• 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

与急性非淋巴细胞白血病的一种特定亚型相关的（6；9）染色体易位，导致9q34上一个靶基因的异常转录。

The (6;9) chromosome translocation, associated with a specific subtype of acute nonlymphocytic leukemia, leads to aberrant transcription of a target gene on 9q34.

作者信息

von Lindern M, Poustka A, Lerach H, Grosveld G

机构信息

Department of Cell Biology and Genetics, Erasmus University, Rotterdam, The Netherlands.

出版信息

Mol Cell Biol. 1990 Aug;10(8):4016-26. doi: 10.1128/mcb.10.8.4016-4026.1990.

DOI:10.1128/mcb.10.8.4016-4026.1990
PMID:2370860
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC360912/
Abstract

The specific (6;9)(p23;q34) chromosomal translocation is associated with a defined subtype of acute nonlymphocytic leukemia (ANLL). The 9q34 breakpoint is located at the telomeric side of the c-abl gene. Through a combination of chromosome jumping, long-range mapping, and chromosome walking, the chromosome 9 breakpoints of several t(6;9) ANLL patients were localized within a defined region of 8 kilobases (kb), 360 kb telomeric of c-abl. Subsequent cDNA cloning revealed that this region represented an intron in the middle of a gene, called Cain (can), encoding a 7.5-kb transcript. Disruption of the can gene by the translocation resulted in the expression of a new 5.5-kb can mRNA from the 6p- chromosome. Isolation of chromosome 6 sequences showed that breakpoints on 6p23 also clustered within a limited stretch of DNA. These data strongly suggest a direct involvement of the translocation in the leukemic process of t(6;9) ANLL.

摘要

特定的(6;9)(p23;q34)染色体易位与急性非淋巴细胞白血病(ANLL)的一种特定亚型相关。9q34断点位于c-abl基因的端粒侧。通过染色体跳跃、长距离定位和染色体步移相结合的方法，几位t(6;9)ANLL患者的9号染色体断点被定位在c-abl基因端粒360 kb处一个8千碱基(kb)的特定区域内。随后的cDNA克隆显示，该区域代表一个基因中部的内含子，该基因名为Cain(can)，编码一个7.5 kb的转录本。易位导致can基因中断，从而使6号染色体短臂(p)上表达一种新的5.5 kb的can mRNA。6号染色体序列的分离表明，6p23上的断点也聚集在一段有限的DNA片段内。这些数据强烈表明，该易位直接参与了t(6;9)ANLL的白血病发生过程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a580/360912/1a0eb4c60af5/molcellb00044-0177-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a580/360912/87ebce969f43/molcellb00044-0172-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a580/360912/40bac6952a81/molcellb00044-0173-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a580/360912/740c6d90deef/molcellb00044-0174-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a580/360912/766520ccc305/molcellb00044-0175-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a580/360912/b075d0dce5ca/molcellb00044-0175-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a580/360912/1a0eb4c60af5/molcellb00044-0177-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a580/360912/87ebce969f43/molcellb00044-0172-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a580/360912/40bac6952a81/molcellb00044-0173-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a580/360912/740c6d90deef/molcellb00044-0174-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a580/360912/766520ccc305/molcellb00044-0175-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a580/360912/b075d0dce5ca/molcellb00044-0175-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a580/360912/1a0eb4c60af5/molcellb00044-0177-a.jpg

相似文献

1
The (6;9) chromosome translocation, associated with a specific subtype of acute nonlymphocytic leukemia, leads to aberrant transcription of a target gene on 9q34.与急性非淋巴细胞白血病的一种特定亚型相关的（6；9）染色体易位，导致9q34上一个靶基因的异常转录。
Mol Cell Biol. 1990 Aug;10(8):4016-26. doi: 10.1128/mcb.10.8.4016-4026.1990.
2
Can, a putative oncogene associated with myeloid leukemogenesis, may be activated by fusion of its 3' half to different genes: characterization of the set gene.Can是一种与髓系白血病发生相关的假定致癌基因，其3'端的一半与不同基因融合时可能被激活：set基因的特征分析。
Mol Cell Biol. 1992 Aug;12(8):3346-55. doi: 10.1128/mcb.12.8.3346-3355.1992.
3
Molecular cytogenetics of chronic myeloid leukemia with atypical t(6;9) (p23;q34) translocation.伴有非典型t(6;9)(p23;q34)易位的慢性髓性白血病的分子细胞遗传学
Leukemia. 1995 Jun;9(6):981-7.
4
Translocation t(6;9) in acute non-lymphocytic leukaemia results in the formation of a DEK-CAN fusion gene.急性非淋巴细胞白血病中的易位t(6;9)导致DEK-CAN融合基因的形成。
Baillieres Clin Haematol. 1992 Oct;5(4):857-79. doi: 10.1016/s0950-3536(11)80049-1.
5
Loss of the Y chromosome associated with translocation t(6;9)(p23;q34) in a patient with acute nonlymphocytic leukemia.一名急性非淋巴细胞白血病患者中与6号和9号染色体易位t(6;9)(p23;q34)相关的Y染色体缺失。
Cancer Genet Cytogenet. 1989 May;39(1):81-7. doi: 10.1016/0165-4608(89)90233-1.
6
The human pim-1 gene is not directly activated by the translocation (6;9) in acute nonlymphocytic leukemia.人类pim - 1基因不会被急性非淋巴细胞白血病中的易位(6;9)直接激活。
Oncogene. 1989 Jan;4(1):75-9.
7
t(8;21) breakpoints on chromosome 21 in acute myeloid leukemia are clustered within a limited region of a single gene, AML1.急性髓系白血病中21号染色体上的t(8;21)断点聚集在单个基因AML1的有限区域内。
Proc Natl Acad Sci U S A. 1991 Dec 1;88(23):10431-4. doi: 10.1073/pnas.88.23.10431.
8
The first BCR gene intron contains breakpoints in Philadelphia chromosome positive leukemia.首个BCR基因内含子在费城染色体阳性白血病中存在断点。
Nucleic Acids Res. 1988 Nov 11;16(21):10069-81. doi: 10.1093/nar/16.21.10069.
9
Molecular cloning of translocation t(1;14)(q21;q32) defines a novel gene (BCL9) at chromosome 1q21.易位t(1;14)(q21;q32)的分子克隆确定了位于1号染色体q21的一个新基因（BCL9）。
Blood. 1998 Mar 15;91(6):1873-81.
10
The translocation (6;9) (p23;q34) shows consistent rearrangement of two genes and defines a myeloproliferative disorder with specific clinical features.6号和9号染色体易位（6；9）（p23；q34）显示两个基因持续重排，并定义了一种具有特定临床特征的骨髓增殖性疾病。
Blood. 1992 Jun 1;79(11):2990-7.

引用本文的文献

1
XPO1-dependency of DEK::NUP214 leukemia.DEK::NUP214白血病对XPO1的依赖性
Leukemia. 2025 May;39(5):1102-1113. doi: 10.1038/s41375-025-02570-1. Epub 2025 Mar 27.
2
Identification of hub genes and potential molecular mechanisms related to drug sensitivity in acute myeloid leukemia based on machine learning.基于机器学习的急性髓系白血病中与药物敏感性相关的枢纽基因及潜在分子机制的鉴定
Front Pharmacol. 2024 Apr 8;15:1359832. doi: 10.3389/fphar.2024.1359832. eCollection 2024.
3
Interstitial Deletions Generating Fusion Genes.形成融合基因的染色体间片段缺失

本文引用的文献

1
Lymphoblastic lymphoma: cytogenetic, pathologic, and immunologic studies.
Int J Cancer. 1982 Sep 15;30(3):273-9. doi: 10.1002/ijc.2910300304.
2
Translocation of the c-myc gene into the immunoglobulin heavy chain locus in human Burkitt lymphoma and murine plasmacytoma cells.在人类伯基特淋巴瘤和鼠浆细胞瘤细胞中，c-myc基因易位至免疫球蛋白重链基因座。
Proc Natl Acad Sci U S A. 1982 Dec;79(24):7837-41. doi: 10.1073/pnas.79.24.7837.
3
Localization of human immunoglobulin kappa light chain variable region genes to the short arm of chromosome 2 by in situ hybridization.通过原位杂交将人免疫球蛋白κ轻链可变区基因定位于2号染色体短臂。
Cancer Genomics Proteomics. 2021 May-Jun;18(3):167-196. doi: 10.21873/cgp.20251.
4
Targeted CRM1-inhibition perturbs leukemogenic NUP214 fusion proteins and exerts anti-cancer effects in leukemia cell lines with rearrangements.靶向CRM1抑制可扰乱致白血病的NUP214融合蛋白，并对具有重排的白血病细胞系发挥抗癌作用。
Oncotarget. 2020 Sep 8;11(36):3371-3386. doi: 10.18632/oncotarget.27711.
5
Disclosing the Interactome of Leukemogenic NUP98-HOXA9 and SET-NUP214 Fusion Proteins Using a Proteomic Approach.采用蛋白质组学方法揭示白血病致癌 NUP98-HOXA9 和 SET-NUP214 融合蛋白的相互作用组。
Cells. 2020 Jul 10;9(7):1666. doi: 10.3390/cells9071666.
6
Pathogenic Variants in NUP214 Cause "Plugged" Nuclear Pore Channels and Acute Febrile Encephalopathy.NUP214 中的致病性变异导致“堵塞”核孔通道和急性发热性脑病。
Am J Hum Genet. 2019 Jul 3;105(1):48-64. doi: 10.1016/j.ajhg.2019.05.003. Epub 2019 Jun 6.
7
NUP214 in Leukemia: It's More than Transport.NUP214 在白血病中的作用：不止是运输。
Cells. 2019 Jan 21;8(1):76. doi: 10.3390/cells8010076.
8
Whole-exome sequence analysis highlights the role of unmasked recessive mutations in copy number variants with incomplete penetrance.外显子组测序分析强调了未掩盖的隐性突变在部分外显率的拷贝数变异中的作用。
Eur J Hum Genet. 2018 Jun;26(6):912-918. doi: 10.1038/s41431-018-0124-4. Epub 2018 Feb 26.
9
[Clinical characteristics of four SET-NUP214 positive acute leukemia patients].[4例SET-NUP214阳性急性白血病患者的临床特征]
Zhonghua Xue Ye Xue Za Zhi. 2017 Dec 14;38(12):1062-1065. doi: 10.3760/cma.j.issn.0253-2727.2017.12.012.
10
-Fusion Identified by RNA-Sequencing of an Acute Myeloid Leukemia with t(9;12)(q34;q15).- 通过RNA测序在伴有t(9;12)(q34;q15)的急性髓系白血病中鉴定出融合现象
Cancer Genomics Proteomics. 2017 Nov-Dec;14(6):437-443. doi: 10.21873/cgp.20053.
Proc Natl Acad Sci U S A. 1982 Aug;79(16):4957-61. doi: 10.1073/pnas.79.16.4957.
4
Human immunoglobulin heavy chain genes map to a region of translocations in malignant B lymphocytes.人类免疫球蛋白重链基因定位于恶性B淋巴细胞的易位区域。
Science. 1982 Apr 16;216(4543):301-3. doi: 10.1126/science.6801764.
5
Assignment of the genes for human lambda immunoglobulin chains to chromosome 22.人类λ免疫球蛋白链基因定位于22号染色体。
Nature. 1981 Nov 12;294(5837):173-5. doi: 10.1038/294173a0.
6
Purification of mouse immunoglobulin heavy-chain messenger RNAs from total myeloma tumor RNA.从小鼠骨髓瘤肿瘤总RNA中纯化小鼠免疫球蛋白重链信使RNA。
Eur J Biochem. 1980 Jun;107(2):303-14. doi: 10.1111/j.1432-1033.1980.tb06030.x.
7
Molecular cloning of the chromosomal breakpoint of B-cell lymphomas and leukemias with the t(11;14) chromosome translocation.伴有t(11;14)染色体易位的B细胞淋巴瘤和白血病染色体断裂点的分子克隆
Science. 1984 Jun 29;224(4656):1403-6. doi: 10.1126/science.6610211.
8
Amplified C lambda and c-abl genes are on the same marker chromosome in K562 leukemia cells.在K562白血病细胞中，扩增的Cλ和c-abl基因位于同一条标记染色体上。
Proc Natl Acad Sci U S A. 1983 Dec;80(23):7289-92. doi: 10.1073/pnas.80.23.7289.
9
Localization of the c-ab1 oncogene adjacent to a translocation break point in chronic myelocytic leukaemia.慢性粒细胞白血病中与易位断点相邻的c-ab1癌基因的定位。
Nature. 1983;306(5940):239-42. doi: 10.1038/306239a0.
10
Lambda replacement vectors carrying polylinker sequences.携带多克隆位点序列的λ置换载体。
J Mol Biol. 1983 Nov 15;170(4):827-42. doi: 10.1016/s0022-2836(83)80190-9.