https://scholars.lib.ntu.edu.tw/handle/123456789/543464
Title: | Anti-angiogenic therapy in patients with advanced gastric and gastroesophageal junction cancer: A systematic review | Authors: | Chen L.-T. Oh D.-Y. Ryu M.-H. KUN-HUEI YEH Yeo W. Carlesi R. Cheng R. Kim J. Orlando M. Kang Y.-K. |
Keywords: | Angiogenesis inhibitors; Esophagogastric junction; Stomach neoplasms; Vascular endothelial growth factors | Issue Date: | 2017 | Publisher: | Korean Cancer Association | Journal Volume: | 49 | Journal Issue: | 4 | Start page/Pages: | 851-868 | Source: | Cancer Research and Treatment | Abstract: | Despite advancements in therapy for advanced gastric and gastroesophageal junction cancers, their prognosis remains dismal. Tumor angiogenesis plays a key role in cancer growth and metastasis, and recent studies indicate that pharmacologic blockade of angiogenesis is a promising approach to therapy. In this systematic review, we summarize current literature on the clinical benefit of anti-angiogenic agents in advanced gastric cancer. We conducted a systematic search of PubMed and conference proceedings including the American Society of Clinical Oncology, the European Society for Medical Oncology, and the European Cancer Congress. Included studies aimed to prospectively evaluate the efficacy and safety of anti-angiogenic agents in advanced gastric or gastroesophageal junction cancer. Each trial investigated at least one of the following endpoints: overall survival, progression-free survival/time to progression, and/or objective response rate. Our search yielded 139 publications. Forty-two met the predefined inclusion criteria. Included studies reported outcomes with apatinib, axitinib, bevacizumab, orantinib, pazopanib, ramucirumab, regorafenib, sorafenib, sunitinib, telatinib, and vandetanib. Second-line therapy with ramucirumab and third-line therapy with apatinib are the only anti-angiogenic agents so far shown to significantly improve survival of patients with advanced gastric cancer. Overall, agents that specifically target the vascular endothelial growth factor ligand or receptor have better safety profile compared to multi-target tyrosine kinase inhibitors. ? 2017 by the Korean Cancer Association. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-85016981672&doi=10.4143%2fcrt.2016.176&partnerID=40&md5=e184e6b525b7234e839c9bab67cb493a https://scholars.lib.ntu.edu.tw/handle/123456789/543464 |
ISSN: | 1598-2998 | DOI: | 10.4143/crt.2016.176 | SDG/Keyword: | angiogenesis inhibitor; apatinib; axitinib; bevacizumab; orantinib; pazopanib; protein tyrosine kinase inhibitor; ramucirumab; regorafenib; sorafenib; sunitinib; telatinib; tumor marker; vandetanib; vasculotropin A; vasculotropin receptor 2; angiogenesis inhibitor; antineoplastic agent; biological marker; epidermal growth factor receptor 2; ERBB2 protein, human; protein kinase inhibitor; vasculotropin A; abdominal pain; advanced cancer; anemia; antiangiogenic therapy; asthenia; bleeding; cancer chemotherapy; cancer growth; cancer survival; decreased appetite; drug efficacy; drug safety; esophagus cancer; fatigue; febrile neutropenia; gastroesophageal junction; gastroesophageal junction cancer; hand foot syndrome; human; hypertension; lethargy; leukopenia; Medline; meta analysis; neutropenia; outcome assessment; overall survival; progression free survival; prospective study; protein targeting; proteinuria; quality of life; Review; stomach cancer; stomatitis; systematic review; thrombocytopenia; thromboembolism; antagonists and inhibitors; cancer staging; clinical trial (topic); esophagus tumor; gastroesophageal junction; metabolism; molecularly targeted therapy; pathology; stomach tumor; treatment outcome; Angiogenesis Inhibitors; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Biomarkers; Clinical Trials as Topic; Esophageal Neoplasms; Esophagogastric Junction; Humans; Molecular Targeted Therapy; Neoplasm Staging; Protein Kinase Inhibitors; Quality of Life; Receptor, ErbB-2; Stomach Neoplasms; Treatment Outcome; Vascular Endothelial Growth Factor A |
Appears in Collections: | 腫瘤醫學研究所 |
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