禽淋巴细胞白血病：淋巴瘤发生机制 - Suppr

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Avian lymphoid leukosis: mechanisms of lymphomagenesis.

作者信息

Ewert D L, de Boer G F

机构信息

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

出版信息

Adv Vet Sci Comp Med. 1988;32:37-55. doi: 10.1016/b978-0-12-039232-2.50006-2.

DOI:10.1016/b978-0-12-039232-2.50006-2

PMID:2847503

Abstract

摘要

相似文献

Avian lymphoid leukosis: mechanisms of lymphomagenesis.禽淋巴细胞白血病：淋巴瘤发生机制

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Normal and neoplastic B cell development in the bursa of fabricius.法氏囊中正常和肿瘤性B细胞的发育

Curr Top Microbiol Immunol. 1986;132:209-14. doi: 10.1007/978-3-642-71562-4_30.

Restrictions that influence avian leukosis virus-induced lymphoid leukosis.影响禽白血病病毒诱导的淋巴细胞白血病的限制因素。

Curr Top Microbiol Immunol. 1986;132:215-20. doi: 10.1007/978-3-642-71562-4_31.

Follicular hyperplasia in the prelymphomatous avian bursa: relationship to the incidence of B-cell lymphomas.淋巴瘤前期禽法氏囊的滤泡增生：与B细胞淋巴瘤发病率的关系

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Formation of a transformed follicle is necessary but not sufficient for development of an avian leukosis virus-induced lymphoma.转化卵泡的形成对于禽白血病病毒诱导的淋巴瘤的发展是必要的，但不是充分的。

Proc Natl Acad Sci U S A. 1985 Jan;82(1):213-6. doi: 10.1073/pnas.82.1.213.

Importance of the medullary macrophage in the replication of lymphoid leukosis virus in the bursa of Fabricius of chickens.髓样巨噬细胞在鸡法氏囊中淋巴白血病病毒复制中的重要性。

Am J Vet Res. 1987 Apr;48(4):613-20.

Development of an antigen in visceral lymphomatosis and splenic lymphoid foci.内脏淋巴瘤病和脾淋巴样病灶中一种抗原的发育。

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Long terminal repeat (LTR) sequences, env, and a region near the 5' LTR influence the pathogenic potential of recombinants between Rous-associated virus types 0 and 1.长末端重复序列（LTR）、包膜蛋白（env）以及5' LTR附近的一个区域会影响劳氏相关病毒0型和1型之间重组体的致病潜力。

J Virol. 1988 Sep;62(9):3431-7. doi: 10.1128/JVI.62.9.3431-3437.1988.

Lymphoid leukosis: detection of group specific viral antigen in chicken spleens by immunofluorescence and complement fixation.淋巴细胞性白血病：通过免疫荧光和补体结合法检测鸡脾脏中的群特异性病毒抗原

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Dynamics of protein 27 of avian leukosis virus and transforming growth factor beta2 in lymphoid leukosis susceptible and resistant broiler chicken breeding stock.

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引用本文的文献

Endogenous Avian Leukosis Virus in Combination with Serotype 2 Marek's Disease Virus Significantly Boosted the Incidence of Lymphoid Leukosis-Like Bursal Lymphomas in Susceptible Chickens.内源性禽白血病病毒与血清型 2 型马立克氏病病毒联合显著增加易感鸡发生淋巴白血病样法氏囊淋巴瘤的发生率。

J Virol. 2019 Nov 13;93(23). doi: 10.1128/JVI.00861-19. Print 2019 Dec 1.

Differential selection of cells with proviral c-myc and c-erbB integrations after avian leukosis virus infection.禽白血病病毒感染后具有原病毒c-myc和c-erbB整合的细胞的差异选择。

J Virol. 1998 Jul;72(7):5517-25. doi: 10.1128/JVI.72.7.5517-5525.1998.

bic, a novel gene activated by proviral insertions in avian leukosis virus-induced lymphomas, is likely to function through its noncoding RNA.Bic是一种在禽白血病病毒诱导的淋巴瘤中由前病毒插入激活的新基因，可能通过其非编码RNA发挥作用。

Mol Cell Biol. 1997 Mar;17(3):1490-502. doi: 10.1128/MCB.17.3.1490.

Identification of EFIV, a stable factor present in many avian cell types that transactivates sequences in the 5' portion of the Rous sarcoma virus long terminal repeat enhancer.鉴定出EFIV，一种存在于多种禽类细胞类型中的稳定因子，它可反式激活劳氏肉瘤病毒长末端重复序列增强子5'部分的序列。

J Virol. 1996 Jan;70(1):393-401. doi: 10.1128/JVI.70.1.393-401.1996.

The VBP and a1/EBP leucine zipper factors bind overlapping subsets of avian retroviral long terminal repeat CCAAT/enhancer elements.VBP和a1/EBP亮氨酸拉链因子与禽逆转录病毒长末端重复CCAAT/增强子元件的重叠亚集结合。

J Virol. 1994 Oct;68(10):6232-42. doi: 10.1128/JVI.68.10.6232-6242.1994.

Tissue-specific lability and expression of avian leukosis virus long terminal repeat enhancer-binding proteins.禽白血病病毒长末端重复序列增强子结合蛋白的组织特异性不稳定性与表达

Mol Cell Biol. 1989 Dec;9(12):5660-8. doi: 10.1128/mcb.9.12.5660-5668.1989.

Multiple proto-oncogene activations in avian leukosis virus-induced lymphomas: evidence for stage-specific events.禽白血病病毒诱导的淋巴瘤中多个原癌基因的激活：阶段特异性事件的证据。

Mol Cell Biol. 1989 Jun;9(6):2657-64. doi: 10.1128/mcb.9.6.2657-2664.1989.

a1/EBP: a leucine zipper protein that binds CCAAT/enhancer elements in the avian leukosis virus long terminal repeat enhancer.a1/EBP：一种亮氨酸拉链蛋白，可结合禽白血病病毒长末端重复增强子中的CCAAT/增强子元件。

J Virol. 1992 Nov;66(11):6578-86. doi: 10.1128/JVI.66.11.6578-6586.1992.

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