Differences between phosphotyrosine accumulation and Neu/ErbB-2 receptor expression in astrocytic proliferative processes: Implications for glial oncogenesis

Kristt, Donald A.; Yarden, Yosef

doi:10.1002/(sici)1097-0142(19960915)78:6<1272::aid-cncr16>3.0.co;2-y

Cited by 22 publications

(14 citation statements)

References 41 publications

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“…Of the cases studied (results from tumour biopsy), the range in results observed for HER2/neu in vivo positivity is wide (20 -90%). Some authors detect HER2/neu positivity without density analysis of receptors, so they report more than 70% positivity (Dietzmann and Von Bossanyi, 1994;Kristt and Yarden, 1996;Westphal et al, 1997;Bian et al, 2000). Some authors consider only the 2 þ and 3 þ tumours as positive, so they report only 20% positivity (Forseen et al, 2002;Koka et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

“…The HER2/neu (also called c-erbB2) receptor is not found in the adult central nervous system (Press et al, 1990), but it appears in tumoral astrocytes. Its expression increases with the degree of astrocytoma anaplasia (Kristt and Yarden, 1996) and becomes frequent in glioblastomas (20 -90%; Bian et al, 2000;Forseen et al, 2002;Koka et al, 2003). Overexpression of HER2/neu seems correlated to higher degree of glioma cells anaplasia (Kristt and Yarden, 1996).…”

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confidence: 99%

“…Its expression increases with the degree of astrocytoma anaplasia (Kristt and Yarden, 1996) and becomes frequent in glioblastomas (20 -90%; Bian et al, 2000;Forseen et al, 2002;Koka et al, 2003). Overexpression of HER2/neu seems correlated to higher degree of glioma cells anaplasia (Kristt and Yarden, 1996). Activated HER2/neu can form homologous complexes, but the major action of HER2/neu results from heterodimerisation of HER2/neu with the other tyrosine kinase family-activated receptors (like epidermal growth factor receptor also called c-erbB1; Harwerth et al, 1993).…”

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confidence: 99%

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Recombinant humanised anti-HER2/neu antibody (Herceptin®) induces cellular death of glioblastomas

et al. 2004

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Glioblastoma multiforme (GBM) remains the most devastating primary tumour in neuro-oncology. Targeting of the human epithelial receptor type 2 (HER2)-neu receptor by specific antibodies is a recent well-established therapy for breast tumours. Human epithelial receptor type 2/neu is a transmembrane tyrosine/kinase receptor that appears to be important for the regulation of cancer growth. Human epithelial receptor type 2/neu is not expressed in the adult central nervous system, but its expression increases with the degree of astrocytoma anaplasia. The specificity of HER2/neu for tumoral astrocytomas leads us to study in vitro treatment of GBM with anti-HER2/neu antibody. We used human GBM cell lines expressing HER2/neu (A172 express HER2/neu more than U251MG) or not (U87MG) and monoclonal humanised antibody against HER2/neu (Herceptin s ). Human epithelial receptor type 2/neu expression was measured by immunohistochemistry and flow cytometry. Direct antibody effect, complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity were evaluated by different cytometric assays. We have shown, for the first time, the ability of anti-HER2/neu antibodies to induce apoptosis and cellular-dependent cytotoxicity of HER2/neu-expressing GBM cell lines. The results decreased from A172 to U251 and were negative for U87MG, in accordance with the decreasing density of HER2/neu receptors.

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Section: Discussionmentioning

confidence: 99%

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Recombinant humanised anti-HER2/neu antibody (Herceptin®) induces cellular death of glioblastomas

et al. 2004

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“…2C, 3B,D). Double-staining studies of ErbB2 and GFAP clearly showed their colocalization on astrocytes, as in a previous observation with human biopsy samples (Kristt and Yarden, 1996). In addition, neuregulin was also detected on GFAP-positive cells (Fig.…”

Section: Expression Of Neuregulin Erbb2 and Erbb3 In Injured Brainsmentioning

confidence: 92%

Regulation of neuregulin expression in the injured rat brain and cultured astrocytes

Tokita¹

2000

Neuroscience Research

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In this report, we investigated whether reactive astrocytes produce neuregulins (glial growth factor 2/heregulin/acetylcholine receptor-inducing activity or neu differentiation factor) and its putative receptors, ErbB2 and ErbB3 tyrosine kinases, in the injured CNS in vivo. Significant immunoreactivities with antineuregulin, anti-ErbB2, and anti-ErbB3 antibodies were detected on astrocytes at the injured site 4 d after injury to the adult rat cerebral cortex. To elucidate the mechanisms for the upregulation of neuregulin expression in astrocytes, primary cultured astrocytes were treated with certain reagents, including forskolin, that are known to elevate the intracellular level of cAMP and induce marked morphological changes in astrocytes. Western blot analysis showed that the expression of a 52 kDa membrane-spanning form of a neuregulin protein was enhanced in cultured astrocytes after administration of forskolin. The upregulation of glial fibrillary acidic protein was also observed in astrocytes treated with forskolin. In contrast, inactivation of protein kinase C because of chronic treatment with phorbol ester 12-O-tetradecanoyl phorbol 13-acetate downregulated the expression of the 52 kDa isoform, although other splice variants with apparent molecular sizes of 65 and 60 kDa were upregulated. These results suggest that the enhancement of neuregulin expression at injured sites is induced, at least in part, by elevation in intracellular cAMP levels and/or a protein kinase C signaling pathway. The neuregulin expressed on reactive astrocytes may stimulate their proliferation and support the survival of neurons surrounding cortical brain wounds in vivo.

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“…As such, this aberrant EGFR does not bind any known EGFR ligand, but is a constitutively active tyrosine kinase which initiates mitosis independent of ligand-binding. The EGFRvIII has been detected in tumour cells only and is thought to play a significant role in the pathogenesis and aggressiveness of cancers (Kristt and Yarden, 1996;Moscatello et al, 1996;Nagane et al, 1996).…”

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Evidence for the differential expression of a variant EGF receptor protein in human prostate cancer

et al. 2000

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SummaryEarlier studies have demonstrated an unexplained depletion of the epidermal growth factor receptor (EGFR) protein expression in prostatic cancer. We now attribute this phenomenon to the presence of a variant EGFR (EGFRvIII) that is highly expressed in malignant prostatic neoplasms. In a retrospective study, normal, benign hyperplastic and malignant prostatic tissues were examined at the mRNA and protein levels for the presence of this mutant receptor. The results demonstrated that whilst EGFRvIII was not present in normal prostatic glands, the level of expression of this variant protein increased progressively with the gradual transformation of the tissues to the malignant phenotype. The selective association of high EGFRvIII levels with the cancer phenotype underlines the role that this mutant receptor may maintain in the initiation and progression of malignant prostatic growth, and opens the way for new approaches in the management of this disease including gene therapy. © 2000 Cancer Research Campaign Keywords: tumour marker; stromal-epithelial interaction; EGFR; prostate/prognostic factors; hormone resistance 186British Journal of Cancer (2000) 82(1), 186-194 © 2000 Cancer Research Campaign Article no. bjoc.1999 Received 24 These results were presented in part at

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Differences between phosphotyrosine accumulation and Neu/ErbB-2 receptor expression in astrocytic proliferative processes: Implications for glial oncogenesis

Cited by 22 publications

References 41 publications

Recombinant humanised anti-HER2/neu antibody (Herceptin®) induces cellular death of glioblastomas

Recombinant humanised anti-HER2/neu antibody (Herceptin®) induces cellular death of glioblastomas

Regulation of neuregulin expression in the injured rat brain and cultured astrocytes

Evidence for the differential expression of a variant EGF receptor protein in human prostate cancer

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