Multiple Sclerosis Treatment and Melanoma Development

Therapy of multiple sclerosis (MS) with disease-modifying agents such as natalizumab or fingolimod has been associated with the development of cutaneous melanoma. Here we briefly revise literature data and report of a case of a 48-year old woman who developed a melanoma and several atypical naevi af...

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Bibliographic Details
Published in:International journal of molecular sciences 2020-04, Vol.21 (8), p.2950
Main Authors: Carbone, Maria Luigia, Lacal, Pedro Miguel, Messinese, Serena, De Giglio, Laura, Pozzilli, Carlo, Persechino, Severino, Mazzanti, Cinzia, Failla, Cristina Maria, Pagnanelli, Gianluca
Format: Article
Language:English
Subjects:
Antirheumatic Agents - adverse effects
Antirheumatic Agents - therapeutic use
Biomarkers
Biopsy
Case Report
Case reports
Cell adhesion & migration
Cell growth
Cell proliferation
Disease
Disease Susceptibility
Drugs
Female
Fingolimod Hydrochloride - adverse effects
Fingolimod Hydrochloride - therapeutic use
Growth factors
Humans
Immunohistochemistry
Immunosuppressive Agents - adverse effects
Immunosuppressive Agents - therapeutic use
Immunotherapy
Lymphocytes
Lymphocytes T
Melanoma
Melanoma - diagnosis
Melanoma - etiology
Melanoma - metabolism
Melanoma - therapy
Melanoma, Cutaneous Malignant
Metastases
Metastasis
Middle Aged
Monoclonal antibodies
Multiple sclerosis
Multiple Sclerosis - complications
Multiple Sclerosis - diagnosis
Multiple Sclerosis - therapy
Natalizumab - adverse effects
Natalizumab - therapeutic use
Nervous system
Patients
Skin Neoplasms - diagnosis
Skin Neoplasms - etiology
Skin Neoplasms - therapy
Tumors
Vascular endothelial growth factor
Vascular Endothelial Growth Factor A - metabolism
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Summary:Therapy of multiple sclerosis (MS) with disease-modifying agents such as natalizumab or fingolimod has been associated with the development of cutaneous melanoma. Here we briefly revise literature data and report of a case of a 48-year old woman who developed a melanoma and several atypical naevi after sub sequential treatment with natalizumab (1 year) and fingolimod (7 years). By immunohistochemistry we observed the presence of T cells and leukocyte infiltration as well as of vascular endothelial growth factor (VEGF)-A expression in the patient melanoma biopsy. Then, we analyzed proliferation, migration and VEGF-A expression in three melanoma cell lines and found out that both natalizumab and fingolimod inhibited tumor cell proliferation but promoted or blocked cell migration depending on the cell line examined. VEGF-A secretion was augmented in one melanoma cell line only after fingolimod treatment. In conclusion, our in vitro data do not support the hypothesis of a direct action of natalizumab or fingolimod on melanoma progression but acting on the tumor microenvironment these treatments could indirectly favor melanoma evolution.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms21082950