Molecular pathogenesis of pediatric thyroid carcinoma

作者
Norisato Mitsutake,Vladimir Saenko
出处
期刊:Journal of Radiation Research [Oxford University Press]
卷期号:62 (Supplement_1): i71-i77 被引量:29
标识
DOI:10.1093/jrr/rraa096
摘要

There has been little understanding of the molecular pathogenesis of pediatric thyroid cancers. Most of them are histologically classified as papillary thyroid carcinoma (PTC). Ionizing radiation is the most important environmental factor to induce PTC, especially in children. Particularly, radiation-related pediatric PTCs after the Chernobyl accident provided invaluable information. In addition, the recent accumulation of sporadic pediatric PTC cases, partly due to advances in diagnostic imaging, has also provided insight into their general pathogenesis. In PTC development, basically two types of genetic alterations, fusion oncogenes, mainly RET/PTC, and a point mutation, mainly BRAFV600E, are thought to play a key role as driver oncogenes. Their frequencies vary depending on patient age. The younger the age, the more prevalent the fusion oncogenes are. Higher incidence of fusion oncogenes was also observed in cases exposed to radiation. In short, fusion oncogenes are associated with both age and radiation and are not evidence of radiation exposure. The type of driver oncogene is shifted toward BRAFV600E during adolescence in sporadic PTCs. However, until about this age, fusion oncogenes seem to still confer dominant growth advantages, which may lead to the higher discovery rate of the fusion oncogenes. It has been postulated that RET/PTC in radiation-induced PTC is generated by ionizing radiation; however, there is an interesting hypothesis that thyroid follicular cell clones with pre-existing RET/PTC were already present, and radiation may play a role as a promoter/progressor but not initiator. Telomerase reverse transcriptase gene (TERT) promoter mutations, which are the strongest marker of tumor aggressiveness in adult PTC cases, have not been detected in pediatric cases; however, TERT expression without the mutations may play a role in tumor aggressiveness. In this paper, the recent information regarding molecular findings in sporadic and radiation-associated pediatric PTCs is summarized.

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
体贴千风完成签到 ,获得积分10
刚刚
1秒前
笋之完成签到,获得积分10
1秒前
2秒前
海绵饱饱完成签到 ,获得积分10
3秒前
3秒前
高佳慧完成签到,获得积分20
4秒前
jhy完成签到 ,获得积分10
4秒前
LL完成签到,获得积分10
4秒前
5秒前
5秒前
nzx发布了新的文献求助10
6秒前
田恬完成签到,获得积分10
6秒前
闪闪完成签到,获得积分10
7秒前
8秒前
羊村长完成签到,获得积分10
9秒前
aa发布了新的文献求助10
9秒前
9秒前
郁是忻发布了新的文献求助10
9秒前
JamesPei的应助被光亮的念珍采纳,获得10
10秒前
10秒前
11秒前
KG的应助被gdsfgdf采纳,获得10
12秒前
烟花的应助被珍蚌好命女采纳,获得10
12秒前
Hello的应助被纳米采纳,获得10
12秒前
kkk完成签到 ,获得积分20
12秒前
luoshiyi完成签到,获得积分20
12秒前
11111111的应助被王大男采纳,获得30
13秒前
无奈的小懒虫完成签到 ,获得积分10
13秒前
沈清酌完成签到,获得积分10
13秒前
13秒前
14秒前
14秒前
困困羊发布了新的文献求助10
14秒前
LL发布了新的文献求助10
15秒前
漏漏漏发布了新的文献求助30
15秒前
15秒前
田様的应助被熙悦采纳,获得10
16秒前
沉静的傲旋完成签到 ,获得积分10
16秒前
16秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
IRTSD: Open-Source Data and Toolset for Electromagnetic Transient Analysis of Disturbances and IBR Control Malfunctions in Transmission Systems 1000
Les Mots du discours 600
A Consideration on Use of Material Grades for Hull Structural Members Based on Fracture Toughness(Second Report) 500
AI Disclosure in Annual Reports: Evolution, Determinants, and Capital Market Participants’ Perceptions 500
5th World Conference on Detergents: Reinventing the Industry : Opportunities and Challenges 500
Erzählte Gnade 500
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 计算机科学 工程类 有机化学 化学工程 生物化学 物理 复合材料 内科学 催化作用 光电子学 人工智能 细胞生物学 无机化学 物理化学 数学
热门帖子
关注 科研通微信公众号,转发送积分 8110045
求助须知:如何正确求助?哪些是违规求助? 9517546
关于积分的说明 21513219
捐赠科研通 7687256
什么是DOI,文献DOI怎么找? 3411481
关于科研通互助平台的介绍 2538628
邀请新用户注册赠送积分活动 2451427