首页> 外文期刊>Cancer biology & therapy >CSHL study shows that malignant tumors can be shut down after all Aggressive tumors lacking p53 protein stop dead in their tracks when p53's sister protein-TAp63-steps in
【24h】

CSHL study shows that malignant tumors can be shut down after all Aggressive tumors lacking p53 protein stop dead in their tracks when p53's sister protein-TAp63-steps in

机译:CSHL研究表明,当所有缺乏p53蛋白的侵袭性肿瘤停止死亡时,p53的姊妹蛋白-TAp63逐步转移,恶性肿瘤可以关闭。

获取原文
获取原文并翻译 | 示例
           

摘要

Oncologists have had their hands tied because more than half of all human cancers have mutations that disable a protein called p53. As a critical anti-cancer watchdog, p53 masterminds several cancer-fighting operations within cells.When cells lose p53, tumors grow aggressively and often cannot be treated.These tumors might be tough, but they're not invincible, suggests a new study from Cold Spring Harbor Laboratory (CSHL). The chink in the tumors' armor, according to CSHL Associate Professor Alea Mills, Ph.D., is a protein called TAp63, an older sibling of p53 that's usually intact and not mutated in most cancers.
机译:肿瘤学家之所以束手无策,是因为所有人类癌症中有一半以上都具有使p53蛋白失活的突变。作为一项重要的抗癌监督者,p53策划了细胞内的几种抗癌行动,当细胞丢失p53时,肿瘤会迅速生长且通常无法治疗,这些肿瘤可能很坚韧,但并非无敌,冷泉港实验室(CSHL)。根据CSHL副教授Alea Mills博士的说法,肿瘤的铠甲中的缝隙是一种称为TAp63的蛋白质,它是p53的较老同胞,在大多数癌症中通常是完整的且不会发生突变。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号