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Prostaglandins in human
brain tumors
Paoletti P, Chiabrando C, Gaetani P, Castelli MG, Butti
G, Martelli L, Rolli M
Department
of Surgery, Universita di Pavia, Italy
It has
been recently observed that arachidonic acid (AA) metabolites may modulate many
of the mechanisms involved in tumor growth and metastasis.
In order to clarify the role played in human brain tumors, authors have
determined AA metabolic profiles in 63 surgical specimen of human intracranial
tumors (mostly neuroepithelial tumors and meningiomas).
The five metabolites via the cyclooxygenase pathway (PGD2, PGE2, TxB2, PGF2a,
6-Keto-PGF1a) were measured by high resolution gas chromatography-mass
spectrometry after "ex vivo" metabolism of endogenous AA by tumor
homogenates.
The overall synthesis capacity of AA metabolites widely varied among different
oncotypes, and, except in two cases of dermoid cysts, was higher than in normal
brain tissue.
AA metabolism seems more active in neuroepithelial tumors with the highest grade
of anaplasia; some changes in the percentage of each metabolite is evident when
anaplastic features changed.
Thromboxane B2 was the most represented and 6-Keto-PGF1a the less abundant
metabolite.
Meningiomas and neuroepithelial tumors showed different relative proportion of
AA metabolites which have in some cases reported to positively or negatively
affect tumor growth.
In histological subgroups of meningiomas AA metabolites synthesis capacity did
not show any statistical difference.
In the six cases of brain metastasis there is a wide range of overall synthesis
capacity, with predominant synthesis of thromboxane B2 and prostaglandin E2,
while the percentage of prostaglandin D2, reported as antimetastatic, is very
low.
PMID:
2674360 [PubMed - indexed for MEDLINE]
Source:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2674360&dopt=Abstract
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