Study reveals why chemotherapy may be compromised in patients with pancreatic cancer
MD安德森新闻发布2015年11月11日
MD安德森新闻Release 11/11/2015
A study at The University of Texas MD Anderson Cancer Center may explain why chemotherapy drugs such as gemcitabine are not effective for many pancreatic cancer patients, and perhaps point to new approaches to treatment including enhancing gemcitabine’s ability to stop tumor growth.
在小鼠中的MD安德森研究表明，抑制被称为上皮 - 间充质组合转化（EMT）与吉西他滨的蜂窝塑性加工，可提高药物的效果。研究结果发表在Nature的11月11日在线版。
“胰腺癌的诊断，预后较差，尽管目前的治疗方法的可用性关联，” Raghu卡鲁，医学博士，博士，教授，肿瘤生物学的椅子上，该研究报告的主要作者。“急需因此新的治疗策略。”
卡鲁的团队观察EMT，由癌细胞劫持，被认为是帮助癌细胞转移到其他器官的胚胎细胞的可塑性程序。通过任一分割（增殖）的癌细胞扩散的疾病，或通过迁移，允许它们转移。当癌细胞采取EMT方案，以促进他们的迁移，他们通常停止分裂。研究结果188bet体育网址表明，EMT线索逮捕癌细胞增殖造成损害化疗敏感性，影响身体的能力，以有效地处理这样的回应。
“Gemcitabine works primarily on cancer cells that are dividing or proliferating,” said Kalluri. “When cancer cells suspend their proliferation – such as when they launch an EMT program – then anti-proliferation drugs like gemcitabine do not target them well.”
“We found that EMT program suppressed drug transporter and concentrative proteins, which inadvertently protected these cancer cells from anti-proliferative drugs such as gemcitabine,” added Kalluri. “The correlation of decreased survival of pancreatic cancer patients with an increased EMT program is likely due to their impaired capacity to respond to chemotherapy, leading to overall poor prognosis and higher incidence of metastasis.”
抑制导致肿瘤对吉西他滨的增强响应EMT程序。
“Collectively, our study offers the opportunity to evaluate the potential of targeting EMT program to enhance efficacy of chemotherapy and likely targeted therapies,” said Kalluri.
安德森的研究团队成员包括Xiaofeng Zheng, Ph.D., Julienne Carstens, Ph.D., Jiha Kim, Ph.D., Matthew Scheible, Judith Kaye, Hikaru Sugimoto, M.D., Ph.D., and Valerie LeBleu, Ph.D., all of Cancer Biology; and Chia-Chin Wu, Ph.D. of Genomic Medicine.
这项研究由癌症预防和得克萨斯州的研究所资助。188bet体育网址