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1
Emergence of tumorigenic cells during the course of Friend virus leukemias.在弗氏病毒白血病病程中致瘤细胞的出现。
Proc Natl Acad Sci U S A. 1981 Jun;78(6):3614-8. doi: 10.1073/pnas.78.6.3614.
2
Detection of tumorigenic cells in Friend virus-infected mice: an in vivo methodological investigation.
J Natl Cancer Inst. 1981 Jun;66(6):1121-7. doi: 10.1093/jnci/66.6.1121.
3
Bone marrow transplantation from Fv-4-resistant donors rescues Friend leukemia virus-infected mice from leukemia: a model of bone marrow transplantation therapy against retroviral infection.来自Fv-4抗性供体的骨髓移植可使感染Friend白血病病毒的小鼠免于白血病:一种针对逆转录病毒感染的骨髓移植治疗模型。
Leukemia. 1994 Dec;8(12):2200-6.
4
The spleen in Friend leukemia. II. Nonleukemic nature of spleen stroma.
J Natl Cancer Inst. 1976 Jun;56(6):1189-95. doi: 10.1093/jnci/56.6.1189.
5
Kinetics of erythroid precursors in mice infected with the anemic or the polycythemic strain of Friend leukemia virus.感染贫血型或红细胞增多型弗氏白血病病毒的小鼠中红系前体细胞的动力学
Proc Natl Acad Sci U S A. 1980 Apr;77(4):2054-8. doi: 10.1073/pnas.77.4.2054.
6
Employment of a [3H]thymidine-incorporation assay to distinguish the effects of different Friend erythroleukemia-inducing retroviruses on erythroid cell proliferation.采用[3H]胸腺嘧啶核苷掺入试验来区分不同的Friend红细胞白血病诱导逆转录病毒对红系细胞增殖的影响。
J Natl Cancer Inst. 1986 Jul;77(1):241-5.
7
Protective influence of lactoferrin on mice infected with the polycythemia-inducing strain of Friend virus complex.乳铁蛋白对感染弗氏病毒复合体红细胞增多症诱导株的小鼠的保护作用。
Cancer Res. 1987 Aug 1;47(15):4184-8.
8
Friend disease in vitro.体外Friend病
J Exp Med. 1981 Sep 1;154(3):594-608. doi: 10.1084/jem.154.3.594.
9
Spontaneous regression in virus-induced murine leukemia. I. Host-virus system.病毒诱导的小鼠白血病中的自发消退。I.宿主-病毒系统。
J Natl Cancer Inst. 1969 Apr;42(4):559-69.
10
Spi-1 oncogene activation in Rauscher and Friend murine virus-induced acute erythroleukemias.
Leukemia. 1990 Jan;4(1):20-3.

引用本文的文献

1
Spi-1/PU.1 transgenic mice develop multistep erythroleukemias.Spi-1/PU.1转基因小鼠会发生多步骤的红白血病。
Mol Cell Biol. 1996 May;16(5):2453-63. doi: 10.1128/MCB.16.5.2453.
2
Protection against retroviral diseases after vaccination is conferred by interference to superinfection with attenuated murine leukemia viruses.接种疫苗后对逆转录病毒疾病的保护作用是通过干扰减毒鼠白血病病毒的重复感染来实现的。
J Virol. 1993 Sep;67(9):5146-52. doi: 10.1128/JVI.67.9.5146-5152.1993.
3
The Ets-related transcription factor PU.1 immortalizes erythroblasts.与Ets相关的转录因子PU.1使成红细胞永生化。
Mol Cell Biol. 1993 Sep;13(9):5670-8. doi: 10.1128/mcb.13.9.5670-5678.1993.
4
Sequences responsible for the distinctive hemolytic potentials of Friend and Moloney murine leukemia viruses are dispersed but confined to the psi-gag-PR region.负责弗瑞德和莫洛尼小鼠白血病病毒独特溶血潜能的序列是分散的,但局限于ψ- gag - PR区域。
J Virol. 1993 Sep;67(9):5478-86. doi: 10.1128/JVI.67.9.5478-5486.1993.
5
Functional interference between the Spi-1/PU.1 oncoprotein and steroid hormone or vitamin receptors.Spi-1/PU.1癌蛋白与类固醇激素或维生素受体之间的功能干扰。
EMBO J. 1993 Dec 15;12(13):5089-96. doi: 10.1002/j.1460-2075.1993.tb06203.x.
6
Rapid capping in alpha-spectrin-deficient MEL cells from mice afflicted with hereditary hemolytic anemia.患有遗传性溶血性贫血的小鼠的α-血影蛋白缺陷型MEL细胞中的快速加帽现象。
J Cell Biol. 1994 Jun;125(5):1057-65. doi: 10.1083/jcb.125.5.1057.
7
A Friend virus mutant encodes a small glycoprotein that causes erythroleukemia.一种Friend病毒突变体编码一种导致红白血病的小糖蛋白。
J Virol. 1994 Jun;68(6):4053-6. doi: 10.1128/JVI.68.6.4053-4056.1994.
8
A nonstructural gag-encoded glycoprotein precursor is necessary for efficient spreading and pathogenesis of murine leukemia viruses.一种非结构的gag编码糖蛋白前体对于鼠白血病病毒的有效传播和发病机制是必需的。
J Virol. 1994 Jun;68(6):3857-67. doi: 10.1128/JVI.68.6.3857-3867.1994.
9
A mouse erythroleukemia cell line possessing friend spleen focus-forming virus gp55 transgene and temperature-sensitive mutant p53 gene.一种具有弗瑞德脾集落形成病毒gp55转基因和温度敏感型突变p53基因的小鼠红白血病细胞系。
Jpn J Cancer Res. 1995 Mar;86(3):284-91. doi: 10.1111/j.1349-7006.1995.tb03052.x.
10
Erythroleukemia induction by Friend leukemia virus. A host gene locus controlling early anemia or polycythemia and the rate of proliferation of late erythroid cells.弗瑞德白血病病毒诱导的红白血病。一个控制早期贫血或红细胞增多症以及晚期红系细胞增殖速率的宿主基因位点。
J Exp Med. 1982 Aug 1;156(2):398-414. doi: 10.1084/jem.156.2.398.

本文引用的文献

1
ASSAY FOR FRIEND LEUKEMIA VIRUS: RAPID QUANTITATIVE METHOD BASED ON ENUMERATION OF MACROSCOPIC SPLEEN FOCI IN MICE.Friend白血病病毒检测:基于小鼠脾脏肉眼可见病灶计数的快速定量方法。
Virology. 1964 Nov;24:513-8. doi: 10.1016/0042-6822(64)90199-0.
2
Tumor formation with transplants of spleen or liver from mice with virus-induced leukemia.用患有病毒诱导白血病的小鼠的脾脏或肝脏移植进行肿瘤形成。
J Natl Cancer Inst. 1960 Dec;25:1279-85.
3
Cell-free transmission in adult Swiss mice of a disease having the character of a leukemia.具有白血病特征的疾病在成年瑞士小鼠中的无细胞传播。
J Exp Med. 1957 Apr 1;105(4):307-18. doi: 10.1084/jem.105.4.307.
4
The molecular biology of Friend virus.弗瑞德病毒的分子生物学
Biochim Biophys Acta. 1980 Sep 22;605(3):305-24. doi: 10.1016/0304-419x(80)90014-1.
5
Friend leukaemia virus-transformed cells, unlike normal stem cells, form spleen colonies in Sl/sld mice.与正常干细胞不同,Friend白血病病毒转化细胞在Sl/sld小鼠体内形成脾集落。
Nature. 1980 Dec 11;288(5791):592-4. doi: 10.1038/288592a0.
6
Release of spleen focus-forming virus (SFFV) from differentiation inducible promyelocytic leukemia cell lines transformed in vitro by Friend leukemia virus.由弗瑞德白血病病毒体外转化的分化诱导早幼粒细胞白血病细胞系中脾脏病灶形成病毒(SFFV)的释放
Virology. 1980 Sep;105(2):425-35. doi: 10.1016/0042-6822(80)90043-4.
7
Anemia- and polycythemia-inducing isolates of Friend spleen focus-forming virus. Biological and molecular evidence for two distinct viral genomes.弗氏脾脏灶形成病毒的贫血和红细胞增多诱导分离株。两种不同病毒基因组的生物学和分子证据。
J Exp Med. 1980 Jun 1;151(6):1477-92. doi: 10.1084/jem.151.6.1477.
8
Malignant myelomonocytic cells after in vitro infection of marrow cells with Friend leukaemia virus.用弗氏白血病病毒体外感染骨髓细胞后产生的恶性骨髓单核细胞
Br J Cancer. 1980 Jan;41(1):33-9. doi: 10.1038/bjc.1980.4.
9
Virus-induced polycythemia in mice: erythropoiesis without erythropoietin.病毒诱导的小鼠红细胞增多症:无促红细胞生成素的红细胞生成
Proc Soc Exp Biol Med. 1968 Jul;128(3):844-9. doi: 10.3181/00379727-128-33139.
10
Regulation of erythropoiesis in the Friend leukemia mouse.对弗氏白血病小鼠红细胞生成的调控
Blood. 1968 Jun;31(6):758-65.

在弗氏病毒白血病病程中致瘤细胞的出现。

Emergence of tumorigenic cells during the course of Friend virus leukemias.

作者信息

Wendling F, Moreau-Gachelin F, Tambourin P

出版信息

Proc Natl Acad Sci U S A. 1981 Jun;78(6):3614-8. doi: 10.1073/pnas.78.6.3614.

DOI:10.1073/pnas.78.6.3614
PMID:6943562
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC319621/
Abstract

Appearance of tumorigenic cells was studied in DBA/2 and ICFW mice infected either with the polycythemia-inducing or the anemia-inducing strain of Friend leukemia virus. Tumorigenicity was defined by transplantability of virus-infected cells into the omentum of an isogeneic preirradiated host. Tumorigenic cells were detected in 50% of the leukemic donors 3 wk after infection by the polycythemia-inducing strain and 7-8 wk after infection by the anemia-inducing strain. These cells appeared first in the spleen and later in peripheral blood, bone marrow, and liver. They consisted of a heterogeneous population at different degrees of malignancy as determined by successive transfers in vivo and in vitro. The observations clearly show that leukemias induced by Friend viruses evolve by multistep processes, in which different stages of malignancy can be detected.

摘要

在感染了诱导红细胞增多或诱导贫血的弗瑞德白血病病毒株的DBA/2和ICFW小鼠中,研究了致瘤细胞的出现情况。致瘤性通过将病毒感染细胞移植到同基因预先照射的宿主的网膜中来定义。在感染诱导红细胞增多病毒株3周后,50%的白血病供体中检测到致瘤细胞;在感染诱导贫血病毒株7 - 8周后,也检测到了致瘤细胞。这些细胞首先出现在脾脏,随后出现在外周血、骨髓和肝脏中。通过体内和体外的连续传代确定,它们由不同恶性程度的异质群体组成。这些观察结果清楚地表明,弗瑞德病毒诱导的白血病是通过多步骤过程发展的,其中可以检测到不同的恶性阶段。