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Rapid and clinically significant response to masitinib in the treatment of mucosal primary esophageal melanoma with somatic KIT exon 11 mutation involving brain metastases: A case report
J. Prosvicova, S. Lukesova, J. Kopecky, J. Grim, Z. Papik, R. Kolarova, B. Navratilova, P. Dubreuil, J. Agopian, C. Mansfield, A. Moussy, O. Hermine
Jazyk angličtina Země Česko
Typ dokumentu kazuistiky, časopisecké články
NLK
Directory of Open Access Journals
od 2001
Free Medical Journals
od 1998
Medline Complete (EBSCOhost)
od 2007-06-01
ROAD: Directory of Open Access Scholarly Resources
od 2001
- MeSH
- exony MeSH
- fatální výsledek MeSH
- inhibitory proteinkinas terapeutické užití MeSH
- lidé středního věku MeSH
- lidé MeSH
- melanom farmakoterapie sekundární MeSH
- mutace genetika MeSH
- nádory jícnu farmakoterapie MeSH
- nádory mozku farmakoterapie sekundární MeSH
- protoonkogenní proteiny c-kit genetika MeSH
- thiazoly terapeutické užití MeSH
- Check Tag
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- kazuistiky MeSH
BACKGROUND: Malignant melanoma in the gastrointestinal tract may be primary or metastatic. Mucosal melanoma is a quite rare and aggressive disease, growing hidden and diagnosed with a certain delay which makes treatment difficult. CASE REPORT: The authors present the first patient with c-kit exon 11 mutated primary esophageal melanoma treated with oral tyrosine kinase inhibitor masitinib. A 55-year-old-man presented with esophageal melanoma metastising into visceral organs and to the brain. The patient showed objective and clinical significant therapeutic response to masitinib. After initiation of masitinib, dysphagia and odynophagia disappeared within 1 week. Following 1 month of treatment, computed tomography showed a regression in the number and size of brain metastatic lesions and regression in visceral lesions. This therapeutic response, despite the aggressive disease on treatment initiation, effectively enabled the patient to have 6 months of quality life. CONCLUSION: This report corroborates the plausibility of treating advanced melanoma carrying a mutation of KIT with masitinib. It also raises the question of masitinib treatment beyond progression. Additionally, the observed masitinib treatment effect on the brain suggests accumulation of therapeutically relevant concentration of masitinib in the central nervous system. This observation has possible ramifications for treatment of intracranial neoplasms.
AB Science Paris France Hospital Necker Paris
CNRS UMR 8147 Department of Hematology Universite Paris 5 Rene Descartes Paris
CNRS UMR7258 Marseille F 13009 France AB Science Paris France
Department of Clinical Oncology and Radiotherapy University Hospital in Hradec Kralove
Department of Clinical Oncology County Hospital Nachod Czech Republic
Department of Histopathology County Hospital Nachod
Endoscopic Centre County Hospital Nachod
Institut Imagine Universite Sorbonne Paris cite Paris France
Citace poskytuje Crossref.org
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- $a BACKGROUND: Malignant melanoma in the gastrointestinal tract may be primary or metastatic. Mucosal melanoma is a quite rare and aggressive disease, growing hidden and diagnosed with a certain delay which makes treatment difficult. CASE REPORT: The authors present the first patient with c-kit exon 11 mutated primary esophageal melanoma treated with oral tyrosine kinase inhibitor masitinib. A 55-year-old-man presented with esophageal melanoma metastising into visceral organs and to the brain. The patient showed objective and clinical significant therapeutic response to masitinib. After initiation of masitinib, dysphagia and odynophagia disappeared within 1 week. Following 1 month of treatment, computed tomography showed a regression in the number and size of brain metastatic lesions and regression in visceral lesions. This therapeutic response, despite the aggressive disease on treatment initiation, effectively enabled the patient to have 6 months of quality life. CONCLUSION: This report corroborates the plausibility of treating advanced melanoma carrying a mutation of KIT with masitinib. It also raises the question of masitinib treatment beyond progression. Additionally, the observed masitinib treatment effect on the brain suggests accumulation of therapeutically relevant concentration of masitinib in the central nervous system. This observation has possible ramifications for treatment of intracranial neoplasms.
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