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Resistance through repopulation

机译:人口增加带来的抵抗

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摘要

Initial or acquired resistance to anticancer drugs limits their effectiveness. Many papers have described mechanisms underlying such drug resistance, but most have evaluated molecular changes in single tumour cells, with the emphasis on stable genetic changes that may be induced by therapy or selected for. However, causes of drug resistance are multiple and complex, and in this issue, Kurtova et al.1 (page 209) explore an alternative mechanism - the repopulation of tumours by cancer stem cells that survive treatment. The authors show that, in certain bladder tumours, repopulation is stimulated by the hormone-like lipid molecule prostaglandin E_2 (PGE_2), which is released from tumour cells that are killed by the initial chemotherapy. Furthermore, the authors show that repopulation can be inhibited by the drug celecoxib, which inhibits PGE_2 synthesis.
机译:最初或获得的抗癌药耐药性限制了其有效性。许多论文描述了这种耐药性的潜在机制,但是大多数论文评估了单个肿瘤细胞中的分子变化,重点是可能由治疗诱导或选择的稳定遗传变化。然而,耐药性的原因是多种多样且复杂的,在这个问题中,Kurtova等人(第209页)探讨了另一种机制-存活下来的癌症干细胞在肿瘤中的繁殖。这组作者表明,在某些膀胱肿瘤中,激素样脂质分子前列腺素E_2(PGE_2)刺激了再增殖,该激素从最初的化疗杀死的肿瘤细胞中释放出来。此外,作者表明,塞来昔布可以抑制PGE_2的合成,从而抑制种群的再繁殖。

著录项

  • 来源
    《Nature》 |2015年第7533期|152-153|共2页
  • 作者

    IAN F. TANNOCK;

  • 作者单位

    Department of Medical Oncology, Princess Margaret Cancer Centre, Toronto, Ontario M5G 2M9, Canada;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

  • 入库时间 2022-08-18 02:52:29

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