[Methyl-C-11] thymidine positron emission tomography in tumoral and non-tumoral cerebral lesions

Citation
J. De Reuck et al., [Methyl-C-11] thymidine positron emission tomography in tumoral and non-tumoral cerebral lesions, ACT NEUR BE, 99(2), 1999, pp. 118-125
Citations number
40
Categorie Soggetti
Neurology
Journal title
ACTA NEUROLOGICA BELGICA
ISSN journal
03009009 → ACNP
Volume
99
Issue
2
Year of publication
1999
Pages
118 - 125
Database
ISI
SICI code
0300-9009(199906)99:2<118:[TPETI>2.0.ZU;2-L
Abstract
Background: No ideal radiopharmaceutical exists for positron emission tomog raphy (PET) that fullfils all clinical requirements for the study of brain tumors. Purpose: The usefulness of a recently developed PET tracer, [methyl-(11) C] thymidine ([methyl-(11) C] TdR) is explored in brain tumors. Patients and Methods: Twenty patients with confirmed tumoral and non-tumora l brain lesions were investigated with [methyl-C-11] TdR PEI: The C-11 acti vity was visually and quantitatively assessed. In two patients, dynamic sca ns were performed. The PET findings were compared to those of magnetic reso nance imaging (MRI) or computed tomography (CT) of the brain and to the fin al diagnosis. Results: Eight out of ten patiens with confirmed tumoral lesions or tumor r ecurrence had increased C-11 activity within the lesion. In ten non-tumoral lesions no increased C-11 uptake was found. The dynamic PET studies showed that [methyl-C-11] TdR first acts as a blood flow tracer, but that later a n the uptake of C-11 activity is due to labeled metabolites, crossing the b lood-brain barrier. Increased tracer activity was only observed in tumoral and not in non-tumoral contrast-enhanced lesions on MRT or CI: Conclusions: [Methyl-C-11] TdR is not a selective PET radiopharmaceutical f or brain tumors, but can be used as a tracer for tumoral blood-brain barrie r disruption.