Literature DB >> 19156926

O(6)-methylguanine DNA methyltransferase immunoexpression in nonfunctioning pituitary adenomas: are progressive tumors potential candidates for temozolomide treatment?

Georg Widhalm1, Stefan Wolfsberger, Matthias Preusser, Adelheid Woehrer, Mark R Kotter, Thomas Czech, Christine Marosi, Engelbert Knosp.   

Abstract

BACKGROUND: Currently, no effective alternative treatment exists for progressive, regrowing, nonfunctioning pituitary adenomas (NFPA) that are resistant to conventional multimodality therapy. Temozolomide (TMZ) was proposed as a treatment option for pituitary carcinomas and aggressive pituitary adenomas. Recently, it was suggested that the responsiveness of pituitary tumors to TMZ depends on the immunoexpression of O(6)-methylguanine DNA methyltransferase (MGMT). Therefore, the authors of this report assessed MGMT expression in a series of patients with progressive, regrowing NFPAs to evaluate whether TMZ may serve as alternative treatment option.
METHODS: On the basis of postoperative magnetic resonance imaging, 45 patients with NFPAs were allocated to either a group with progressive, regrowing tumors (n = 24) or a tumor-free group (n = 21), which served as a control. MGMT expression was assessed semiquantitatively by immunohistochemistry (low expression was defined as <or=50% immunostained adenoma cells, and high expression was defined as >50% immunostained adenoma cells) and was compared between the 2 groups.
RESULTS: At the time of initial surgery, low MGMT expression was observed in 12 of 24 patients (50%) in the study group with progressive, regrowing NFPAs. In the control group of tumor-free patients, only 5 of 21 patients (24%) exhibited low MGMT expression. A comparable distribution of MGMT expression was observed in the specimens from repeat surgeries. A shorter interval to second surgery was observed in patients who had low MGMT expression.
CONCLUSIONS: The current data has suggested that half of the patients with progressive, regrowing NFPAs exhibit low MGMT expression and are potential candidates for treatment with TMZ. These findings provide a rationale for the use of TMZ as an alternative treatment approach in this subgroup if conventional therapy, including reoperation, radiosurgery, and radiotherapy, fails. (c) 2009 American Cancer Society.

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Year:  2009        PMID: 19156926     DOI: 10.1002/cncr.24053

Source DB:  PubMed          Journal:  Cancer        ISSN: 0008-543X            Impact factor:   6.860


  15 in total

Review 1.  Temozolomide responsiveness in aggressive corticotroph tumours: a case report and review of the literature.

Authors:  A K Annamalai; A F Dean; N Kandasamy; K Kovacs; H Burton; D J Halsall; A S Shaw; N M Antoun; H K Cheow; R W Kirollos; J D Pickard; H L Simpson; S J Jefferies; N G Burnet; M Gurnell
Journal:  Pituitary       Date:  2012-09       Impact factor: 4.107

2.  Temozolomide for corticotroph pituitary adenomas refractory to standard therapy.

Authors:  Troy H Dillard; S Humayun Gultekin; Johnny B Delashaw; Chris G Yedinak; Edward A Neuwelt; Maria Fleseriu
Journal:  Pituitary       Date:  2011-03       Impact factor: 4.107

Review 3.  Molecular status of pituitary carcinoma and atypical adenoma that contributes the effectiveness of temozolomide.

Authors:  Akira Matsuno; Mineko Murakami; Katsumi Hoya; Shoko M Yamada; Shinya Miyamoto; So Yamada; Jae-Hyun Son; Hajime Nishido; Fuyuaki Ide; Hiroshi Nagashima; Mutsumi Sugaya; Toshio Hirohata; Akiko Mizutani; Hiroko Okinaga; Yudo Ishii; Shigeyuki Tahara; Akira Teramoto; R Yoshiyuki Osamura
Journal:  Med Mol Morphol       Date:  2013-08-17       Impact factor: 2.309

4.  MGMT promoter methylation and immunoexpression in aggressive pituitary adenomas and carcinomas.

Authors:  Fateme Salehi; Bernd W Scheithauer; Johann M Kros; Queenie Lau; Michael Fealey; Dana Erickson; Kalman Kovacs; Eva Horvath; Ricardo V Lloyd
Journal:  J Neurooncol       Date:  2011-02-11       Impact factor: 4.130

5.  Temozolomide treatment for aggressive pituitary tumors: correlation of clinical outcome with O(6)-methylguanine methyltransferase (MGMT) promoter methylation and expression.

Authors:  Zachary M Bush; Janina A Longtine; Tracy Cunningham; David Schiff; John A Jane; Mary Lee Vance; Michael O Thorner; Edward R Laws; M Beatriz S Lopes
Journal:  J Clin Endocrinol Metab       Date:  2010-07-28       Impact factor: 5.958

6.  Temozolomide (Temodar®) and capecitabine (Xeloda®) treatment of an aggressive corticotroph pituitary tumor.

Authors:  Marie S Thearle; Pamela U Freda; Jeffrey N Bruce; Steven R Isaacson; Yoomi Lee; Robert L Fine
Journal:  Pituitary       Date:  2011-12       Impact factor: 4.107

Review 7.  MGMT immunoexpression in aggressive pituitary adenoma and carcinoma.

Authors:  Queenie Lau; Bernd Scheithauer; Kalman Kovacs; Eva Horvath; Luis V Syro; Ricardo Lloyd
Journal:  Pituitary       Date:  2010-12       Impact factor: 4.107

8.  MGMT expression and pituitary tumours: relationship to tumour biology.

Authors:  Ann McCormack; Warren Kaplan; Anthony J Gill; Nicholas Little; Raymond Cook; Bruce Robinson; Roderick Clifton-Bligh
Journal:  Pituitary       Date:  2013-06       Impact factor: 4.107

9.  LOW O6-METHYLGUANINE-DNA METHYTRANSFERASE (MGMT) AND PAN-CYTOKERATIN (PAN-CK) EXPRESSION VIA IMMUNOHISTOCHEMISTRY IN PITUITARY ADENOMAS.

Authors:  R Basaran; M Onoz; F H Bolukbasi; M Efendioglu; A Sav
Journal:  Acta Endocrinol (Buchar)       Date:  2017 Jul-Sep       Impact factor: 0.877

Review 10.  Temozolomide in aggressive pituitary adenomas and carcinomas.

Authors:  Leon D Ortiz; Luis V Syro; Bernd W Scheithauer; Fabio Rotondo; Humberto Uribe; Camilo E Fadul; Eva Horvath; Kalman Kovacs
Journal:  Clinics (Sao Paulo)       Date:  2012       Impact factor: 2.365

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