Effect of a newly developed bisphosphonate, YH529, on osteolytic bone metastases in nude mice

双膦酸盐 骨溶解 医学 病理 牙科 骨质疏松症
作者
Akira Sasaki,Kazuyuki Kitamura,Rafael E. Alcalde,Toshimitsu Tanaka,Atushi Suzuki,Y Etoh,Tomohiro Matsumura
出处
期刊:International Journal of Cancer [Wiley]
卷期号:77 (2): 279-285 被引量:69
标识
DOI:10.1002/(sici)1097-0215(19980717)77:2<279::aid-ijc18>3.0.co;2-6
摘要

YH529, [1-hydroxy-2-(imidazo [1,2-a] pyridin-3-yl) ethylidene]-bisphosphonic acid monohydrate, is a newly developed third-generation bisphosphonate with a potent inhibitory activity toward osteoclastic bone resorption. The primary cellular mechanism of osteolysis associated with metastatic cancer is osteoclast-mediated. It is likely that bisphosphonates would be efficacious in this situation. In the present study, we examined the effect of YH529 in a nude mice bone metastasis model, in which the intracardiac injection of a human breast cancer cell line, MDA-MB-231 (MDA-231), leads to osteolytic bone metastases. To examine whether YH529 would prevent such bone metastasis, we administered YH529 s.c. to nude mice simultaneously with cancer cell inoculation through the entire experimental period (protocol 1) or performed short-term prophylactic administration before inoculation of the MDA-231 cells (protocol 2). In addition, to examine the possible therapeutic effects of the drug on established bone metastases, we injected YH529 after radiographically small but distinct osteolytic bone metastases had been detected (protocol 3). In all protocols, YH529 (2 microg/mouse/day) markedly inhibited bone metastases as well as the progression of established metastatic foci that were quantified on the radiographs. Histological examination and histomorphometrical analysis revealed that YH529 markedly reduced the number of osteoclasts and the size of the tumor at the metastatic bone sites. Our results suggest that YH529 may suppress metastasis formation and tumor growth in bone through inhibition of osteoclastic bone resorption.

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
www完成签到,获得积分10
1秒前
斯文听筠应助西西采纳,获得10
3秒前
专注芹完成签到,获得积分10
4秒前
msd2phd完成签到,获得积分10
5秒前
yoyoyo完成签到,获得积分10
5秒前
5秒前
shinble发布了新的文献求助10
7秒前
无咎0623完成签到 ,获得积分10
8秒前
9秒前
科研熊发布了新的文献求助10
10秒前
池鱼思故渊完成签到,获得积分10
11秒前
宏哥完成签到,获得积分10
11秒前
yangsouth发布了新的文献求助10
12秒前
虚心臻发布了新的文献求助10
13秒前
14秒前
执生完成签到,获得积分10
15秒前
16秒前
lucky应助woaizuoshiyan采纳,获得10
18秒前
Essence应助woaizuoshiyan采纳,获得10
18秒前
cdercder应助woaizuoshiyan采纳,获得10
18秒前
123发布了新的文献求助10
20秒前
21秒前
青帝完成签到 ,获得积分10
21秒前
慕青应助不知道就嘿嘿采纳,获得10
22秒前
Dan完成签到,获得积分10
23秒前
徐六硕完成签到 ,获得积分10
25秒前
kanryu完成签到,获得积分10
25秒前
科研通AI6.2应助yhb采纳,获得10
25秒前
科研通AI6.4应助专注芹采纳,获得10
25秒前
123完成签到,获得积分10
27秒前
领导范儿应助RC采纳,获得10
29秒前
张欢馨应助呜哈哈采纳,获得10
30秒前
32秒前
34秒前
35秒前
35秒前
islazheng应助Yuki采纳,获得10
37秒前
37秒前
37秒前
yehen完成签到,获得积分10
38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
Reducing Compassion Fatigue, Secondary Traumatic Stress and Burnout 600
China Pluperfect I: Epistemology of Past and Outside in Chinese Art 520
Matrix Methods in Data Mining and Pattern Recognition Second Edition 510
Mammalian Synthetic Biology 500
Auslegungsgeschichte 500
Cosmos as Art Object: Studies in Plato's Timaeus and Other Dialogues 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 工程类 有机化学 化学工程 生物化学 计算机科学 内科学 物理 复合材料 催化作用 细胞生物学 无机化学 光电子学 物理化学 电极 基因
热门帖子
关注 科研通微信公众号,转发送积分 7638954
求助须知:如何正确求助?哪些是违规求助? 9212138
关于积分的说明 19761294
捐赠科研通 7205817
什么是DOI,文献DOI怎么找? 3275926
关于科研通互助平台的介绍 2437509
邀请新用户注册赠送积分活动 2273206