Prognostic Implication of Clinical and Pathologic Features in Patients with Glioblastoma Multiforme Treated with Concomitant Radiation plus Temozolomide

Donato, Vittorio; Papaleo, Antonella; Castrichino, Annamaria; Banelli, E; Giangaspero, Felice; Salvati, Maurizio; Delfini, Roberto

doi:10.1177/030089160709300304

Cited by 50 publications

(35 citation statements)

References 46 publications

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“…PTEN mutations have been found in 15 to 40% of glioblastoma [26,27]. In several previous studies PTEN mutations were not associated with prognosis of glioblastoma [28,29]. In our series we report 7 missense mutations mostly in the region of homologous tensin, auxlin and dual specificity phosphatases thereby possibly resulting in the gliomogenesis in the samples harboring these mutations.…”

Section: Discussionsupporting

confidence: 44%

“…Most of the previous studies concluded that patient's age had the greatest effect on survival. Vittorio Donato in 2007 observed that patients under 61 years of age had a significantly prolonged survival [29]. We observed that Median Overall survival was better i.e, 15 months in patients with KPS >70 compared to 13 (7,19) months in patients with KPS ≤ 70 (p>0.05) .…”

Section: Discussionmentioning

confidence: 56%

“…We observed that Median Overall survival was better i.e, 15 months in patients with KPS >70 compared to 13 (7,19) months in patients with KPS ≤ 70 (p>0.05) . Most of the previous studies have also concluded that Median OS is better in patients with good pre-operative KPS [29,30].…”

Section: Discussionmentioning

confidence: 98%

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EGFR and PTEN Gene Mutation Status in Glioblastoma Patients and their Prognostic Impact on Patient's Survival

A¹

2015

J Carcinog Mutagen

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Glioblastoma multiforme (GBM) is the most aggressive form of glioma. Genetic analysis of GBM tumorigenesis has identified several alterations in particular EGFR and PTEN genes. The purpose of the present study was to analyze the frequency and distribution of EGFR/PTEN mutations in GBM and to determine their relationship with different clinicopathological characteristics.The paired tumor and adjacent normal tissue specimens of 40 consecutive patients with GBM were examined and DNA preparations were evaluated for the occurrence of EGFR/PTEN gene mutations by PCR-SCCP and DNA sequencing.In total, 20 of 40 (50%) GBM tumours had mutation of either an EGFR or PTEN. EGFR gene mutation was present in 13 (32.5%) and PTEN gene mutations in 07 of 40 (17.5%) patients. Both EGFR/PTEN mutations were found in 03 of 40 samples (7.5%). The samples which showed EGFR mutations but were negative for PTEN were detected in 10 of 40 (25%) patients (EGFR+ve/PTEN-ve). The samples with PTEN +ve/EGFR -ve were present in 04 of 40 (10%) patients. Median PFS and Median OS was better in patients with EGFR +ve/PTEN -ve (p>0.05).EGFR and PTEN gene mutations exist in our population with GBM and play a significant role in its development with better survival for patients for EGFR+ve/PTE -ve mutation status.

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Section: Discussionsupporting

confidence: 44%

Section: Discussionmentioning

confidence: 56%

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EGFR and PTEN Gene Mutation Status in Glioblastoma Patients and their Prognostic Impact on Patient's Survival

A¹

2015

J Carcinog Mutagen

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“…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;…”

Section: Studies Selection and Characteristicsmentioning

confidence: 99%

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

Chen

He²,

Tang³

et al. 2015

Asian Pacific Journal of Cancer Prevention

119

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“…3 In contrast, there are publications opposing a prognostic relevance. 4,5 Currently, the possibility of EGFRtargeted therapies has initiated the development of a variety of agents directed either towards the extracellular ligand-binding domain or the intracellular tyrosine kinase domain including the monoclonal antibody Erbitux (IMC-C225, ImClone/Bristol Myers Squibb), and the EGFR tyrosine kinase inhibitors Gefitinib (ZD1839, Iressa, AtraZeneca) and Erlotinib (OSI-774, OSI/Genentech/Roche). 6 Although these EGFR-targeted therapies are already in phase III clinical trials, it still remains to be determined, which subgroup of patients will most likely benefit.…”

Section: Introductionmentioning

confidence: 99%

Comparison of automated silver enhanced in situ hybridization and fluorescence in situ hybridization for evaluation of epidermal growth factor receptor status in human glioblastomas

et al. 2009

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The epidermal growth factor receptor (EGFR) is amplified in approximately 40% of glioblastomas making it a compelling molecular target for therapy. Before starting a therapy targeting the EGFR pathway, accurate determining of EGFR status is a prerequisite. We evaluated the reliability of the novel automated silver enhanced in situ hybridization for the detection of EGFR gene amplification in human glioblastomas. EGFRamplification status was assessed in 93 cases of glioblastoma by silver enhanced in situ hybridization and compared with results of fluorescence in situ hybridization and immunohistochemistry. In a second cohort, silver enhanced in situ hybridization status was correlated with EGFR gene expression data. The EGFR gene was amplified in 25/90 tumours (28%) by silver enhanced in situ hybridization, and in 28/93 tumours (30%) by fluorescence in situ hybridization. The concordance rate for silver enhanced in situ hybridization and fluorescence in situ hybridization was 98%. Two glioblastomas were scored as being amplified by fluorescence in situ hybridization but not by silver enhanced in situ hybridization. Polymerase chain reaction-based EGFRamplification data were highly correlated with EGFR silver enhanced in situ hybridization. Altogether, 81 of 91 cases (89%) showed positivity for EGFR expression by immunohistochemistry. Although EGFR protein over expression was associated with gene amplification (r ¼ 0.40, Po0.001), there were 29 of 91 cases that showed a high EGFR protein level and no EGFR amplification by fluorescence in situ hybridization. The high concordance rate of silver enhanced in situ hybridization and fluorescence in situ hybridization for the detection of EGFR amplification in paraffin-embedded glioblastomas samples demonstrates that silver enhanced in situ hybridization is a valid and attractive alternative to fluorescence in situ hybridization. Silver enhanced in situ hybridization combines the advantages of bright field microscopy with fully automated analysis in a costeffective way thereby emphasizing its use for routine application in surgical pathology.

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Prognostic Implication of Clinical and Pathologic Features in Patients with Glioblastoma Multiforme Treated with Concomitant Radiation plus Temozolomide

Cited by 50 publications

References 46 publications

EGFR and PTEN Gene Mutation Status in Glioblastoma Patients and their Prognostic Impact on Patient's Survival

EGFR and PTEN Gene Mutation Status in Glioblastoma Patients and their Prognostic Impact on Patient's Survival

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

Comparison of automated silver enhanced in situ hybridization and fluorescence in situ hybridization for evaluation of epidermal growth factor receptor status in human glioblastomas

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