How Do Telomere Abnormalities Regulate the Biology of Neuroblastoma?

How Do Telomere Abnormalities Regulate the Biology of Neuroblastoma?
复制标题

DOI:
10.3390/biom11081112
复制
发表时间:
2021-07-28
期刊:
影响因子:
5.5
通讯作者:
Kamijo T
Kamijo T
中科院分区:
生物学2区
文献类型:
--
作者:
Akter J;Kamijo T

文献摘要

参考文献

被引文献

相似文献

端粒的维持在基因组稳定和细胞增殖中起着重要作用。肿瘤细胞通过激活端粒维持机制(TMM)(端粒酶,一种逆转录酶)或端粒延长(ALT)机制获得复制永生。TMM的遗传和分子特征的最新进展表明,端粒酶激活和ALT定义了具有不良结局的不同神经母细胞瘤(NB)亚组,并代表了高危神经母细胞瘤(HRNB)的有希望的治疗靶点,HRNB是一种侵袭性儿童实体瘤,占所有儿科癌症死亡的15%。HRNB患者经常出现广泛转移性疾病,肿瘤携带复发性遗传畸变(MYCN扩增、TERT重排和ATRX突变),这些畸变相互排斥,能够促进TMM。这篇综述提供了我们对NB肿瘤中TMM的理解的最新见解,并强调了新兴的治疗策略作为端粒酶和ALT阳性肿瘤的潜在治疗方法。
Telomere maintenance plays important roles in genome stability and cell proliferation. Tumor cells acquire replicative immortality by activating a telomere-maintenance mechanism (TMM), either telomerase, a reverse transcriptase, or the alternative lengthening of telomeres (ALT) mechanism. Recent advances in the genetic and molecular characterization of TMM revealed that telomerase activation and ALT define distinct neuroblastoma (NB) subgroups with adverse outcomes, and represent promising therapeutic targets in high-risk neuroblastoma (HRNB), an aggressive childhood solid tumor that accounts for 15% of all pediatric-cancer deaths. Patients with HRNB frequently present with widely metastatic disease, with tumors harboring recurrent genetic aberrations (MYCN amplification, TERT rearrangements, and ATRX mutations), which are mutually exclusive and capable of promoting TMM. This review provides recent insights into our understanding of TMM in NB tumors, and highlights emerging therapeutic strategies as potential treatments for telomerase- and ALT-positive tumors.
DOI: 10.1126/science.aat6768
发表时间: 2018-12-07
期刊: Science (New York, N.Y.)
影响因子: --
作者:
Ackermann S;Cartolano M;Hero B;Welte A;Kahlert Y;Roderwieser A;Bartenhagen C;Walter E;Gecht J;Kerschke L;Volland R;Menon R;Heuckmann JM;Gartlgruber M;Hartlieb S;Henrich KO;Okonechnikov K;Altmüller J;Nürnberg P;Lefever S;de Wilde B;Sand F;Ikram F;Rosswog C;Fischer J;Theissen J;Hertwig F;Singhi AD;Simon T;Vogel W;Perner S;Krug B;Schmidt M;Rahmann S;Achter V;Lang U;Vokuhl C;Ortmann M;Büttner R;Eggert A;Speleman F;O'Sullivan RJ;Thomas RK;Berthold F;Vandesompele J;Schramm A;Westermann F;Schulte JH;Peifer M;Fischer M
通讯作者: Fischer M
31种癌症类型的端粒长度和躯体改变的系统分析。
DOI: 10.1038/ng.3781
发表时间: 2017-03
期刊: Nature genetics
影响因子: 30.8
作者:
Barthel FP;Wei W;Tang M;Martinez-Ledesma E;Hu X;Amin SB;Akdemir KC;Seth S;Song X;Wang Q;Lichtenberg T;Hu J;Zhang J;Zheng S;Verhaak RG
通讯作者: Verhaak RG
DOI: 10.1126/science.1170633
发表时间: 2009-11-13
期刊: Science (New York, N.Y.)
影响因子: --
作者:
de Lange T
通讯作者: de Lange T
DOI: 10.1016/j.ejca.2005.08.025
发表时间: 2005-12-01
影响因子: 8.4
作者:
Binz, N;Shalaby, T;Grotzer, MA
通讯作者: Grotzer, MA
DOI: 10.1002/j.1460-2075.1995.tb00098.x
发表时间: 1995-09-01
期刊: EMBO JOURNAL
影响因子: 11.4
作者:
BRYAN, TM;ENGLEZOU, A;REDDEL, RR
通讯作者: REDDEL, RR