Advances in treatment for tenosynovial giant cell tumors
Autor: | Eric L. Staals, Davide Maria Donati, Alessandra Longhi, Emanuela Palmerini |
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Přispěvatelé: | Palmerini, Emanuela, Longhi, Alessandra, Donati, Davide, Staals, Eric L. |
Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
colony-stimulating factor 1 (CSF1)
medicine.drug_class medicine.medical_treatment Pigmented villonodular synoviti Emactuzumab Pexidartinib Monoclonal antibody surgery 03 medical and health sciences 0302 clinical medicine TGCT medicine Pharmacology (medical) Giant Cell Tumors Pharmacology Toxicology and Pharmaceutics (miscellaneous) 030203 arthritis & rheumatology PVNS treatment business.industry tenosynovial giant cell tumor Health Policy Imatinib CSF1R medicine.disease Radiation therapy Nilotinib Pigmented villonodular synovitis 030220 oncology & carcinogenesis Cancer research business medicine.drug |
Popis: | Introduction: Tenosynovial giant cell tumor (TGCT) is a benign clonal neoplastic proliferation arising from the synovium often causing pain, swelling, joint stiffness, and reduced quality of life. The optimal treatment strategy in patients with diffuse-type TGCT (dt-TGCT) is unclear. The purpose of this review is to describe recent advances in the knowledge of TGCT pathogenesis and potential therapeutic implications. Areas covered: Current treatment options for TGCT are discussed, including surgery and radiotherapy. Recent evidence that TGCT cells overexpress colony-stimulating factor 1 (CSF1), resulting in recruitment of CSF1 receptor (CSF1R) positive tumor-associated macrophage and contributing to tumor growth, has created new opportunities for systemic treatments of dt-TGCT. Results of clinical trials with CSF1R inhibitors are now available. These inhibitors include small molecules such as imatinib, nilotinib, pexidartinib, and monoclonal antibodies like emactuzumab, MCS110, and cabiralzumab. Expert opinion: TGCT impairs patients’ quality of life significantly. The confirmation that the pathogenetic loop of TGCT can be inhibited through targeted agents could potentially change the therapeutic armamentarium for this condition. |
Databáze: | OpenAIRE |
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