ECE2010 Poster Presentations Endocrine tumours & neoplasia (<emphasis role="italic">Generously supported by Novartis</emphasis>) (82 abstracts)
Temozolomide treatment in aggressive pituitary tumors and pituitary carcinomas: a French multicenter experience
Gerald Raverot 1, , Nathalie Sturm 3 , Florence De Fraipont 3 , Philippe Caron 4 , Marie Muller 3 , Christine Cortet-Rudelli 5 , Sylvie Salenave 6 , Richard Assaker 3 , Henry Dufour 7 , Stephan Gaillard 8 , Patrick François 9 , Emmanuel Jouanneau 1, , Michèle Bernier 8 , Dominique Figarella-Branger 7 , Claude-Alain Maurage 5 , Jacqueline Trouillas 1, , Françoise Borson-Chazot 1 & Thierry Brue 7
1Groupement Hospitalier Est, Hospices Civils de Lyon, Lyon, France; 2INSERM, U842, Université de Lyon, Lyon 1, UMR-S842, Faculté de Médecine Lyon-Est, Lyon, France; 3CHU Grenoble, Grenoble, France; 4CHU de Toulouse, Toulouse, France; 5CHRU Lille, Lille, France; 6Groupement hospitalier universitaire Sud, AP-HP, LE KREMLIN-BICETRE, France; 7Assistance-Publique Hôpitaux de Marseille and Université de la Méditerranée, Marseille, France; 8Hôpital Foch, Suresnes, France; 9CHRU, Hôpital Bretonneau, Tours, France.
Context: To date ten publications reporting only 16 patients with pituitary aggressive tumors or carcinomas treated with temozolomide are available. Expression of O6-methylguanine-DNA-methyltranferase (MGMT), a DNA repair protein implicated in the resistance to temozolomide, was studied in only 10 out of these 16 patients. It has been suggested that low expression of MGMT could predict temozolomide efficacy.
Objective: The aim of this study was to describe the effects of temozolomide treatment in a larger number of patients with aggressive pituitary tumors or carcinomas and to evaluate the possible prognostic significance of MGMT promoter methylation and protein expression.
Patient: From a French multicenter study, we report eight patients; five carcinomas (three PRL and two ACTH) and three aggressive pituitary tumors (one PRL and two ACTH); treated with temozolomide administered orally for 4–24 cycles. Three out of the eight patients were considered as responder to temozolomide because of significant tumoral shrinkage and decreased of PRL/ACTH secretion.
Design: MGMT expression, assessed by immunohistochemistry and MGMT promoter methylation analysed by pyrosequencing, were studied in seven patients.
Results: Temozolomide treatment was effective in three out of the eight patients (two ACTH and one PRL tumors). Three cycles of temozolomide were sufficient to identify patients responding to temozolomide treatment; in non-responders, additional cycles did not improve treatment efficacy even in association with carboplatine and etoposide. Tumoral response to temozolomide was not predicted by MGMT expression since MGMT expression was positive (30%) in one responder and negative in two out the five non-responders patients. Similarly, MGMT promoter methylation (3/7 tumors) did not predict MGMT expression.
Conclusion: Temozolomide treatment could be an effective option for some aggressive pituitary tumors or carcinomas but MGMT status is a poor predictor of treatment outcome that cannot be used to select patients who may benefit from this treatment.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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