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  cell carcinoma
Regulation of matrix metalloproteinase-9 transcription in squamous cell carcinoma of uterine cervix: the role of human papilloma
      
Matrix metalloproteinase-9 (MMP-9) plays an important role in initiation and progression of squamous cell carcinoma (SCC) of human uterine cervix.
      
Extended terminal deletions (56%) prevailed over shorter internal and multiple deletions and dominated (65%) in the most aggressive histopathological kidney cancer subtype, clear-cell carcinoma.
      
Semiquantitative RT-PCR revealed elevated transcription of RHOA in tumors (45 cases of breast cancer, renal cell carcinoma, and epithelial ovarian carcinoma; p >amp;lt; 10-4).
      
The NOLA2 and RPS3A genes as highly informative markers of human squamous cell carcinoma of lung
      
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  cell carcinomas
To reveal early genetic alterations of chromosome 6 that are important for CC progression, we analyzed the loss of heterozygosity (LOH) in DNAs from 45 CIN cases, 47 microcarcinomas, and 19 invasive squamous cell carcinomas stage IB.
      
No change in the reactivity for HBGA was detected in the stratified epithelium overlying squamous cell or basal cell carcinomas, whereas a considerable loss of LAMPs was detected.
      
We investigated 37 head and neck squamous cell carcinomas (HNSCC) at different stages, using immunohistochemical staining for CD4+ infiltrates and real-time reverse transcription polymerase chain reaction (RT-PCR) detection of CD4 mRNA.
      
Signet ring cell carcinomas frequently contained strong CD97stalk and CD55-staining.
      
Effect of the Hypoxic Cell Sensitizer Isometronidazole on Local Control of Two Human Squamous Cell Carcinomas after Fractionated
      
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  cell cancer
The transcription levels of TIMP3, DAPK1, and AKR1B10 were compared for normal and tumor lung tissues of patients with squamous-cell cancer (SCC) by RT-PCR.
      
Decreased expression of the human immunoglobulin J-chain gene in squamous cell cancer and adenocarcinoma of the lungs
      
The content of the J chain and the transcription level of its gene were studied in normal and tumor cells at various stages of squamous cell cancer and adenocarcinoma of the lungs by RT-PCR and immunoblotting.
      
Anti-human lung giant cell cancer (PG) effect of human LAK cellsin vitro and in nude mice
      
The positive expression rate (87.5%) and nuclear expression rate of adenocarcinoma (62.5%) were apparently higher than those of squamous cell cancer (40.0% and 17.1%) (P>amp;lt;0.01).
      
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  carcinoma
Immunohistochemical analysis revealed a high expression level of hSef in kidney, testis, and the corresponding carcinoma tissues.
      
Effect of down-regulating VEGF on proliferation of colon carcinoma cell HT-29
      
Cancer-related genes harbored in the loss regions containing a high frequency of hepatocellular carcinoma (HCC) were selected.
      
The purified 19peptide directly inhibited proliferation and migration of murine B16 melanoma cells, SMMC-7721hepatoma carcinoma cells and human umbilical vein endothelial cells (HUVEC).
      
We recognized and honoured the important contributions of these Chinese pioneers in portal hypertension, recurrent pyogenic cholangitis, hepatocellular carcinoma and liver transplantation.
      
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  其他


Observations on the localization of AFP in rat liver tissue in correlation to serum AFP dynamics during 3'-MeDAB carcinogenesis were carried out by the immunoenzyme technique and the radio-rocket-electrophoresis autography.The following results were obtained:(1) During the precancerous stage, AFP was found in a few liver cells in the pseudolobules, in the cells of the basophilio anaplastic regenerative nodules and in some of the "survival" liver cells and "transitional" cells. Most of these cells showed basophilio...

Observations on the localization of AFP in rat liver tissue in correlation to serum AFP dynamics during 3'-MeDAB carcinogenesis were carried out by the immunoenzyme technique and the radio-rocket-electrophoresis autography.The following results were obtained:(1) During the precancerous stage, AFP was found in a few liver cells in the pseudolobules, in the cells of the basophilio anaplastic regenerative nodules and in some of the "survival" liver cells and "transitional" cells. Most of these cells showed basophilio cytoplasm and appeared dedifferentiated.(2) AFP was not detected in the bile duct carcinomas nor in most of the liver cell carcinomas of low grade malignancy, but was demonstrated in the poorly differentiated liver cell carcinomas. The intensity of AFP synthesis in liver cell carcinomas increased in coincidence with their activity in cell growth and cell proliferation but decreased with cell differentiation. AFP synthesis was not directly related to whether or not the cell was in the mitotic stage.(3) In the liver cell carcinomas, the extent of AFP positive reaction as visualized by the immunoenzyme technique basically paralleled the serum AFP level.The possible mechanism and the histologic basis of the serum AFP "saddle shaped" curve during 3'-MeDAB carcinogenesis are discussed, and a preliminary postulation on the histogenesis of liver cancer so induced is suggested.

本工作采用放射火箭电泳自显术和免疫酶标记定位技术,对大鼠3'-MeDAB诱癌过程血清和肝组织甲胎蛋白(AFP)的动态变化和定位情况进行了观察。发现(1)肝硬化假小叶内的少数肝细胞、嗜碱性间变再生结节细胞、少数“幸存肝细胞”及少数“过渡性细胞”,具有合成AFP的能力。未见肝内其他类型细胞合成AFP。合成AFP的细胞大多具有胞浆嗜碱性、生长活跃和形态上去分化的特点。(2)未见胆管癌细胞合成AFP。肝细胞癌分化好的癌细胞绝大多数也未见合成AFP,分化差的癌细胞合成AFP的能力,基本上与其生长活跃程度呈正相关,与分化程度呈负相关,而与癌细胞是否处于核分裂阶段关系不大。(3)肝癌组织AFP酶标的强度和范围与血清AFP水平之间基本上有平行关系。此外,本文还就什么细胞合成AFP、血清AFP“马鞍型”变化的成因及病理组织学基础等进行了讨论,并根据实验结果,对大鼠3'-MeDAB肝癌的组织发生提出了初步的设想。

Histological observations are reported of the normal development of embryonic and neonatal rat liver with simultaneous observations by the immunoenzyme technique of AFP synthesis in these tissues. It was found that the hepatocellular carcinomas of Ⅰ~Ⅳ grade malignancy during 3'-MeDAB carcinogenesis morphologically reflected the retrogression of the normal developmental differentiation of liver cells, presenting a process of dedifferentiation. However, AFP synthesis in these liver cancers did not coincide with...

Histological observations are reported of the normal development of embryonic and neonatal rat liver with simultaneous observations by the immunoenzyme technique of AFP synthesis in these tissues. It was found that the hepatocellular carcinomas of Ⅰ~Ⅳ grade malignancy during 3'-MeDAB carcinogenesis morphologically reflected the retrogression of the normal developmental differentiation of liver cells, presenting a process of dedifferentiation. However, AFP synthesis in these liver cancers did not coincide with that in the embryonic livers of corresponding degrees of differentiation. AFP synthesis in embryonic tissues other than liver was also observed and discussed.

本文报导大鼠胚肝及新生鼠肝正常发育的组织学观察和利用免疫酶标技术观察胚鼠及新生鼠肝内AFP的分布情况。发现3'-MeDAB诱癌过程中所见一至四级分化的肝细胞癌,其细胞形态基本上反映了正常肝细胞分化发育的逆转,反映了肝细胞的去分化。但是AFP在这些癌细胞里的重现却与AFP在相应分化程度的胚肝细胞中的合成情况不完全一致。本文并就肝外其他胚胎组织合成AFP的问题进行了一些观察和讨论。

In connection with the study of the mechanism of carcinogenesis,we have underta-ken an investigation on the relative changes in activities of the proliferating enzymesuch as aspartate carbamyl transferase(ACT)and the tissue-specific enzymes such asornithine carbamyl transferase(OCT)and carbamyl phosphate synthetase(CPS_1)in amodel system of hepatocarcinogenesis of rats induced by diethylnitrosamine(DENA).Similar observations have also been made during development of rat liver.(1)Based on the pathological study...

In connection with the study of the mechanism of carcinogenesis,we have underta-ken an investigation on the relative changes in activities of the proliferating enzymesuch as aspartate carbamyl transferase(ACT)and the tissue-specific enzymes such asornithine carbamyl transferase(OCT)and carbamyl phosphate synthetase(CPS_1)in amodel system of hepatocarcinogenesis of rats induced by diethylnitrosamine(DENA).Similar observations have also been made during development of rat liver.(1)Based on the pathological study and enzymatic changes of liver in the presentexperiment,the process of carcinogenesis may be tentatively divided into three stages:(1)stage of simple hyperplasia—the early 6 weeks of DENA feeding.Changes in therelative ratio of ACT,OCT,and CPS_1 activities in this stage are reversible,similar tothose observed in the regenerating liver.(2)stage of malignant transformation—fromthe 6th to the 16th week of feeding the carcinogen.In this stage there appears anaplastichyperplasia of liver cells characterized by an irreversible change of the relative ratioof enzyme activities and (3)stage of the development of hepatocellular carcinoma—fromthe 16th to the 30th week of carcinogenesis.(2)During carcinogenesis of rat liver(after the 6th week of feeding DENA),activities of OCT and CPS_1 decreased while those of ACT increased gradually till theformation of cancer.In hepatocellular carcinoma the activities of OCT and CPS_1 areabout 10~20% of the normal liver,while those of ACT being about 2~3 times higher than the normal liver.The pattern of relative changes in activities of both groups ofenzyme during carcinogenesis was found to be the reverse of those observed in thedevelopment of rat liver.(3)The above enzymes in hepatocellular carcinoma and normal liver are probablyidentical entities,as shown by the similarities of pH optima and distribution patternsof enzyme activity in polyacrylamide gel electrophoresis.Similar K_m values anddifferent V_m values of OCT and ACT in hepatocellular carcinoma and normal liverpreparations suggested that changes in enzyme activities during carcinogenesis maypossibly be the result of an alteration in the amount of enzyme proteins.Furthermore,the specific activities of OCT and CPS_1 in the mitochondria of hepatocellular carcinomahave been found to be much lower than those of normal liver,although the proteincontent in the mitochondria of hepatocellular carcinoma decreased to an extent of about40% of that of normal liver.(4)The possible correlation between cell proliferation and differentiation to themechanism of carcinogenesis is discussed.As seen from Fig.3,the process of carcinogenesisseems to be a reversal of that of normal differentiation(development).Changes in enzymeactivities during carcinogenesis may be explained as a result of repression andderepression of the tissue-specific operons and mitotic operons,which are closelylinked and mutually repressed.It appears likely that cell proliferation may provide afundamental condition for the malignant transformation of the hepatocytes,while lossor decrease in the activities of tissue-specific function may be of primary importance tothe initiation of carcinogenesis.It is thus concluded that carcinogenesis would be dueto a random impairment of the control mechanism for gene activities of certain tissue-specific operons,leading to irreversible changes in nucleic acid biosynthesis and intissue-specific metabolism and their key enzyme activities which in turn give rise to anirreversible disturbance of the normal balance between cell proliferation and tissue-specific function,resulting in an abnormal growth and finally the formation of cancer.

本实验以二乙基亚硝胺诱发大鼠肝癌为动物模型,结合病理形态学研究了细胞增殖与组织特异代谢关键性酶ACT 及OCT,CPS_1活性的相互改变及其与癌变的关系,同时作了鼠肝发育过程中酶活性变化的比较研究。(1)根据DENA 引癌过程中酶活性CPS_Ⅰ/ACT,OCT/ACT 及ACT/CPS_Ⅰ,ACT/OCT 相对比值的变化,以及病理形态观察结果,DENA 引癌过程大致可分为三个阶段:喂DENA6周以内为单纯性增生期。此时期酶活性相对比值的改变是可逆的,与再生肝相似。第6周以后至16周为癌变期。此时期出现肝细胞异型性增生及癌变病灶。酶活性相对比值的改变是不可逆的。16周到30周为癌变细胞发展成为肝细胞癌期。(2)癌变过程中(喂DENA6周以后),OCT 及CPS_Ⅰ活性持续降低,同时ACT 活性持续增高。肝癌结节中OCT 及CPS_Ⅰ活性约为正常肝的10~20%,ACT 活性约为正常肝的2倍。癌变过程中这两类酶活性的相互改变与发育过程中的情况正好相反。在发育过程中,胚胎肝内OCT 及GPS_Ⅰ活性较成年水平低,而ACT 活性则较高。新生后CPS_Ⅰ及OCT 活性升高,同时ACT 活性降低。(3)肝与肝...

本实验以二乙基亚硝胺诱发大鼠肝癌为动物模型,结合病理形态学研究了细胞增殖与组织特异代谢关键性酶ACT 及OCT,CPS_1活性的相互改变及其与癌变的关系,同时作了鼠肝发育过程中酶活性变化的比较研究。(1)根据DENA 引癌过程中酶活性CPS_Ⅰ/ACT,OCT/ACT 及ACT/CPS_Ⅰ,ACT/OCT 相对比值的变化,以及病理形态观察结果,DENA 引癌过程大致可分为三个阶段:喂DENA6周以内为单纯性增生期。此时期酶活性相对比值的改变是可逆的,与再生肝相似。第6周以后至16周为癌变期。此时期出现肝细胞异型性增生及癌变病灶。酶活性相对比值的改变是不可逆的。16周到30周为癌变细胞发展成为肝细胞癌期。(2)癌变过程中(喂DENA6周以后),OCT 及CPS_Ⅰ活性持续降低,同时ACT 活性持续增高。肝癌结节中OCT 及CPS_Ⅰ活性约为正常肝的10~20%,ACT 活性约为正常肝的2倍。癌变过程中这两类酶活性的相互改变与发育过程中的情况正好相反。在发育过程中,胚胎肝内OCT 及GPS_Ⅰ活性较成年水平低,而ACT 活性则较高。新生后CPS_Ⅰ及OCT 活性升高,同时ACT 活性降低。(3)肝与肝癌上述酶可能是相同的。因为酶活性的最适pH 和在聚丙烯酰胺凝胶电泳图上的分布都是一致的。肝与肝癌OCT 及ACT 的K_m 相同而V_m 不同,说明癌变过程中酶活性的变化,主要是由于酶蛋白量的改变。此外,肝癌线粒体的蛋白量减少,但OCT 及CPS_Ⅰ的比活性(单位/毫克线粒体蛋白)仍较正常肝线粒体的低。(4)讨论了增生和分化与癌变的关系。初步认为,肝细胞的癌变是反分化(分化逆转)问题,和正常分化一样系由于基因表现的改变,不一定包含基因结构的改变。就与癌变有关的细胞增殖和分化的矛盾而言,细胞增殖及其有关酶活性的增高,可能是癌变发生的基础,而组织特异功能及其关键性酶活性的降低,可能与癌变的关系更为密切。因此癌变的发生,可能是由于在细胞分裂过程中致癌物使肝细胞特异功能基因的调节控制失常,从而引起增生代谢与特异代谢关键性酶活性不可逆的改变,使之失去肝细胞增殖与特异功能的正常平衡,而代之以不受控制的增生,最后形成癌细胞。

 
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