• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

Nonrandom chromosome changes involving the Ig gene-carrying chromosomes 12 and 6 in pristane-induced mouse plasmacytomas.

作者信息

Ohno S, Babonits M, Wiener F, Spira J, Klein G, Potter M

出版信息

Cell. 1979 Dec;18(4):1001-7. doi: 10.1016/0092-8674(79)90212-5.

DOI:10.1016/0092-8674(79)90212-5
PMID:519762
Abstract

The karyotypes of pristane-induced mouse plasmacytomas were studied by G banding. Only primary tumors or early passage generations were analyzed. In contrast to murine T cell leukemias that showed a regular trisomy of chromosome 15, all plasmacytomas showed a consistent translocation of the distal part of chromosome 15 to either chromosome 6 [rcpT(6;15)] or 12 [T(12;15)]. The specific breakpoints were at 6C, 15D3/E ro D2/3 and 12F2. Early passage generations often showed a mixed population with two different translocations, suggesting polyclonal origin. Considered together with the known karyotypic features of murine and human lymphomas, these findings support the theory that the nonrandom chromosomal changes in lymphoproliferative malignancies are associated with the type of the target cell, rather than with the etiological agent. Moreover, the involvement of the chromosomes known to carry the heavy chain (12) and the light chain (6) determinants, respectively, raises the question of whether the translocations may be related to the DNA level rearrangements known to occur during the differentiation of normal plasma cells.

摘要

相似文献

1
Nonrandom chromosome changes involving the Ig gene-carrying chromosomes 12 and 6 in pristane-induced mouse plasmacytomas.
Cell. 1979 Dec;18(4):1001-7. doi: 10.1016/0092-8674(79)90212-5.
2
Specific chromosome translocation in pristane-induced plasmacytomas of NZB mice.NZB小鼠中 pristane 诱导的浆细胞瘤的特定染色体易位。
J Natl Cancer Inst. 1984 Feb;72(2):347-53.
3
Chromosomal translocations activating myc sequences and transduction of v-abl are critical events in the rapid induction of plasmacytomas by pristane and abelson virus.激活myc序列的染色体易位以及v-abl的转导是 pristane 和 Abelson 病毒快速诱导浆细胞瘤过程中的关键事件。
J Exp Med. 1984 Jun 1;159(6):1762-77. doi: 10.1084/jem.159.6.1762.
4
High resolution banding analysis of the involvement of strain BALB/c- and AKR-derived chromosomes No. 15 in plasmacytoma-specific translocations.对BALB/c品系和AKR品系来源的第15号染色体参与浆细胞瘤特异性易位情况的高分辨率显带分析。
J Exp Med. 1984 Jan 1;159(1):276-91. doi: 10.1084/jem.159.1.276.
5
DNA sequence associated with chromosome translocations in mouse plasmacytomas.与小鼠浆细胞瘤中染色体易位相关的DNA序列。
Proc Natl Acad Sci U S A. 1982 Nov;79(21):6622-6. doi: 10.1073/pnas.79.21.6622.
6
[Chromosome translocations and the activation of C-myc oncogene in mouse plasmacytomas].[小鼠浆细胞瘤中的染色体易位与C-myc癌基因激活]
Gan To Kagaku Ryoho. 1984 Mar;11(3 Pt 2):587-96.
7
Hemizygous interstitial deletion of chromosome 15 (band D) in three translocation-negative murine plasmacytomas.三个易位阴性小鼠浆细胞瘤中15号染色体(D带)的半合子间质性缺失
Proc Natl Acad Sci U S A. 1984 Feb;81(4):1159-63. doi: 10.1073/pnas.81.4.1159.
8
Functional homology between N-myc and c-myc in murine plasmacytomagenesis: plasmacytoma development in N-myc transgenic mice.N-myc与c-myc在小鼠浆细胞瘤发生中的功能同源性:N-myc转基因小鼠中的浆细胞瘤发展
Oncogene. 1992 Jun;7(6):1241-7.
9
Non-random chromosomal changes involving chromosomes 6 and 7 in spontaneous rat immunocytomas.自发大鼠免疫细胞瘤中涉及6号和7号染色体的非随机染色体变化。
Int J Cancer. 1982 Apr 15;29(4):431-7. doi: 10.1002/ijc.2910290412.
10
Cytogenetic studies on IgA/lambda-producing murine plasmacytomas: regular occurrence of a T(12;15) translocation.产生IgA/λ的小鼠浆细胞瘤的细胞遗传学研究:T(12;15)易位的常见发生情况
Somatic Cell Genet. 1980 Nov;6(6):731-8. doi: 10.1007/BF01538972.

引用本文的文献

1
Is cancer progression caused by gradual or simultaneous acquisitions of new chromosomes?癌症进展是由新染色体的逐渐获得还是同时获得引起的?
Mol Cytogenet. 2018 Jan 15;11:4. doi: 10.1186/s13039-017-0350-4. eCollection 2018.
2
KSHV Latency Locus Cooperates with Myc to Drive Lymphoma in Mice.卡波西肉瘤相关疱疹病毒潜伏位点与Myc协同作用驱动小鼠淋巴瘤发生。
PLoS Pathog. 2015 Sep 1;11(9):e1005135. doi: 10.1371/journal.ppat.1005135. eCollection 2015 Sep.
3
The emerging complexity of gene fusions in cancer.癌症中基因融合的新兴复杂性。
Nat Rev Cancer. 2015 Jun;15(6):371-81. doi: 10.1038/nrc3947.
4
c-MYC-induced genomic instability.c-MYC诱导的基因组不稳定。
Cold Spring Harb Perspect Med. 2014 Apr 1;4(4):a014373. doi: 10.1101/cshperspect.a014373.
5
Duplication of Subcytoband 11E2 of Chromosome 11 Is Regularly Associated with Accelerated Tumor Development in v-abl/myc-Induced Mouse Plasmacytomas.11号染色体亚细胞带11E2的复制与v-abl/myc诱导的小鼠浆细胞瘤中肿瘤的加速发展经常相关。
Genes Cancer. 2010 Aug;1(8):847-58. doi: 10.1177/1947601910382897.
6
Deregulation of c-Myc Confers distinct survival requirements for memory B cells, plasma cells, and their progenitors.c-Myc 的失调赋予记忆 B 细胞、浆细胞及其祖细胞不同的生存需求。
J Immunol. 2008 Dec 1;181(11):7537-49. doi: 10.4049/jimmunol.181.11.7537.
7
AID-deficient Bcl-xL transgenic mice develop delayed atypical plasma cell tumors with unusual Ig/Myc chromosomal rearrangements.AID 缺陷的 Bcl-xL 转基因小鼠会发展出具有异常 Ig/Myc 染色体重排的延迟性非典型浆细胞瘤。
J Exp Med. 2007 Nov 26;204(12):2989-3001. doi: 10.1084/jem.20070882. Epub 2007 Nov 6.
8
Rearrangements of the telomeric region of mouse chromosome 11 in Pre-B ABL/MYC cells revealed by mBANDing, spectral karyotyping, and fluorescence in-situ hybridization with a subtelomeric probe.通过mBANDing、光谱核型分析以及使用亚端粒探针进行荧光原位杂交,揭示了前B细胞ABL/MYC细胞中小鼠11号染色体端粒区域的重排。
Chromosome Res. 2004;12(8):777-85. doi: 10.1007/s10577-005-5264-z.
9
Novel targeted deregulation of c-Myc cooperates with Bcl-X(L) to cause plasma cell neoplasms in mice.c-Myc的新型靶向性失调与Bcl-X(L)协同作用导致小鼠浆细胞瘤。
J Clin Invest. 2004 Jun;113(12):1763-73. doi: 10.1172/JCI20369.
10
The impact of p53 loss on murine plasmacytoma development.p53缺失对小鼠浆细胞瘤发生发展的影响。
Chromosome Res. 2002;10(3):239-51. doi: 10.1023/a:1015200307448.