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calcium-dependent uptake of phenylalanine, both in vivo and in vitro, thus affecting the initial steps of
the melanogenesis.
Now, from the pathogenesis to the treatment. Tacrolimus has been succesfully used for the treatment
of the vitiligo but how it works and why? Lan observes like in vitro, tacrolimus is able to act directly
on keratinocytes by inducing CSF and MMP2 release. Through this mechanism it promotes
melanocyte growth and proliferation and it could represent the cellular basis for the effectiveness in
the treatment of the vitiligo. Falabella proposes an overview of the actual surgical methods and
remarks that the appropriate selection of the patients is necessary to achieve the best results. Mulekar
reports a 6-year follow-up of 142 patients treated with autologous non-cultured
melanocyte/keratinocyte transplantation. He shows that the transplantation of a fresh non-cultured
suspension of melanocyte/keratinocyte can give good repigmentation but the result obtained is
independent of previous repigmentation in another area or test graft. It is thus possible that the disease
can be active even if the lesions are apparently stable. The suggestion of Mulekar is in agreement with
the idea of an intrinsic melanocyte defect which is more or less clinically evident. However, until now
the panel of methods used for melanocyte or melanocyte/keratinocyte isolation is wide and the culture
for in vitro or in vivo study is not univocal and obvious. Lin suggests the utilization of chitosan-coated
membranes to improve the growth of the melanocytes. The chitosan-induced spheroid morphology
does not affect the phenotype of the melanocytes that are able to return to the normal dendrititc
morphology after the reinoculation on collagen-coated surface. The method could be useful both for
preliminary culture for cell transplantation in vitiligo patients and in vitro culture of melanocytes from
vitiligo subjects. Hartmann performed a trial vs placebo (four-quarters comparison) for the evaluation
of the effectiveness of a combinatory therapy narrow-band UVB plus topical calcipotriol. In agreement
with current literature, the authors report a higher effectiveness of the narrow-band UVB compared
with broad-band UVB but they cannot indicate an improvement of UVB therapy by the topical
application of calcipotriol.
A lot of in vivo and in vitro evidence suggest that melanoma and vitiligo can be considered the
opposite face of the same phenomenon. The understanding of vitiligo pathogenesis could represent a
lesson for the approaches to the melanoma. Palermo hypothesizes that if in both diseases there is an
abnormal (different degree of avidity) immune response against the same antigen, it is possible to
utilize the peripheral cytotoxic melanocyte-specific TCD8 cells from vitiligo subjects for the treatment
of melanoma. Obviously, a HLA compatiblity between vitiligo and melanoma patients is the crucial
requisite,. The results of the in vivo trial could open a new scenario for melanoma treatment in the near
future. Regarding melanoma: Tonks demonstrates a different role in vivo and in vitro for pocket
proteins during proliferation of the melanocytes and progression of melanoma. A further update on the
role of a-MSH and ET-1 was provided by Kadekaro. She indicates a possible intracellular pathway
involving a-MSH, MC1R, Akt, CREB and Mitf and counteracting the apoptotic effect of UV. In
normal melanocytes, thus, the UV-induced ET-1 production protects the cells from the apoptosis and
from mutagenesis (associated with hydrogen peroxide production and DNA damage) whereas loss of
function mutations of MC1R increases a risk of melanoma. An in vitro study (from a molecular
approach) of the role of p53 in melanoma, paying partucular attention to its changes in stability,
localization, and activity based on different DNA-damaging agents, represents the aim of the paper of
Razorenova. Using two different melanoma cell lines, Mangahas shows that ET1, through ETB
receptor, activates CXCL1 and CXCL8 in melanoma but not in normal melanocyte cell lines. The
biological relevance is evident because ET1 downregulates e-cadherin, which inhibits the tumor
invasion, and activates metalloproteinases, which promote the migration and invasion processes.
Two papers sorted from PubMed are clinical studies. Guerra-Tapia describes, in a young subject, a
case of vitiligo in congenital divided nevus evolving in halo nevus. The clinical pattern is interesting
and requires, as suggested by the authors, a prolonged follow-up but it is improbable a common
pathogenesis for vitiligo and halo nevus. The other paper is that of Loquai which describes a case of
confetti-like lesions with hyperkeratosis in a 33 year old white man affected by vitiligo and mycosis
fungoides. The electron microscopy and the histology corroborate a different entity for the confetti-like
spots compared to the white vitiligo lesions in the same subjects.
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