慢粒白血病abl癌基因表达的研究

选择分别位于ｂｃｒ／ａｂｌ嵌合基因的Ｍｂｃｒｌ第二外显子和ａｂｌ的第二外显子上的两条引物，对１８例慢粒白血病及２例急淋白血病标本进行逆转录ＰＣＲ（ＲＴ－ＰＣＲ）检测。结果：在１８例包括ｐｈ（＋）和ｐｈ（－）不同病期的慢粒白血病患者血中均检出ｂｃｒ／ａｂｌ嵌合基因的表达，其中１４例为Ｋ－２８型表达，１例为Ｌ－６型表达，３例为Ｋ－２８型，Ｌ－６型同时表达；２例急淋白血病标本中１例为Ｋ－２８型表达。研究结果表明，１．ｂｃｒ／ａｂｌ嵌合基因是慢粒白血病的一个重要分子生物学特征；２．ｐｈ（＋）和ｐｈ（－）慢粒白血病的分子生物学基础相同，即均有ｂｃｒ／ａｂｌ嵌合基因；３．至少部分急淋白血病与慢粒白血病有相同的分子生物学基础；４．ｂｃｒ的断裂点位置可能有一定的临床意义，但有待进一步研究；５．同时表达Ｌ－６型和Ｋ－２８型的情况多见于急变区，此现象提示体内可能同时有两类不同嵌合的白血病细胞或白血病急变期ｂｃｒ出现新的重排。     

Amplification of the c-erbB oncogene is associated with malignancy in primary tumours of neuroepithelial tissue

Summary In various primary brain tumours of neuroepithelial tissue recombinant DNA techniques were used to demonstrate changes of the epidermal growth factor receptor gene, which is homologous to the c-erbB oncogene. Twenty-one of 40 grade III/IV tumours, but only 1 of 16 grade I/II tumours were found to contain amplified and/or rearranged c-erbB sequences. This highly significant difference suggest that c-erbB amplification, rearrangement, or both, are important steps in malignant transformation in a subset of patients with neuroepithelial tumours.     

三氧化二砷抑制体外培养小鼠气道成纤维细胞增殖及c-myc与c-sis表达

目的：探讨三氧化二砷 (As2O3))对体外培养的小鼠气道成纤维细胞 (FB)增殖及原癌基因c-myc与c-sis表达的影响。 方法： 按不同药物分7组，在体外培养的FB中分别加入浓度为0.25、0.5、1.0、2.0和4.0 μmol/L的As2O3，在1、3、5和7 d后用记数法观察FB生长情况，并用流式细胞仪（FCM）检测不同浓度药物 对各组FB增殖的影响及各组c-myc与c-sis的阳性表达率。 结果： 各种实验浓度的As2O3对FB均有抑制作用，并有时间剂量效应。流式细胞仪分析显示，随着浓度的增高，G1期细胞比例逐渐增高，G2/M期细胞比例降低，浓度为2.0和4.0 μmol/L的As2O3能显著抑制c-myc与c-sis的表达。 结论： As2O3能抑制FB的增生，其机理可能与其下调c-myc与c-sis的表达有关。     

Natural mechanisms protecting against cancer

Carcinogenesis is a multistage process. At each step of this process, there are natural mechanisms protecting against development of cancer. The majority of cancers in humans is induced by carcinogenic factors present in our environment including our food. However, some natural substances present in our diet or synthesized in our cells are able to block, trap or decompose reactive oxygen species (ROS) participating in carcinogenesis. Carcinogens can also be removed from our cells. If DNA damage occurs, it is repaired in most of the cases. Unrepaired DNA alterations can be fixed as mutations in proliferating cells only and mutations of very few strategic genes can induce tumor formation, the most relevant are those activating proto-oncogenes and inactivating tumor suppressor genes. A series of mutations and/or epigenetic changes is required to drive transformation of a normal cell into malignant tumor. The apparently unrestricted growth has to be accompanied by a mechanism preserving telomeres which otherwise shorten with succeeding cell divisions leading to growth arrest. Tumor can not develop beyond the size of 1–2 mm in diameter without the induction of angiogenesis which is regulated by natural inhibitors. To invade the surrounding tissues epithelial tumor cells have to lose some adhesion molecules keeping them attached to each other and to produce enzymes able to dissolve the elements of the basement membrane. On the other hand, acquisition of other adhesion molecules enables interaction of circulating tumor cells with endothelial cells facilitating extravasation and metastasis. One of the last barriers protecting against cancer is the activity of the immune system. Both innate and adaptive immunity participates in anti-tumor effects including the activity of natural killer (NK) cells, natural killer T cells, macrophages, neutrophils and eosinophils, complement, various cytokines, specific antibodies, and specific T cytotoxic cells. Upon activation neutrophils and macrophages are able to kill tumor cells but they can also release ROS, angiogenic and immunosuppressive substances. Many cytokines belonging to different families display anti-tumor activity but their role in natural anti-tumor defense remains largely to be established.     

交链孢酚激活人胎食管上皮组织细胞癌基因的研究

本文报道食管癌高发区粮食中优势污染菌互隔交链孢霉代谢产物交链孢酚(AOH)对人胎儿食管上皮组织癌基因的激活。结果表明,体外培养的人胎儿食管上皮组织经10gg/ml AOH作用4h后,其DNA具有转化活性,可转化NIH/3T3细胞。一轮转化率为0.17Foci/μg DNA,二轮转化率为0.58Foci/μg DNA(P<0.01)。转化细胞中含有人特异性高重复序列Alu,提示转化系人DNA转染所致。Southern blot检测表明,AOH处理后的人胎儿食管上皮组织内有H-ras和myc基因的扩增,经其转染的NIH/3T3细胞中亦有H-ras基因持久而稳定的扩增。对照组胎儿食管上皮和正常NIH/3T3细胞中均未发现相应的同源序列,说明正常胎儿食管组织中的H-ras和myc基因可经AOH短期处理而激活。该结果对AOH可能系人食管癌病因之一提供了直接证据。     

慢性重型乙型肝炎患者血浆内毒素与肝组织FasL和血清sFasL的关系

目的　探讨慢性重型肝炎血浆内毒素脂多糖 (LPS)与肝组织Kuppfer细胞自杀因子配体 (FasL)表达和血清可溶性FasL(sFasL)的关系。　方法　检测 1 2例慢性重型肝炎患者血浆内毒素LPS的水平 ,同步观察肝组织FasL表达与血清sFasL的水平 ,并与 1 6例慢性乙型肝炎患者进行对照。　结果　慢性重型肝炎组LPS水平、sFasL、FasL表达阳性率及阳性强度均高于慢性乙型肝炎组 ,P <0 .0 1。　结论　肝细胞功能严重受损时 ,血中肠源性LPS增高 ,并促使肝组织FasL表达增强。     

胃肠道恶性肿瘤及其周边组织中c-myc基因mRNA表达与临床意义

目的　探讨胃肠道恶性肿瘤及其周围边组织中c -mycmRNA表达与手术切缘的安全性关系。方法　用RT -PCR方法检测了 12例胃癌和 16例肠癌标本肿瘤中心及周边组织中c-mycmRNA的表达。结果　肿瘤的各种分型与各个分期c -mycmRNA的表达无显著性差异。肿瘤周边组织中 ,距肿瘤边缘 4cm处c -mycmRNA表达率显著下降 (P <0 .0 5 ) ,距肿瘤边缘 5cm以远表达率为 0。结论　根据c -mycmRNA表达 ,距肿瘤边缘 5cm处可定为肿瘤较安全的切缘     

大肠癌新相关基因HSU17714的染色体定位研究

目的确定大肠癌新相关基因ＨＳＵ１７７１４的染色体定位。方法采用强化荧光原位杂交技术（ＦＩＳＨ）,以生物素化酪胺强化荧光原位杂交信号。结果８０．０％（１２８／１６０）的间期细胞和５９．８％（１０４／１７４）的中期分裂相可见到明显集中的ＨＳＵ１７７１４基因的杂交信号,相应荧光Ｒ带分析中,８５．１％（４０／４７）在２２号染色体上１区３带处有杂交信号。结论ＨＳＵ１７７１４基因定位于２２ｑ１３。     

子宫颈癌组织中nm23-H1基因表达与淋巴结转移及预后的关系

目的：探讨ｎｍ２３－Ｈ１基因在宫颈癌组织中表达及其意义。方法：采用免疫组化法检测宫颈腺癌及鳞癌各３９例癌组织标本中ｎｍ２３－Ｈ１基因表达，采用统计学χ２检验方法，对ｎｍ２３－Ｈ１表达与临床病理因素及预后的关系进行分析。结果：腺癌与鳞癌的表达阳性率分别为４４．６％和３９．２％。在腺癌病例中，Ⅰ期的阳性率为６１．１％，高于Ⅱ期的２８．６％，差异有显著性；术后复发组的阳性率为２１．５％，低于无复发组的５６．０％，差异有显著性；盆腔淋巴结转移组的阳性率为２８．６％，低于无转移组的５２．０％，虽差异无显著意义，然而，淋巴结转移的１４例患者中无１例ｎｍ２３－Ｈ１呈强阳性表达，而淋巴结无转移组２５例中有７例呈强阳性表达，差异有显著性；ｎｍ２３－Ｈ１阳性组的５年生存率（８２．４％），较阴性组（５２．５％）为高，差异有显著性。ｎｍ２３－Ｈ１表达与鳞癌的各临床病理学因素及预后未见明显关系。结论：ｎｍ２３－Ｈ１表达与宫颈腺癌的生物学行为相关，与鳞癌未显示明显关系。