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在v-src诱导的肉瘤消退过程中产生的肿瘤免疫。

Tumor immunity generated in the course of regression of v-src-induced sarcomas.

作者信息

Wisner T W, England J M, Pan D Y, Stoker A W, Halpern M S

机构信息

Wistar Institute of Anatomy and Biology, Philadelphia, Pennsylvania 19104.

出版信息

J Virol. 1991 Dec;65(12):7020-4. doi: 10.1128/JVI.65.12.7020-7024.1991.

DOI:10.1128/JVI.65.12.7020-7024.1991
PMID:1658394
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC250820/
Abstract

Previous studies have indicated that the regression versus progression of v-src-DNA-induced sarcomas is dependent on chicken line. As a first step in analyzing the role of tumor immunity as a determinant of this line dependence, experiments were undertaken to ascertain whether an antisarcoma immune response is generated in the course of sarcoma growth in TK chickens, a regressor line. To assay for this response, test TK chickens in which v-src-induced wing web sarcomas had regressed, as well as control TK chickens that had not been exposed to v-src, were challenged in protocols known to yield v-src-dependent sarcoma formation and monitored for challenge sarcoma growth. Compared with the control chickens, the test chickens showed a significant resistance to the sarcomagenic challenge. These results raise the possibility that the antisarcoma response that is inducible in regressor lines, as demonstrated here in terms of a protective effect against a subsequent sarcomagenic challenge, may also underlie the regression of v-src-induced primary sarcomas.

摘要

先前的研究表明,v-src-DNA诱导的肉瘤的消退与进展取决于鸡的品系。作为分析肿瘤免疫作为这种品系依赖性决定因素的作用的第一步,开展了实验以确定在TK鸡(一种消退型品系)的肉瘤生长过程中是否会产生抗肉瘤免疫反应。为了检测这种反应,对v-src诱导的翼蹼肉瘤已经消退的受试TK鸡以及未接触过v-src的对照TK鸡,按照已知能产生v-src依赖性肉瘤形成的方案进行攻击,并监测攻击后肉瘤的生长情况。与对照鸡相比,受试鸡对致肉瘤攻击表现出显著的抗性。这些结果增加了一种可能性,即在此处就针对后续致肉瘤攻击的保护作用而言,在消退型品系中可诱导的抗肉瘤反应,可能也是v-src诱导的原发性肉瘤消退的基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3534/250820/0f70c8aea11e/jvirol00055-0659-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3534/250820/f12483e14ca3/jvirol00055-0658-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3534/250820/0f70c8aea11e/jvirol00055-0659-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3534/250820/f12483e14ca3/jvirol00055-0658-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3534/250820/0f70c8aea11e/jvirol00055-0659-a.jpg

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本文引用的文献

1
Tumor induction by direct injection of cloned v-src DNA into chickens.通过将克隆的v-src DNA直接注射到鸡体内诱导肿瘤
Proc Natl Acad Sci U S A. 1983 Jan;80(2):353-7. doi: 10.1073/pnas.80.2.353.
2
The immune status of avian sarcoma virus-infected chickens as a determinant of sarcoma growth pattern and viral antigen expression.禽肉瘤病毒感染鸡的免疫状态作为肉瘤生长模式和病毒抗原表达的决定因素。
J Immunol. 1987 May 1;138(9):3014-8.
3
A nonviral, virus strain-specific antigen expressed on rat cells transformed by avian sarcoma virus.一种由禽肉瘤病毒转化的大鼠细胞上表达的非病毒、病毒株特异性抗原。
Immunogenetics. 1994;40(4):257-65. doi: 10.1007/BF00189970.
4
Tumor cells induced by the v-src oncogene are heterogeneous for expression of markers of mesenchyme differentiation.由v-src癌基因诱导的肿瘤细胞在间充质分化标志物的表达上具有异质性。
Virchows Arch. 1994;424(1):83-8. doi: 10.1007/BF00197397.
Cancer Res. 1986 Nov;46(11):5864-8.
4
Concomitant immunity leads to retardation or acceleration of the growth of Rous sarcomas in genetically resistant or susceptible inbred lines of chickens.伴随免疫会导致罗氏肉瘤在基因抗性或易感的近交系鸡中的生长迟缓或加速。
Folia Biol (Praha). 1986;32(5):334-48.
5
Efficient transformation by Prague A Rous sarcoma virus plasmid DNA requires the presence of cis-acting regions within the gag gene.布拉格A株劳氏肉瘤病毒质粒DNA的高效转化需要gag基因内顺式作用区域的存在。
J Virol. 1987 Nov;61(11):3401-9. doi: 10.1128/JVI.61.11.3401-3409.1987.
6
v-src induces clonal sarcomas and rapid metastasis following transduction with a replication-defective retrovirus.v-src在用复制缺陷型逆转录病毒转导后可诱导克隆性肉瘤并迅速转移。
Proc Natl Acad Sci U S A. 1989 Dec;86(24):10123-7. doi: 10.1073/pnas.86.24.10123.
7
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Jpn J Cancer Res. 1989 Sep;80(9):879-86. doi: 10.1111/j.1349-7006.1989.tb01730.x.
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Jpn J Cancer Res. 1988 Mar;79(3):365-74. doi: 10.1111/j.1349-7006.1988.tb01600.x.
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