Amplification of the c-erbB oncogene is associated with malignancy in primary tumours of neuroepithelial tissue

Diedrich, U; Soja, Sabine; Behnke, J.; Zoll, Barbara

doi:10.1007/bf00314785

Cited by 19 publications

(11 citation statements)

References 13 publications

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“…When glioblastoma cells are cultured in vitro, they lose both their amplified EGFR genes and double-minute chromosomes [93]. Although amplification of the EGFR gene is associated with increasing histologic grade of tumors (e.g., glioblastoma versus anaplastic astrocytoma), within patients with glioblastomas the presence or absence of EGFR gene amplification was not correlated with a tumor's morphologic characteristics or with survival [78,94]. However, recent studies have reported a shorter median survival in patients with amplification, indicating that amplification may be a significant prognostic factor [95].…”

Section: Molecular and Cytogenetic Studiesmentioning

confidence: 99%

Genetics of primary brain tumors: a review

et al. 1994

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In this review we provide evidence for the existence of genes associated with primary malignant brain tumors. We summarize the current knowledge from studies of familial cancer aggregation, hereditary syndromes, and molecular and cytogenetic studies. The epidemiologic evidence is suggestive but inconclusive for an association between brain tumors and cancers in other family members, including cancers of the breast, lung and colon. Central nervous system (CNS) tumors have been associated with several hereditary syndromes including the Li-Fraumeni cancer family syndrome, neurofibromatosis (types 1 and 2), tuberous sclerosis, nevoid basal cell carcinoma syndrome, familial polyposis, and von Hippel-Lindau disease. Significant studies leading to the recognition of molecular and cytogenetic abnormalities in malignant gliomas are described in detail. The genetic studies conducted thus far suggest a role for inherited susceptibility in some CNS tumors.

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Section: Molecular and Cytogenetic Studiesmentioning

confidence: 99%

Genetics of primary brain tumors: a review

et al. 1994

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“…Increased levels of EGFR expression have been demonstrated in the majority of oligodendrogliomas and are rarely due to EGFR gene amplification (137,(201)(202)(203)(204). Based on the approximately equal incidence of EGFR overexpression in both lowand high-grade oligodendrogliomas, this alteration is most likely an early event in oligodendroglial tumor development and not associated with malignant progression of these tumors (201).…”

Section: Egfrmentioning

confidence: 99%

Genetic alterations in adult diffuse glioma: occurrence, significance, and prognostic implications

Smith

Jenkins²

2000

Front Biosci

146

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Our understanding of diffuse glioma development and progression has expanded remarkably over the past decade. As the genetic alterations responsible for these tumors are identified, molecular models of glioma pathogenesis are emerging and hold great promise to explain the biologic mechanisms of these neoplasms. Although these models continue to evolve and remain highly simplified, some of the genetic alterations that they encompass appear to be prognostically useful. Among the astrocytic gliomas, age and tumor grade are the most powerful indicators of patient survival, however, a wide range of variability remains, particularly among the lowgrade and anaplastic astrocytomas. Recent reports indicate that alterations of the PTEN tumor suppressor gene are independent predictors of overall survival for anaplastic astrocytoma patients, helping to distinguish the cases with behavior resembling their more malignant counterparts, the glioblastomas.Among the oligodendroglial tumors, alterations of the 1p and 19q chromosome arms have emerged as potentially powerful predictors of overall patient survival and in vivo chemotherapeutic response, while alterations of the p16/CDKN2A tumor suppressor gene suggest shorter overall survival. As our molecular models continue to improve, through functional analyses and the identification of additional genetic contributors, we will expand our capacity to more effectively prognose these patients and to design rational therapeutic strategies. INTRODUCTIONDiffuse gliomas exhibit an inherent tendency to progress to more malignant phenotypes and a broad range of clinical behavior. Classification of diffuse gliomas by histologic subtype (figure 1) and malignancy grade (figure 2),

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“…[3] In oligodendrogliomas, increased mRNA and protein expression was observed in up to 80%. [134], [135], [147]- [153] Similar expression levels for EGFR were found in Grades II and III oligodendrogliomas, indicating that this alteration is an early event in tumorigenesis. However, in contrast to high-grade astrocytomas, most studies reported only EGFR amplification in a few samples of anaplastic oligodendrog-lioma.…”

Section: Oncogenesmentioning

confidence: 97%

“…Only in a few samples, amplification of EGFR and PDGFRA was seen in anaplastic oligodendrogliomas. [79], [115], [134]- [137] Promoter hypermethylation in oligodendrogliomas Epigenetic silencing may play an important role in the induction and progression of oligodendrogliomas. [86], [138] In fact, a high throughput approach identified large numbers of hypermethylated genes.…”

Section: Allelic Loss Of Chromosome 1p and 19qmentioning

confidence: 99%

“…However, in contrast to high-grade astrocytomas, most studies reported only EGFR amplification in a few samples of anaplastic oligodendrog-lioma. [79], [115], [134]- [136] The ligand PDGF-AA (platelet-derived growth factor) is a major mitogen for oligodendrocyte O2A progenitors, indicating a role in oligodendrocyte differentiation. [154] Increased expression of PDGF-A and the receptor PDGFR-á was found in up to 94% of Grades II and III oligodendrogliomas, suggesting autocrine and paracrine stimulation.…”

Section: Oncogenesmentioning

confidence: 99%

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Oligodendrogliomas: Impact of molecular genetics on treatment

Hartmann

Deimling

2005

Neurol India

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The interest in oligodendrogliomas has increased since it became evident that a subset of these tumors respond to chemotherapy or radiation. This interest was augmented when the combined loss of the short arm of chromosome 1 and the long arm of chromosome 19 was identified as a powerful prediction factor for response. Lack of stringent morphological criteria allow high-interobserver variation with regard to classification and grading of oligodendroglial tumors. The prospect of beneficial chemotherapy prompted neuropathologists to diagnose more 'oligodendroglioma' than before. Therefore, there is great demand for unambiguous classification of oligodendroglial tumors. Supplementary analysis of the integrity of chromosomal arms 1p and 19q may greatly assist diagnostic characterization of tumors with oligodendroglial phenotype. The underlying mechanisms for these deletions are not known. Tumor suppressor genes on 1p and 19q relevant for oligodendroglioma have not yet been identified. Knowledge of these genes and the mechanisms of their inactivation might help to understand why oligodendroglial tumors do respond better to chemotherapy and radiotherapy than astrocytomas. This review compiles clinical, pathological and molecular genetic findings on oligodendrogliomas and oligoastrocytomas of WHO Grades II and III to present a brief overview on recent developments.

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Amplification of the c-erbB oncogene is associated with malignancy in primary tumours of neuroepithelial tissue

Cited by 19 publications

References 13 publications

Genetics of primary brain tumors: a review

Genetics of primary brain tumors: a review

Genetic alterations in adult diffuse glioma: occurrence, significance, and prognostic implications

Oligodendrogliomas: Impact of molecular genetics on treatment

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