New knowledge of the mechanisms of sorafenib resistance in liver cancer
By Yan-jing Zhu, Bo Zheng, Hong-Yang Wang, Lei Chen. Acta Pharmacologica Sinica, 2017
616 citations recorded by the source corpus.
Sorafenib is an oral multikinase inhibitor that suppresses tumor cell proliferation and angiogenesis and promotes tumor cell apoptosis. It was approved by the FDA for the treatment of advanced renal cell carcinoma in 2006, and as a unique target drug for advanced hepatocellular carcinoma (HCC) in 2007. Sorafenib can significantly extend the median survival time of patients but only by 3–5 months. Moreover, it is associated with serious adverse side effects, and drug resistance often develops. Therefore, it is of great importance to explore the mechanisms underlying sorafenib resistance and to develop individualized therapeutic strategies for coping with these problems. Recent studies have revealed that in addition to the primary resistance, several mechanisms are underlying the acquired resistance to sorafenib, such as crosstalk involving PI3K/Akt and JAK-STAT pathways, the activation of hypoxia-inducible pathways, and epithelial-mesenchymal transition. Here, we briefly describe the function of sorafenib, its clinical application, and the molecular mechanisms for drug resistance, especially for HCC patients.
Subfields: Cancer Research, Hepatology, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/2f0e82390bcc2faa1bc6a700b06f5db1d5fa2283
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Citations in the corpus
- Challenges in liver cancer and possible treatment approaches (2019, background): “Moreover, 10% of patients treated with sorafenib may develop cutaneous squamous cell carcinomas [55, 56].”