药物三联疗法被发现可阻断胰腺癌的耐药性。
Drug trio found to block tumour resistance in pancreatic cancer

原始链接: https://www.drugtargetreview.com/news/192714/drug-trio-found-to-block-tumour-resistance-in-pancreatic-cancer/

## 胰腺癌治疗的突破性进展 来自西班牙国家癌症研究中心的最新研究揭示了一种三联药物组合,在临床前模型中**诱导了胰腺肿瘤的完全且持久的消退**。 这为克服胰腺导管腺癌(PDAC)的治疗抵抗力提供了一种潜在的解决方案,这是一种特别致命的癌症。 该疗法同时靶向三个关键信号通路——RAF1、EGFR家族受体和STAT3,使用的药物为RMC-6236、Afatinib和SD36。 在包括人肿瘤组织在内的多种小鼠模型中进行的测试表明,不仅肿瘤显著减少,而且**癌症被完全清除,超过200天未复发**。 重要的是,该组合似乎**可以防止药物耐药性的发展**,这是癌症治疗中的一个主要挑战,因为它攻击了肿瘤信号网络中的多个点。 该治疗在动物模型中耐受性良好,表明未来人体临床试验可能具有有利的安全特性。 这些发现代表着开发更有效胰腺癌疗法的重要一步。

黑客新闻 新的 | 过去的 | 评论 | 提问 | 展示 | 工作 | 提交 登录 发现三种药物可以阻断胰腺癌的肿瘤耐药性 (drugtargetreview.com) 10 分,由 axiomdata316 1小时前发布 | 隐藏 | 过去的 | 收藏 | 4 条评论 ngriffiths 1分钟前 | 下一个 [–] 在小鼠身上。(公平地说,也在一些其他更好的小鼠身上)。https://jamesheathers.medium.com/in-mice-explained-77b61b598... 回复 jonshariat 8分钟前 | 上一个 [–] 我最近和孩子们玩太多宝可梦了,把这读成了“Dugtrio” JohnMakin 0分钟前 | 父评论 | 下一个 [–] 我也是 j-bos 5分钟前 | 父评论 | 上一个 [–] 一样,我再也无法以同样的方式看待它们了。 指南 | 常见问题 | 列表 | API | 安全 | 法律 | 申请YC | 联系 搜索:
相关文章

原文

A new study reports that a triple-targeted drug combination can drive complete and lasting regression of pancreatic tumours in preclinical models, potentially overcoming treatment resistance in one of the deadliest cancers.

Researchers at the Spanish National Cancer Research Centre have announced a potential breakthrough combination therapy that induces complete regression of pancreatic tumours and prevents tumour resistance in preclinical models. 

The study describes a targeted combination therapy that simultaneously targets three key signalling pathways in pancreatic ductal adenocarcinoma (PDAC), the most common and lethal type of pancreatic cancer. 

Triple inhibition strategy

Pancreatic cancer remains notoriously difficult to treat, with very poor survival rates and limited effective therapies. The new research aims to combat this by targeting RAF1, EGFR family receptors and STAT3 signalling – nodes that are crucial for tumour growth and survival.  

According to the authors, “genetic ablation of three independent nodes involved in downstream (RAF1), upstream (EGFR) and orthogonal (STAT3) KRAS signalling pathways leads to complete and permanent regression of orthotopic PDACs induced by KRAS/TP53 mutations.”

The triple treatment combines three drugs:

  • RMC-6236 (daraxonrasib): targeting KRAS
  • Afatinib: an EGFR family inhibitor
  • SD36: a selective STAT3 degrader

These agents together were tested in orthotopic mouse models of PDAC, where tumour cells are implanted in a location that closely resembles their natural environment in the pancreas. The results demonstrated the therapy not only reduced tumour size but also entirely stopped tumour growth with no evidence of tumour resistance for more than 200 days after treatment.

Broad efficacy in preclinical models

Researchers extended their observations beyond engineered mouse models. The combination therapy also led to significant regression in genetically engineered mouse tumours and in human cancer tissues grown in lab mice, known as patient-derived tumour xenografts (PDX).

These results should guide the development of new clinical trials that may benefit PDAC patients.

These powerful anti-tumour effects were achieved with a therapy that was well tolerated in the animals, which could provide a favourable safety profile for future clinical testing.

“These results should guide the development of new clinical trials that may benefit PDAC patients,” said the authors.

A step towards overcoming resistance

One of the most significant hurdles in targeted cancer therapies is the development of resistance. This new combination strategy appears to prevent this relapse, at least in preclinical models, by attacking multiple nodes of tumour signalling simultaneously.

According to commentary from scientists involved in the work: “Overcoming therapeutic resistance in PDAC requires coordinated inhibition of KRAS downstream (RAF1), upstream (EGFR) and parallel survival pathways (STAT3).”

Clinical implications

While more research will be needed before trials in humans can begin, these findings are an important advancement in the search for better pancreatic cancer therapies. By demonstrating complete and durable tumour regression without resistance in preclinical models, there is now strong potential for clinical development of multi-targeted approaches in the future.

联系我们 contact @ memedata.com