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Joseph Samaha, Jim Dagher, Shayan Abdollah Zadegan

Huntington’s disease (HD) is a neurodegenerative disease inherited in an autosomal dominant manner. It is caused by an expansion of cytosine, adenine, guanine (CAG) repeats within the huntingtin (HTT) gene, which is located on chromosome 4. This pathological expansion of CAG repeats results in the production of a mutant huntingtin protein with an abnormally long polyglutamine […]

Temozolomide in the Treatment of Aggressive Pituitary Tumours – An Overview of Existing Knowledge and Future Perspectives

Ann McCormack
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Published Online: Jan 23rd 2013 European Neurological Review, 2012;7(4):228-233 DOI: http://doi.org/10.17925/ENR.2012.07.04.228
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Abstract

The management of aggressive pituitary tumours remains a challenge, however, the recent identification of temozolomide as a chemotherapeutic agent with significant efficacy against these tumours has heralded a new therapeutic era. There has been an exponential growth in the international experience with temozolomide over the past five years, now totalling 50 published cases. Overall, 67 % of cases demonstrated a response to temozolomide. Prolactin- and adrenocorticotrophic hormone (ACTH)-secreting tumours respond more frequently than non-functioning tumours. Response is typically evident in the first three months of treatment. Adverse effects occur in almost half of patients, although the majority are mild. The expression of a DNA repair enzyme, 06-methylguanine-DNA methyltransferase (MGMT), as determined by immunohistochemistry, appears to be the primary determinant of response to temozolomide in pituitary tumours. There is suggestion that MGMT may also play a role in pituitary tumorigenesis. Over the nextfew years we will see temozolomide used earlier in the treatment algorithm of aggressive pituitary tumours, making it imperative tocollect global long-term data on its use.

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