Signaling proteins and transcription factors in normal and malignant early B cell development.

Bone Marrow Research Pub Date : 2011-01-01 Epub Date: 2011-05-20 DOI:10.1155/2011/502751
Patricia Pérez-Vera, Adriana Reyes-León, Ezequiel M Fuentes-Pananá
{"title":"Signaling proteins and transcription factors in normal and malignant early B cell development.","authors":"Patricia Pérez-Vera,&nbsp;Adriana Reyes-León,&nbsp;Ezequiel M Fuentes-Pananá","doi":"10.1155/2011/502751","DOIUrl":null,"url":null,"abstract":"<p><p>B cell development starts in bone marrow with the commitment of hematopoietic progenitors to the B cell lineage. In murine models, the IL-7 and preBCR receptors, and the signaling pathways and transcription factors that they regulate, control commitment and maintenance along the B cell pathway. E2A, EBF1, PAX5, and Ikaros are among the most important transcription factors controlling early development and thereby conditioning mice homeostatic B cell lymphopoiesis. Importantly, their gain or loss of function often results in malignant development in humans, supporting conserved roles for these transcription factors. B cell acute lymphoblastic leukemia is the most common cause of pediatric cancer, and it is characterized by unpaired early B cell development resulting from genetic lesions in these critical signaling pathways and transcription factors. Fine mapping of these genetic abnormalities is allowing more specific treatments, more accurately predicting risk profiles for this disease, and improving survival rates.</p>","PeriodicalId":9220,"journal":{"name":"Bone Marrow Research","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2011-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2011/502751","citationCount":"30","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Bone Marrow Research","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1155/2011/502751","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2011/5/20 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 30

Abstract

B cell development starts in bone marrow with the commitment of hematopoietic progenitors to the B cell lineage. In murine models, the IL-7 and preBCR receptors, and the signaling pathways and transcription factors that they regulate, control commitment and maintenance along the B cell pathway. E2A, EBF1, PAX5, and Ikaros are among the most important transcription factors controlling early development and thereby conditioning mice homeostatic B cell lymphopoiesis. Importantly, their gain or loss of function often results in malignant development in humans, supporting conserved roles for these transcription factors. B cell acute lymphoblastic leukemia is the most common cause of pediatric cancer, and it is characterized by unpaired early B cell development resulting from genetic lesions in these critical signaling pathways and transcription factors. Fine mapping of these genetic abnormalities is allowing more specific treatments, more accurately predicting risk profiles for this disease, and improving survival rates.

Abstract Image

Abstract Image

Abstract Image

正常和恶性早期B细胞发育中的信号蛋白和转录因子。
B细胞的发育始于骨髓,由造血祖细胞向B细胞谱系转移。在小鼠模型中,IL-7和pre - bcr受体及其调控的信号通路和转录因子,沿着B细胞通路控制承诺和维持。E2A, EBF1, PAX5和Ikaros是控制早期发育的最重要的转录因子,从而调节小鼠的稳态B细胞淋巴生成。重要的是,它们功能的获得或丧失通常会导致人类的恶性发展,支持这些转录因子的保守作用。B细胞急性淋巴细胞白血病是儿童癌症最常见的病因,其特点是由于这些关键信号通路和转录因子的遗传病变导致早期B细胞发育不配对。这些基因异常的精细图谱允许更具体的治疗,更准确地预测这种疾病的风险概况,并提高生存率。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信