Expression of the neurotrophin receptors Trk A and Trk B in adult human astrocytoma and glioblastoma

Wadhwa, Shashi; Nag, Tapas Chandra; Jindal, Animesh; Kushwaha, Rahul; Mahapatra, Ashok Kumar; Sarkar, Chitra

doi:10.1007/bf02706217

Cited by 59 publications

(36 citation statements)

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“…Neurotrophin Trk A and Trk B receptors have been implied in tumor pathogenesis in an early stage. They respond to signals that elicit glial proliferation and are regarded as a factor of progression towards malignancy in low grade lesions where high levels of immunoreactivity are present 50 .…”

Section: Review Of the Literaturementioning

confidence: 99%

Giant cell glioblastoma: review of the literature and illustrated case

et al. 2008

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SummaryGiant cell glioblastoma is an infrequent variety of glioblastoma (5% of the cases). It has deserved a separate category in the World Health Organization classification of grade IV tumors. The clinical, imaging, histological and immunohistochemical characteristics, and the genetic alterations are reviewed. Treatment and prognosis are discussed and updated. The case of a patient that survived 19 months and died of spinal leptomeningeal metastases is illustrated.KEYWORDS: Giant cell glioblastoma. Leptomeningeal metastases. Surgery. Temozolomide. Radiotherapy.Glioblastoma de células gigantes: revisión de la literatura e ilustración de un caso Resumen El glioblastoma de células gigantes es una variante rara dentro de los glioblastomas (5% de los casos). En la clasificación de la Organización Mundial de la Salud esta entidad ha merecido una categoría aparte en los tumores de grado IV. Se revisan las características clínicas, radiológicas, histológicas, inmunohistoquímicas y las alteraciones genéticas que caracterizan este tumor. El tratamiento y el pronóstico son discutidos aportando información actualizada. Finalmente se presenta un caso clínico ilustrado, en el cual el paciente sobrevivió durante 19 meses, falleciendo como consecuencia de una diseminación espinal leptomeníngea.PALABRAS CLAVE: Glioblastoma de células gigantes. Metástasis leptomeníngeas. Cirugía. Temozolomida. Radioterapia IntroductionUnlike the "common" glioblastoma, giant cell glioblastoma is not encountered in everyday practice and it probably comes as an unexpected diagnosis most of the times. Despite certain similarities between the two disease processes, there are differences that may be of relevance for the management of the occasional patient harboring this lesion. A case of giant cell glioblastoma managed at the authors' institution is reported and the key features of giant cell glioblastoma are reviewed. Clinical caseA 54 year-old man presented with headache and motor dysphasia of short duration. MR disclosed a voluminous mass in the left temporal lobe (figure 1-A&B). The patient was operated. A frontotemporal approach was employed. The lesion had a good cleavage plane, was moderately hemorrhagic and was totally resected in a piece meal fashion. The postoperative course was uneventful. Histological examination disclosed a highly cellular neoplasm with marked pleomorphism. Prominent giant cells and numerous atypical mitotic figures were found (figure 1-C). Reticulin was abundant in the stroma. Immunohistochemistry showed positivity for GFAP, S100 protein and p53. The picture was consistent with giant cell glioblastoma. Adjuvant radiotherapy (60Gy) and chemotherapy (temozolomide) were given. There was no evidence of relapse at the 14 month follow up MR ( figure 1-D). The patient was symptom free and had no neurological deficits at that time. Three months after, the patient complained of backache, lower limb weakness and deteriorating general condition. MR disclosed spinal leptomeningeal metastases (figure 1-E). Curiously there was no ev...

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Section: Review Of the Literaturementioning

confidence: 99%

Giant cell glioblastoma: review of the literature and illustrated case

et al. 2008

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“…It has been shown that expression of TrkA and TrkC correlates with a favorable outcome in neuroblastoma and medulloblastoma patients. In GBM, immunoreactivity for TrkA was shown to be inversely associated with the grade of malignancy (24). Moreover, TrkA overexpression was found to induce autophagic cell death that was mediated through the JNK pathway (25,26).…”

Section: Discussionmentioning

confidence: 99%

EGFR signaling in the HGG-02 glioblastoma cell line with an unusual loss of EGFR gene copy

et al. 2013

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Abstract. Epidermal growth factor receptor (EGFR) gene amplification and the overexpression of EGFR are described as common features of glioblastoma multiforme (GBM). Nevertheless, we previously reported the loss of EGFR gene copy in a GBM specimen from a patient with an unusually favorable course of the disease, and the HGG-02 cell line with this aberration was successfully derived from this tumor. Here, we present a detailed analysis of changes in gene expression and cell signaling in the HGG-02 cell line; the GM7 reference cell line with a standard EGFR gene copy number derived from a very aggressive GBM was used as a control. We confirmed the downregulation of EGFR expression and signaling in HGG-02 cells using different methods (RTK analysis, gene profiling and RT-PCR). Other changes that may have contributed to the non-aggressive phenotype of the primary tumor were identified, including the downregulated phosphorylation of the Axl and Trk receptors, as well as increased activity of JNK and p38 kinases. Notably, differences in PDGF signaling were detected in both of these cell lines; HGG-02 cells preferentially expressed and signaled through PDGFRα, and PDGFRβ was strongly overexpressed and phosphorylated in the GM7 reference cell line. Using expression profiling of cancer-related genes, we revealed the specific profile of HGG-02 cells that included upregulated tumor-suppressors as well as downregulated genes associated with the extracellular matrix. This study represents the first comprehensive analysis of gene expression and cell signaling in glioblastoma cells with lower EGFR gene

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“…3,4 By systematically screening a library of human tyrosine kinases for their oncogenic potential in astrocytoma formation and then characterizing functional features and molecular mechanisms associated with TrkB-induced oncogenesis, Ni et al have provided compelling findings indicating that TrkB can play a role in astrocytoma formation. 1 It is worth pointing out that previous studies not cited by Ni et al 1 had already identified an increase in TrkB expression in both low-grade astrocytoma and glioblastoma, 5,6 and a role for TrkB signaling in the growth of gliomas and other types of brain tumors or peripheral tumors of possible neural origin has been previously proposed. For example, BDNF-induced activation of TrkB increases the viability of brain-tumor stem cells (BTSCs) isolated from gliomas through activation of the extracellular-regulated kinase (ERK) and Akt pathways, whereas TrkB knockdown or pharmacological inhibition reduces BTSC growth and BDNF-dependent ERK activation.…”

Section: Targeting Tyrosine Receptor Kinase B In Gliomasmentioning

confidence: 91%