英国科学家发现潜在的脑肿瘤药物靶点

英国利兹大学的一项研究已经发现，通过靶向一个分子帮助细胞恢复他们的DNA，可能为一些侵袭性脑肿瘤带来新的治疗方式。

研究人员发现，在实验室关闭RAD51分子，杀死恶性胶质瘤细胞，提高了放射治疗的效果。

恶性胶质瘤是成年人常见的脑肿瘤类型。他们也是难治疗的，每100人当中少于5个人在诊断之后存活超过5年。

这个研究是由英国癌症研究院资助的，在《干细胞报告》期刊上发表。首席研究员、Susan Short博士说“用抑制剂靶向RAD51能够让这些GSCs 对化疗效果更加的敏感，有助于肿瘤的移动。”

英国癌症研究院的高级科学信息官Justine Alford博士说，胶质母细胞瘤迫切需要新的、更好的治疗。

   “这个具有前景的研究在细胞和老鼠里面也许已经找到了一个切断肿瘤燃料供应的方法，”她补充说。

 如果这个方法在对人进行大量研究中，证明是安全和有效的，它“可能有一天可以帮助治疗，从而更准确和有效地靶向疾病，”Alford说。

研究人员已经建议一些特殊种类的恶性胶质瘤细胞可以繁殖，复制出相同的拷贝从而更加的耐治疗。利兹大学的研究人员发现，这个亚组称为成胶质细胞瘤干细胞（GSCs），具有较高水平的RAD51分子。

首席研究员Susan Short教授说，RAD51帮助癌细胞修复放射治疗对其DNA造成的损伤。

这个修复允许癌细胞在治疗之后返回，重新回到肿瘤中。但是与老鼠一起工作，这个团队使用靶向RAD51的实验药物或抑制剂来改变这些效应。

   “通过抑制剂靶向RAD1能够让这些GSCs 对化疗效果更加的敏感，有助于肿瘤的移动”，Short说。

   “在放疗后，RAD51在细胞中的存活进一步增加的确切原理尚不清楚，但我们的研究提供了强有力的证明，这种蛋白正好靶向这种侵袭性脑癌的治疗。

    研究中使用的实验药物尚不适合临床试验，因此下一步将是开发一种类似的药物，不仅在实验室中具有相同的效果，并且对人能进行安全测试。（麻省医疗国际漆琳编译）

Scientists uncover potential brain tumour drug target

    Targeting a molecule that helps cells repair their DNA could lead to a new treatment for some aggressive brain tumours, a University of Leeds study has found .

Researchers discovered that switching off the RAD51 molecule increased the effectiveness of radiotherapy to kill glioblastoma cells in the lab.

Glioblastomas are the most common type of brain tumour in adults. They are also the hardest to treat, with fewer than 5 in every 100 people surviving their disease for at least 5 years after diagnosis.

    The study, funded by Cancer Research UK,was published in the journal Stem Cell Reports.

“By targeting RAD51 with an inhibitor we were able to make these GSCs more sensitive to the effects of radiotherapy, helping remove the tumour.” - Dr Susan Short, lead author

Dr Justine Alford, Cancer Research UK’s senior science information officer, said that new, kinder treatments for glioblastoma were urgently needed.

   “This promising study in cells and mice may have found a way to cut off the tumour’s fuel supply,” she added.

    If the approach proves safe and effective in larger studies with people, it “could one day help treatments target the disease more precisely and effectively”, said Alford.

    Researchers had suggested that some specialised groups of glioblastoma cells can reproduce to make identical copies that are more resistant to treatment.

And the Leeds researchers found that this subgroup, called glioblastoma stem cells (GSCs), have high levels of the RAD51 molecule.

    RAD51 helps cancer cells repair the damage that radiotherapy causes to their DNA, said Professor Susan Short, lead author of the study.

     This repair allows the cancer cells to bounce back after treatment and repopulate the tumour. But working with mice, the team were able to reverse these effects using an experimental drug – or inhibitor – that targets RAD51.  

   “By targeting RAD51 with an inhibitor we were able to make these GSCs more sensitive to the effects of radiotherapy, helping remove the tumour,” said Short.

   “The exact mechanism by which RAD51 becomes increased in cells that survive radiotherapy is not yet known, but our study provides strong evidence that this is the right protein to target in the treatment of this aggressive brain cancer.”

    The experimental drugs used in this study are not yet suitable for clinical trials, so the next step will be to develop a similar drug that has the same effects in the lab and can be safely tested in people.

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