Reviews:
Genetic progression in gastrointestinal stromal tumors: mechanisms and molecular interventions
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Abstract
Ke Li1,2*, Haibo Cheng4,5,6*, Zhang Li1,2, Yuzhi Pang1,2, Xiaona Jia1,2, Feifei Xie1,2, Guohong Hu2, Qingping Cai7 and Yuexiang Wang1,2,3
1 SIBS (Institute of Health Sciences), Changzheng Hospital Joint Center for Translational Medicine, Institute of Health Sciences, Shanghai Changzheng Hospital, Institutes for Translational Medicine (CAS-SMMU), University of Chinese Academy of Sciences, Shanghai, China
2 Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences and Shanghai Jiao Tong University School of Medicine, Shanghai, China.
3 Collaborative Innovation Center of Systems Biomedicine, Shanghai Jiao Tong University School of Medicine, Shanghai, China
4 The First Clinical Medical College, Nanjing University of Chinese Medicine, Nanjing, China.
5 Key Laboratory of SATCM for Empirical Formulae Evaluation and Achievements Transformation, Nanjing, China.
6 Collaborative Innovation Center of Jiangsu Province Chinese Medicine in Cancer Prevention and Treatment, Nanjing, China
7 Department of Gastro-intestinal Surgery, Changzheng Hospital, Second Military Medical University, Shanghai, China
* These authors have contributed equally to this work
Correspondence to:
Yuexiang Wang, email:
Qingping Cai, email:
Keywords: gastrointestinal stromal tumors, dystrophin, small molecules, targeted therapy
Received: January 25, 2017 Accepted: March 02, 2017 Published: March 08, 2017
Abstract
Gastrointestinal stromal tumors (GISTs) are the most common sarcomas in humans. Constitutively activating mutations in the KIT or PDGFRA receptor tyrosine kinases are the initiating oncogenic events. Most metastatic GISTs respond dramatically to therapies with KIT/PDGFRA inhibitors. Asymptomatic and mitotically-inactive KIT/PDGFRA-mutant “microGISTs” are found in one third of adults, but most of these small tumors never progress to malignancy, underscoring that a progression of oncogenic mutations is required. Recent studies have identified key genomic abnormalities in GIST progression. Novel insights into the genetic progression of GISTs are shedding new light on therapeutic innovations.
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