The positive rate of p16 protein in 30 cases paired primary and lymph node metastatic gastric carcinoma: There was 46.67% (14/30) in primary gastric carcinoma, 16.67% (5/30) in lymph node metastatic gastric carcinoma. The positive rate of lymph node metastatic carcinoma was significantly lower than that of primary carcinoma (P < 0.05). There was of p16 gene mutation in exon 2, but 5 cases displayed deletion of p16 gene in exon 2 in the 25 primary gastric carcinomas. CONCLUSIONS: The expression loss of p16 protein related to the gastric carcinogenesis, gastric carcinoma histopathological subtypes and lymph metastasis. The mutation of p16 gene in exon 2 may not be involved in gastric carcinogenesis. But the deletion of p16 gene in exon 2 may be involved in gastric carcinogenesis.     

Expression, deleton and mutation of p16 gene in human gastric cancer

AIM To investigate the relationship between the expression of p16 gene and the gastric carcinogenesis,depth of invasion and lymph node metastases, and to evaluate the deletion and mutation of exon 2 in p16 gene in gastric carcinoma. METHODS The expression of P16 protein was examined by streptavidin-peroxidase conjugated method (S-P); the deletion and mutation of p16 gene were respectively examined by polymerase chain reaction (PCR) and polymerase chain reaction single-strand conformation polymorphism analysis (PCR-SSCP) in gastric carcinoma. RESULTS Expression of P16 protein was detected in 96.25% (77/80) of the normal gastric mucosa, in 92.00% (45/50) of the dysplastic gastric mucosa and in 47.54% (58/122) of the gastric carcinoma. The positive rate of P16 protein expression in gastric carcinoma was significantly lower than that in normal gastric mucosa and dysplastic gastric mucosa (P＜0.05). The positive rate of P16 protein expression in mucoid carcinoma 10.00% (1/ 10) was significantly lower than that in poorly differentiated carcinoma 51.22% ( 21/ 41 ),undifferentiated carcinoma 57.69% (15/26) and signet ring cell carcinoma 62.50% (10/ 16) (P＜0.05). The positive rate of p16 protein in 30 cases paired primary and lymph node metastatic gastric carcinoma: There was 46.67% (14/30) in primary gastric carcinoma, 16.67% (5/30) in lymph node metastatic gastric carcinoma. The positive rate of lymph node metastatic carcinoma was significantly lower than that of primary carcinoma (P＜0.05). There was of p16 gene mutation in exon 2, but 5 cases displayed deletion of p16 gene in exon 2 in the 25 primary gastric carcinomas. CONCLUSIONS The expression loss of P16 protein related to the gastric carcinogenesis, gastric carcinoma histopathological subtypes and lymph metastasis. The mutation of p16 gene in exon 2 may not be involved in gastric carcinogenesis. But the deletion of p16 gene in exon 2 may be involved in gastric carcinogenesis.     

Study of differential polymerase chain reaction of C-erbB-2 oncogene amplification in gastric cancer

ＭＥＴＨＯＤＳＣｅｒｂＢ２ｏｎｃｏｇｅｎｅａｍｐｌｉｆｉｃａｔｉｏｎｗａｓｅｘａｍｉｎｅｄｂｙｕｓｉｎｇｄｉｆｅｒｅｎｔｉａｌｐｏｌｙｍｅｒａｓｅｃｈａｉｎｒｅａｃｔｉｏｎ（ｄＰＣＲ）ｉｎｓｕｒｇｉｃａｌａｎｄｅｎｄｏｓｃｏｐｉｃｓｐｅｃｉｍｅｎ...     

Expression of bcl-2 protein in gastric carcinoma and its significance

Ｅｘｐｒｅｓｓｉｏｎｏｆｂｃｌ２ｐｒｏｔｅｉｎｉｎｇａｓｔｒｉｃｃａｒｃｉｎｏｍａａｎｄｉｔｓｓｉｇｎｉｆｉｃａｎｃｅＬＩＵＨａｉＦｅｎｇ,ＬＩＵＷｅｉＷｅｎ,ＦＡＮＧＤｉａｎＣｈｕｎａｎｄＭＥＮＲｏｎｇＰｕＳｕｂｊｅｃｔｈｅａｄｉｎｇｓ...     

Expression and significance of proapoptotic gene Bax in gastric carcinoma

ＩＮＴＲＯＤＵＣＴＩＯＮＲｅｃｅｎｔｉｎｖｅｓｔｉｇａｔｉｏｎｓｈａｖｅｄｅｍｏｎｓｔｒａｔｅｄｔｈａｔａｐｏｐｔｏｓｉｓｐｌａｙｓａｓｉｇｎｉｆｉｃａｎｔｒｏｌｅｉｎｔｈｅｐａｔｈｏｇｅｎｅｓｉｓｏｆｔｕｍｏｒｓ［１,２］．Ｅｍｐｈａｓｉｓｈａｓ...     

胃癌及癌前病变粘膜中呈高表达6个基因片段的筛选及其临床意义

目的　筛选数个在胃癌及癌前病变粘膜中检出率高的差异表达基因片段并探讨其临床意义．方法　以筛选出的ｇｃｙｓ１ 至ｇｃｙｓ１８ 的新基因片段作为研究对象,采用定量ＲＴＰＣＲ 技术检测４８ 例胃癌、１６ 例其他肿瘤及１１０ 例活检的胃粘膜标本．结果　①在４８ 例胃癌中,表达检出率高的６ 个片段依次为：ｇｃｙｓ１０ 为９０－５ ％ ,ｇｃｙｓ１ 为８０－９ ％ ,ｇｃｙｓ１８ 为６９－５ ％ ,ｇｃｙｓ１１为６１－９ ％ ,ｇｃｙｓ４ 为４２－８ ％ ,ｇｃｙｓ８ 为３５－７ ％ ,在癌旁组织中检出率＜ １０ ％ ;６ 个片段的检出率在胃癌及癌旁组织中存在显著性差异（ Ｐ ＜ ０－０１） ;②在１６ 例其他肿瘤中, 表达率依次为：ｇｃｙｓ１０ 为３７－５ ％ ,ｇｃｙｓ１ 为１４－３ ％ ,ｇｃｙｓ１８ 为２７－５ ％ ,ｇｃｙｓ１１为４３－７ ％ ,ｇｃｙｓ４ 为１４－３ ％ ,ｇｃｙｓ８ 为３１－３ ％ ;③３３ 例萎缩性胃炎中,表达率依次为：ｇｃｙｓ１０ 是４０－５ ％ ,ｇｃｙｓ１ 是１６－７ ％ ,ｇｃｙｓ１８ 为４４－５ ％ ,ｇｃｙｓ１１ 为４３－３ ％ ,ｇｃｙｓ４ 为３３－３ ％ ,ｇｃｙｓ８为４８－３ ％ ;２８ 例肠腺化生     

BCL—2,Fas基因蛋白在胃癌及癌前病变组织中的表达

探讨基因蛋白ｂｃｌ－２,Ｆａｓ的表达变化与胃癌及癌前病变之间的关系。方法采用免疫组化ＳＰ法,分别检测浅表性胃炎组织２０例,萎缩性胃炎３２例,肠化生３２例,胃癌３６例基因蛋白ｂｅｌ－２,Ｆａｓ的表达变化。结果Ｆａｓ基因蛋白的表达,浅表性胃炎组６５％（１３／２０）较肠化生组２１．８％（７／３２）及胃癌组１９．６％７／３６）明显增高（Ｐ＜０．００５）;ｂｃｌ－２基因蛋白表达,胃癌组织３３．３％（１２／３６）,其中高一中分化腺癌阳性表达５６．２５％（９／１６）较低分化腺癌１６．６％（２／１２）及未分化癌１２．５％（１／８）明显增高（Ｐ＜０．０５）,浅表性胃炎组无回例表达;胃炎与胃癌组之间Ｆａｓ和ｂｃｌ－２表达呈负相关,两者比较有显著性差异（Ｐ＜０．０５）。结论ｂｃｌ－２基因的异常表达对胃癌及癌前病变的形成发挥一定作用;Ｆａｓ基因的过度表达诱导胃炎发生,而弱表达又为胃粘膜细胞癌变提供了条件;ｂｃｌ－２与Ｆａｓ基因的表达失衡可能与胃癌的发生有关。     

食管癌核基质抗体的免疫组化研究

目的研究食管癌核基质抗体的肿瘤特异性和组织学特异性．方法用人食管癌组织提取核基质抗原，制备核基质抗体，采用免疫组织化学方法对食管癌４１例（男２６例，女１５例，年龄５３岁±７２岁）、正常食管粘膜８例、食管粘膜异型增生１５例、肺鳞癌１０例、喉癌１０例、胃腺癌１０例以及大鼠食管癌５例进行免疫组化染色．结果食管癌核基质抗体在食管癌组织中表达有特异性（３２／４１，７８０％），与正常食管粘膜（１／８，１２５％）及胃腺癌（２／１０，２００％）有非常显著差异（Ｐ＜００１），与食管异常增生（７／１５，４６７％）、肺鳞癌（３／１０，３００％）、喉鳞癌（４／１０，４００％）差异明显（Ｐ＜００５），但与大鼠食管癌组织（２／５，４００％）差异不明显．食管癌核基质的表达，在不同分化程度的食管癌组织中无明显差异（Ｐ＞００５）；在淋巴结转移阳性组高于淋巴结转移阴性组（１７／１８，９４４％ｖｓ１５／２３，６５２％，Ｐ＜００５）．结论食管癌核基质抗体具有较好肿瘤和组织学特异性，对肿瘤转移有一定影响，可作为食管癌的一项新标记物．     

早期胃癌cyclin E表达的生物学意义

目的研究早期胃癌ｃｙｃｌｉｎＥ表达的生物学意义．方法用免疫组化法检测１０８例早期胃癌组织中ｃｙｃｌｉｎＥ和Ｐ５３的表达．结果正常胃腺体细胞几乎不染色,３３％（３６／１０８）的胃癌呈棕黄色．ＣｙｃｌｉｎＥ的总阳性率,在幽门部为４８％（２４／５０）,肉眼观混合型４６％（６／１３）,组织学分化型４０％（３１／７８）,Ｐ５３阳性者５４％（１９／３５）,均显著高于对照组．ＣｙｃｌｉｎＥ的强阳性率,在癌侵入粘膜下者是１８％（９／５１）,侵入静脉者２８％（５／１８）,侵入淋巴管者２８％（９／３２）,侵入淋巴结者３０％（４／１３）,都显著高于对照组．ＣｙｃｌｉｎＥ强阳性者五年生存率４０％（４／１０）,显著低下．结论ＣｙｃｌｉｎＥ阳性尤其是强阳性者恶性程度高     

Gastric and intestinal phenotypes of gastric carcinoma with reference to expression of brain (fetal)-type glycogen phosphorylase

PURPOSE: Although reports have suggested that differentiated gastric carcinomas have different phenotypes, i.e., gastric and intestinal type, this classification is complicated and can be confusing. Our previous studies have demonstrated a close relationship between carcinogenesis in differentiated-type gastric cancer and the expression of brain (fetal)-type glycogen phosphorylase (BGP). The purpose of this study was to investigate the relationship between the mucin phenotype of gastric carcinoma and BGP expression. METHODS: Ninety-six specimens of gastric carcinoma were studied using specific anti-BGP antibody. Correlation of BGP expression with intestinal and gastric phenotypes was determined with the anti-mucin antibodies, HGM, CD10, and MUC2. RESULTS: BGP was expressed in 82.6% (38/46) of differentiated type and in 24.0% (12/50) of undifferentiated type carcinomas. The incidence of BGP positivity was significantly greater in the differentiated-type carcinoma than in the undifferentiated type (P < 0.001). The proportions of gastric, mixed and intestinal types in differentiated and undifferentiated gastric carcinomas were 13.0%, 47.8%, and 39.2%, and 56.0%, 32.0%, and 12.0%, respectively. In both differentiated and undifferentiated types, the phenotype of gastric and intestinal mucin expression corresponded very well with BGP expression, that is, more than 90% of carcinomas with gastric type did not express BGP, whereas approximately 90% of carcinomas with intestinal type did express BGP. CONCLUSIONS: The classification of gastric and intestinal phenotypes of gastric carcinoma in terms of BGP expression was simpler and clearer than such classification in terms of mucin immunohistochemistry. It is suggested that BGP is a useful biomarker for the classification of intestinal and gastric type carcinoma of the human stomach, including classification from the carcinogenetic point of view.