Proliferation and aneusomy predict survival of young patients with astrocytoma grade II

Abstract

The clinical course of astrocytoma grade II (AII) is highly variable and not reflected by histological characteristics. As one of the best prognostic factors, higher age identifies rapid progressive A II. For patients over 35 years of age, an aggressive treatment is normally propagated. For patients under 35 years, there is no clear guidance for treatment choices, and therefore also the necessity of histopathological diagnosis is often questioned. We studied the additional prognostic value of the proliferation index and the detection of genetic aberrations for patients with A II. The tumour samples were obtained by stereotactic biopsy or tumour resection and divided into two age groups, that is 18 -34 years (n ¼ 19) and X35 years (n ¼ 28). Factors tested included the proliferation (Ki-67) index, and numerical aberrations for chromosomes 1, 7, and 10, as detected by in situ hybridisation (ISH). The results show that age is a prognostic indicator when studied in the total patient group, with patients above 35 years showing a relatively poor prognosis. Increased proliferation index in the presence of aneusomy appears to identify a subgroup of patients with poor prognosis more accurately than predicted by proliferation index alone. We conclude that histologically classified cases of A II comprise a heterogeneous group of tumours with different biological and genetic constitution, which exhibit a highly variable clinical course. Immunostaining for Ki-67 in combination with the detection of aneusomy by ISH allows the identification of a subgroup of patients with rapidly progressive A II. This is an extra argument not to defer stereotactic biopsy in young patients with radiological suspicion of A II.

Ki-67 is a Valuable Prognostic Factor in Gliomas: Evidence from a Systematic Review and Meta-analysis

“…Of the candidate studies, 13 articles failed to completely describe the available survival data. Finally, 51 published studies in total were included in the analysis after eliminating articles unsatisfying the selection criteria and duplicates (Jaros et al, 1992;Torp et al, 1992;Montine et al, 1994;Ellison et al, 1995;Heegaard et al, 1995;Kros et al, 1996;Coons et al, 1997;Pollack et al, 1997;Dehghani et al, 1998;McKeever et al, 1998;Ritter et al, 1998;Figarella-Branger et al, 2000;Rodriguez-Pereira et al, 2000;Ho et al, 2001;ReaveyCantwell et al, 2001;Zhong et al, 2001;Bredel et al, 2002;Pollack et al, 2002;Bowers, 2003;Chiang et al, 2003;Neder et al, 2003;Wessels et al, 2003;Zamecnik et al, 2003;Preusser et al, 2005;Uematsu et al, 2005;Kleinschmidt-DeMasters et al, 2006;Donato et al, 2007;Kanamori et al, 2008;Kuo et al, 2009;Laks et al, 2009;Li et al, 2009;Armstrong et al, 2010;Nabika et al, 2010;Watanabe et al, 2010;Yoshida et al, 2010;Habberstad et al, 2011;Margraf et al, 2011;Qiang et al, 2011;Shen et al, 2011;Zawrocki et al, 2011;…”

Η Έκφραση Της Τελομεράσης Ως Προγνωστικός Παράγων Σε Όγκους Εγκεφάλου

“…έχουν επίσης καταγραφεί, χωρίς μέχρι τώρα να έχει καταστεί δυνατή η εξήγηση του μηχανισμού πρόκλησης των μεταλλάξεων αυτών και της κλινικής τους σημασίας. (7,56,91,92,111) Πίνακας 1: Χρωμοσωμιακές και γονιδιακές αλλαγές σε όγκους εγκεφάλου. και τα νευρινώματα που προέρχονται από τα κύτταρα των ελύτρων των εγκεφαλικών νεύρων με ποσοστό 3%.…”