Magnetic Resonance Imaging Characteristics Predict Epidermal Growth Factor Receptor Amplification Status in Glioblastoma

Aghi, Manish K.; Gaviani, Paola; Henson, John W.; Batchelor, Tracy T.; Louis, David N.; Barker, Fred G.

doi:10.1158/1078-0432.ccr-05-0713

Cited by 99 publications

(70 citation statements)

References 23 publications

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“…Moreover, BTL3 cells demonstrated reduced proliferative and migratory potential. This suggests loss of several features of glioblastoma aggressiveness in BTL3 probably based on lower EGFR-mediated signals (Aghi et al, 2005;Kang et al, 2005;Lamszus et al, 2005). Loss of chromosome 7 copy numbers was also observed in the recurrent tumour of GL5, showing only a borderline gain of chromosome 7, whereas the primary tumour displayed chromosome 7 amplification (data not shown).…”

Section: Discussionmentioning

confidence: 78%

Dynamics of chemosensitivity and chromosomal instability in recurrent glioblastoma

et al. 2007

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Glioblastoma multiforme is characterised by invasive growth and frequent recurrence. Here, we have analysed chromosomal changes in comparison to tumour cell aggressiveness and chemosensitivity of three cell lines established from a primary tumour and consecutive recurrences (BTL1 to BTL3) of a long-term surviving glioblastoma patient together with paraffin-embedded materials of five further cases with recurrent disease. Following surgery, the BTL patient progressed under irradiation/ lomustine but responded to temozolomide after re-operation to temozolomide. The primary tumour -derived BTL1 cells showed chromosomal imbalances typical of highly aggressive glioblastomas. Interestingly, BTL2 cells established from the first recurrence developed under therapy showed signs of enhanced chromosomal instability. In contrast, BTL3 cells from the second recurrence resembled a less aggressive subclone of the primary tumour. Although BTL2 cells exhibited a highly aggressive phenotype, BTL3 cells were characterised by reduced proliferative and migratory potential. Despite persistent methylation of the O 6 -methylguanine-DNA methyltransferase promoter, BTL3 cells exhibited the highest temozolomide sensitivity. A comparable situation was found in two out of five glioblastoma patients, both characterised by enhanced survival time, who also relapsed after surgery/chemotherapy with less aggressive recurrences. Taken together, our data suggest that pretreated glioblastoma patients may relapse with highly chemosensitive tumours confirming the feasibility of temozolomide treatment even in case of repeated recurrence.

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Section: Discussionmentioning

confidence: 78%

Dynamics of chemosensitivity and chromosomal instability in recurrent glioblastoma

et al. 2007

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“…In oligodendrogliomas the sharpness of the T 2 weighted abnormality did not predict invasive behaviour, but did predict the presence of loss of heterozygosity of chromosomes 1p and 19q, which is a marker of good prognosis and response to chemotherapy [19]. In glioblastomas, tumours with a low T 2 weighted border sharpness and a high ratio of the volume of the T 2 weighted abnormality to the T 1 weighted area correlated with increased expression of epidermal growth factor receptor (EGFR) [20], a molecular marker that is known to be associated with invasive behaviour [21].…”

Section: Problems With Conventional Imagingmentioning

confidence: 99%

Imaging biomarkers of brain tumour margin and tumour invasion

Price

Gillard²

2011

BJR

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ABSTRACT. Invasion of tumour cells into the normal brain is one of the major reasons of treatment failure for gliomas. Although there is a good understanding of the molecular and cellular processes that occur during this invasion, it is not possible to detect the extent of the tumour with conventional imaging. However, there is an understanding that the degree of invasion differs with individual tumours, and yet they are all treated the same. Newer imaging techniques that probe the pathological changes within tumours may be suitable biomarkers for invasion. Imaging methods are now available that can detect subtle changes in white matter organisation (diffusion tensor imaging), tumour metabolism and cellular proliferation (using MR spectroscopy and positron emission tomography) occurring in regions of tumour that cannot be detected by conventional imaging. The role of such biomarkers of invasion should allow better delineation of tumour margins, which should improve treatment planning (especially surgery and radiotherapy) and provide information on the invasiveness of an individual tumour to help select the most appropriate therapy and help stratify patients for clinical trials.

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“…The textural patterns between voxel intensities and their surrounding neighbors provide further insight to tissue microstructure and the local environment. 11,12 Numerous studies have correlated both MRI signal and texture analysis with genetic profiles in GBM, 5,11,[13][14][15][16][17][18][19][20][21] yet these have been limited in resolving the challenge of GBM's intratumoral heterogeneity. A major reason is that most groups use nonlocalizing biopsies to determine a single representative profile for an entire tumor.…”

Section: Introductionmentioning

confidence: 99%

Radiogenomics to characterize regional genetic heterogeneity in glioblastoma

et al. 2016

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Background. Glioblastoma (GBM) exhibits profound intratumoral genetic heterogeneity. Each tumor comprises multiple genetically distinct clonal populations with different therapeutic sensitivities. This has implications for targeted therapy and genetically informed paradigms. Contrast-enhanced (CE)-MRI and conventional sampling techniques have failed to resolve this heterogeneity, particularly for nonenhancing tumor populations. This study explores the feasibility of using multiparametric MRI and texture analysis to characterize regional genetic heterogeneity throughout MRI-enhancing and nonenhancing tumor segments. Methods. We collected multiple image-guided biopsies from primary GBM patients throughout regions of enhancement (ENH) and nonenhancing parenchyma (so called brain-around-tumor, [BAT]). For each biopsy, we analyzed DNA copy number variants for core GBM driver genes reported by The Cancer Genome Atlas. We co-registered biopsy locations with MRI and texture maps to correlate regional genetic status with spatially matched imaging measurements. We also built multivariate predictive decision-tree models for each GBM driver gene and validated accuracies using leave-one-out-cross-validation (LOOCV). Results. We collected 48 biopsies (13 tumors) and identified significant imaging correlations (univariate analysis) for 6 driver genes: EGFR, PDGFRA, PTEN, CDKN2A, RB1, and TP53. Predictive model accuracies (on LOOCV) varied by driver gene of interest. Highest accuracies were observed for PDGFRA (77.1%), EGFR (75%), CDKN2A (87.5%), and RB1 (87.5%), while lowest accuracy was observed in TP53 (37.5%). Models for 4 driver genes (EGFR, RB1, CDKN2A,

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Magnetic Resonance Imaging Characteristics Predict Epidermal Growth Factor Receptor Amplification Status in Glioblastoma

Cited by 99 publications

References 23 publications

Dynamics of chemosensitivity and chromosomal instability in recurrent glioblastoma

Dynamics of chemosensitivity and chromosomal instability in recurrent glioblastoma

Imaging biomarkers of brain tumour margin and tumour invasion

Radiogenomics to characterize regional genetic heterogeneity in glioblastoma

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