Targeting TAM to Tame Pancreatic Cancer

被引:6
|
作者
von Itzstein, Mitchell S. [1 ,2 ]
Burke, Michael C. [1 ,2 ]
Brekken, Rolf A. [3 ]
Aguilera, Todd A. [4 ]
Zeh, Herbert J. [3 ]
Beg, Muhammad Shaalan [1 ,2 ]
机构
[1] UT Southwestern Med Ctr, Div Hematol Oncol, Dept Internal Med, 5323 Harry Hines Blvd, Dallas, TX 75390 USA
[2] Univ Texas Southwestern Med Ctr Dallas, Div Hematol & Med Oncol, Dallas, TX 75390 USA
[3] Univ Texas Southwestern Med Ctr Dallas, Div Surg Oncol, Dallas, TX 75390 USA
[4] Univ Texas Southwestern Med Ctr Dallas, Dept Radiat Oncol, Dallas, TX 75390 USA
关键词
RECEPTOR TYROSINE KINASE; EPITHELIAL-MESENCHYMAL TRANSITION; DRUG-RESISTANCE; MEDIATES RESISTANCE; TUMOR INVASION; TYRO3; RECEPTOR; PROTEIN-S; IN-VIVO; AXL; ACTIVATION;
D O I
10.1007/s11523-020-00751-9
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Pancreatic cancer is expected to become the second leading cause of cancer-related death within the next few years. Current therapeutic strategies have limited effectiveness and therefore there is an urgency to develop novel effective therapies. The receptor tyrosine kinase subfamily TAM (Tyro3, Axl, MerTK) is directly implicated in the pathogenesis of the metastatic, chemoresistant, and immunosuppressive phenotype in pancreatic cancer. TAM inhibitors are promising investigational therapies for pancreatic cancer due to their potential to target multiple aspects of pancreatic cancer biology. Specifically, recent mechanistic investigations and therapeutic combinations in the preclinical setting suggest that TAM inhibition with chemotherapy, targeted therapy, and immunotherapy should be evaluated clinically.
引用
收藏
页码:579 / 588
页数:10
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