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Anti-angiogenic
activity of melatonin in advanced cancer patients
Lissoni P, Rovelli F, Malugani F, Bucovec R, Conti A,
Maestroni GJ
Division
of Radiation Oncology, San Gerardo Hospital, 20052 Monza, Milan, Italy
Objectives.
The anticancer activity of the indole melatonin has been explained to be due to
its immunomodulatory, anti-prolferative and anti-oxidant effects, whereas at
present no data are available about its possible influence on the angiogenesis,
which has been shown to be one of the main biological mechanisms responsible for
tumor dissemination. Vascular endothelial growth factor (VEGF) is the most
active angiogenic factor, and the evidence of abnormally high blood levels or
VEGF has been proven to be associated with poor prognosis in cancer patients.
To
investigate the influence of melatonin on angiogenesis, in this preliminary
study we have evaluated the effects of melatonin therapy on VEGF blood levels in
advanced cancer patients.
Material
and Methods. The study included 20 metastatic patients, who progressed on
previous conventional antitumor therapies and for whom no other effective
treatment was available.
Melatonin was given orally at 20 mg/day in the evening
for at least 2 months.
Serum levels of VEGF were measured by an enzyme
immunoassay on venous blood samples collected at 15-day intervals.
Results.
The clinical response consisted of minor response (MR) in 2, stable disease (SD)
in 6 and progressive disease (PD) in the remaining 12 patients.
VEGF mean levels
decreased on therapy, without, however, statistical differences with respect to
the pre-treatment values.
In contrast, by evaluating changes in VEGF levels in
relation to the clinical response, non-progressing patients (MR + SD) showed a
significant decline in VEGF mean concentrations, whereas no effect was achieved
in progressing patients.
Conclusions.
This study, by showing that melatonin-induced control or the neoplastic growth
is associated with a decline in VEGF secretion, would suggest that the pineal
hormone may control tumor growth at least in part by acting as a natural
anti-angiogenic molecule, with a following opposition or angiogenesis-dependent
cancer proliferation.
PMID:
11335879 [PubMed - indexed for MEDLINE]
Source:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11335879&dopt=Abstract
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