凋亡的分子生物学途径和肿瘤细胞凋亡

研究肿瘤的发生、发展已成为当前医学的热门课题。肿瘤的发生常常是由于肿瘤细胞凋亡失控造成肿瘤组织的无限增长 ,在肿瘤细胞凋亡的过程中线粒体 (ｍｉｔｏ ｃｈｏｎｄｒｉａｍｔ)起着非常重要的作用 ,线粒体是哺乳动物细胞中唯一含有自身的遗传物质的效应器 ,同时它又是各种损伤因子作用的敏感部位。因此细胞中线粒体损伤导致其中的遗传物质即线粒体ＤＮＡ的释放事件可能时有发生。已经证实[1] ,癌细胞核基因组中存在线粒体ＤＮＡ的同源序列 ,在生理状态下 ,任何细胞的线粒体ＤＮＡ游离片段都可能具有潜在的转化活性 ,因而从理论上可以推…     

早期食管癌的病理形态观察及组织发生学探讨

目的探讨早期食管癌的组织发生学.方法对109例早期食管癌及癌周病变进行病理观察.结果其中20例的一点癌(黄豆大小),3例双原发癌,1例小细胞癌.癌周伴有不同程度的鳞状上皮异形增生和不典型增生.结论早期食管具有多样性生长的特点.提示临床医生在胃镜检查应注意多点取材,以防漏诊;以及正确确定手术范围,防止手术残留.     

大鼠胃黏膜癌变过程细胞凋亡及相关癌基因bcl—2、c—myc的动态表达

目的：探讨大鼠胃黏膜癌变发生发展过程中细胞凋亡及其相关基因的关系。方法：采用MNNG,10％NaCl及酒精灌胃建立了大鼠胃黏膜癌变模型,设立正常空白组,模型组,分别用TUNEL,原位杂交技术及免疫组化大鼠检测胃黏膜细胞凋亡指数,bcl-2,c-myc基因表达。结果：本造模方法成功率较高。从正常胃黏膜到胃癌,细胞凋亡指数逐渐下降,bcl-2,c-myc基因表达逐渐增高,大鼠胃黏膜细胞凋亡受到抑制与bcl-2,c-myc基因高表达具有高度的一致性,结论：细胞凋亡失控是胃黏膜癌变发生发展的机制之一,bcl-2,c-myc基因可能参与了对大鼠胃黏膜癌变细胞凋亡的调控。     

84例肝炎肝硬变癌变AFP检测临床分析

通过对８４例肝炎肝硬变癌变患者（称ＨＣＣ给）及同期收住的４４３例肝炎肝硬变患者（称ＬＣ组）的ＡＦＰ（ＲＩＡ法）检测,结果显示ＨＣＣ级ＡＦＰ总阳性率为７５％明显高于ＬＣ组１７．６１％（Ｐ〈０．００１）。在ＨＣＣ组中,中晚期ＨＣＣ患者ＡＦＰ阳性率８２．１４％明显高于早期患才６０．７１％,（Ｐ〈０．０５）。提示ＡＦＰ在肝癌诊断中仍然是良好指标之一,但在部分早期肝癌诊断中,易漏诊或延误诊断。衣采用ＡＦＰ与     

185例大肠息肉患者的临床表现、内镜下及组织学特点

对 18 5例大肠息肉患者的临床表现 ,内镜及组织学资料进行分析 ,结果显示 :大肠息肉主要症状为粘液血便 ,多分布于左半结肠 ,大小 <1.0cm ,有蒂和腺瘤为主 ,息肉越大越易癌变 (P <0 .0 1和 0 .0 5) ,广基息肉易癌变 (P <0 .0 5) ,腹瘤组织类型不同癌变率不同 (P >0 .0 5和 <0 .0 1)。     

口腔粘膜病癌变的临床分析

验交流近年来,口腔癌发病呈上升的趋势,其中多数由起于粘膜的鲮状细胞癌组成。口腔粘膜癌变患者多伴有先期口腔粘膜疾病,由于口腔粘膜病多具有慢性迁延性的特点,同时口腔粘膜癌变又较为隐蔽,不易早期发现,给治疗带来了较大的困难。本文结合临床实际情况,对临床常见的口腔粘膜病癌变的可疑因素进行初步探讨,以助口腔内科医师在诊治此类患者时能早期做出正确疹断并及时采取相应的措施。１材料和方法自１９８８～１９９８年在我科就诊的粘膜病人进行初步统计。临床诊断严格采用同一标准。１．１白斑（ＯＬＫ）发生于口腔粘膜上的白色角…     

胆囊息肉样病变临床病理与癌变关系的探讨

目的　探讨胆囊息肉样病变 (PLG)的临床及病理特征与癌变的关系。方法　回顾性分析经手术切除的15 0例PLG患者临床及病理资料。结果　胆固醇息肉 10 3例 ,占 6 8.7% ;炎性息肉、腺肌瘤及腺瘤样增生 30例 ,占2 0 .0 % ,无恶变 ;腺瘤 17例 ,占 11.3% ,其中癌变 6例 ,恶变率为 35 .0 %。6例癌变者年龄 5 2～ 6 9岁 ,均为广基单发 ,大小为 15mm× 18mm× 2 0mm以上。结论　PLG中年龄 >5 0岁、广基单发、直径 >10mm ,位于颈部的息肉均为癌变的高危因素 ,病理类型以腺瘤最易癌变 ,应早期手术切除。     

妇科肿瘤癌变的基础研究现状

恶性肿瘤是进行性发展的疾病 ,临床发现时多属晚期 ,治疗亦无过多回旋余地 ,病人的生活质量急剧下降 ,故早期诊断、早期治疗极为重要 ,而早期识别癌前病变则是防止肿瘤发生发展并做出早期治疗的重要环节。1　子宫颈癌子宫颈癌是危害妇女健康的主要恶性肿瘤之一 ,近 4 0年来国内外广泛开展了巴氏涂片和宫颈癌普查普治工作 ,使其发病率及病死率都明显下降。但近年来由于人乳头瘤病毒 (HPV)感染增多 ,宫颈癌发病率有明显上升趋势 ,且患者趋于年轻化 ,故针对癌前病变的基础研究引起人们普遍关注。1.1　HPV感染与宫颈癌前病变自 1976年首次从…     

幽门螺杆菌感染与c-myc、p16表达在胃粘膜癌变中的相关性研究

目的 观察胃粘膜癌变过程中幽门螺杆菌(Hp)和c-myc、p16的表达状况，探讨Hp感染与c-myc、p16表达在胃粘膜癌变中的相关性。方法 通过内镜活检和外科手术获取171例胃组织标本，Hp培养确定有无Hp感染；免疫组织化学法检测组织标本中c-myc、p16表达。结果 胃癌(GC)组织中c-myc表达率最高，慢性浅表性胃炎(CSG)和慢性萎缩性胃炎(CAG)伴轻度肠化(IM)组p16表达率显高于其它各组(P＜0．05)。在CAG伴中、重度IM、异型增生(Dys)组中，Hp阳性亚组的c-myc表达率显高于Hp阴性亚组(P＜0．01)，p16阳性表达率显低于Hp阴性亚组(P＜0．01)。结论 Hp感染可能通过激活c-myc、抑制p16，刺激胃粘膜过度增殖，使其具有较高恶变倾向。     

Effects of Imbalance of Apoptosis and Proliferation on Large Bowel Carcinogenesis in Mice

OBJECTIVE To observe the pattern of changes in the proliferation and apoptosis at different stages of large bowel carcinoma in mice, and to explore the effects of the imbalance of apoptosis and proliferation at different stages of large-intestine carcinogenesis.METHODS An experimental animal model for large intestine carcinogenesis of KUNMING-strain mice was used. The carcinomas were induced by subcuteneous injection of dimethylhydrazine (DMH) and the distribution and density changes of proliferating and apoptotic cells observed through multistages toward cancer formation. The animals were killed in groups at the 12th, 18th, 24th,and 32nd weeks of carcinoma induction. The apoptotic and proliferating cells were labeled separately using TUNEL and PCNA immunohistochemical staining methodsRF, RESULTS In the normal mouse mucosa, all the apoptotic cells were situated in the superficial layers, however, the proliferating cells were situated in the basement layers, and the amount of both were small. In the early stage of carcinoma induction, the proliferation and the apoptotic cells slightly increased in amount, but there were no obvious changes in their ratio. In the medium stage, the densities of both distinctly increased, but there were no obvious changes in the ratio. In the late stage, the densities of the proliferating and the apoptotic cells in the non-carcinoma mucosa were higher than those at other stages. The proliferating cells in the dysplastic mucosa increased progressively with the increasing degree of the lesions. Although the apoptotic cells increased, their changes did not occur with the degree of the lesions. Their ratio showed a decreasing tendency with the degree of the lesions.CONCLUSIONS (①The presence of an imbalance between cell proliferation and apoptosis was confirmed in the course of large intestine carcinogenesis in a mouse model. ②In the early stage of carcinoma induction both proliferation and apoptosis were at a low level; in the medium stage, they were both at a high level; and in the late stage (that is in carcinoma), proliferation was at a very high level, while apoptosis was at a low level. ③The proliferating cells increased progressively with the degree of dysplasia. There were no obvious changes in the apoptotic cells and their ratio to the proliferating cell sshowed a progressively increasing tendency. ④In the stage of cancer formation, the most essential change was the excessive decrease in the ratio of apoptosis to proliferation. These results support the hypothesis of “Cell Selective Proliferation“, which was raised by authors previously in a study on human large bowel carcinoma.