Coexpression of platelet-derived growth factor (PDGF) and PDGF-receptor genes by primary human astrocytomas may contribute to their development and maintenance.

Maxwell, Marius; Naber, Stephen P.; Wolfe, Hubert J.; Galanopoulos, T; Hedley‐Whyte, E. T.; Black, Perry; Antoniades, Harry N.

doi:10.1172/jci114675

Cited by 190 publications

(95 citation statements)

References 36 publications

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“…[17] Several growth factors are said to involve in glioma angiogenesis, notably platelet-derived growth factor (PDGF), [7] basic fibroblast growth factor (bFGF), [8] epidermal growth factor (EGF),[9] transforming growth factor beta (TGF-B), [18] and vascular endothelial growth factor (VEGF). [10][11][12][13] Among angiogenic agents, VEGF is the most studied one, and its role in driving the angiogenic process in glioma is well known.…”

Section: Discussionmentioning

confidence: 99%

“…Angiogenesis markers such as platelet-derived growth factor (PDGF), basic fibroblast growth factor (bFGF), epidermal growth factor (EGF), transforming growth factor beta (TGF-B) and vascular endothelial growth factor (VEGF) have been mentioned to play a role in this process. [7][8][9][10][11][12][13] However, there has not been any published report explaining the angiogenesis profile of RECK in glioma. Therefore in this study, we aimed at exploring RECK role in angiogenesis of glioma by performing immunohistochemistry study and comparing it with other well-known angiogenesis markers such as CD34 and VEGF.…”

Section: Introductionmentioning

confidence: 99%

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Expression of RECK in endothelial cells of glioma: comparison with CD34 and VEGF expressions

Rahmah

Sakai

et al. 2011

J Neurooncol

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2 AbstractPurpose: Angiogenesis is thought to involve in progression of glioma grades, and RECK has been said to involve in maturation of vessels. In this study, we aimed to determine whether high micro-vessel density (MVD) expressed by RECK in glioma tissue is correlated with grades of glioma. We also compared RECK expression with that of the formerly known vessel marker, CD34 and VEGF.Methods: RECK, CD34 and VEGF immuno-reactivities of 72 glioma tissues were studied.Results: RECK was seen in microvessels of glioma tissues. CD34 showed similar pattern to RECK, whereas VEGF showed positive staining in cytoplasm of tumor cells and endothelial cells. Average MVD with RECK was 107.6 microvessels (range: 7-290).RECK was positively correlated with grades of glioma. RECK and CD34 also showed strong correlation (P= 0.001). Higher frequency of VEGF staining was also correlated with higher grade of glioma.Conclusions: This is the first study describing expression of RECK in glioma, and its angiogenesis-related nature may provide a potential therapeutic target for glioma treatment in the future.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Expression of RECK in endothelial cells of glioma: comparison with CD34 and VEGF expressions

Rahmah

Sakai

et al. 2011

J Neurooncol

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“…1,2 The most important limitations of the chemotherapy are the intrinsic or acquired resistance of tumor cells to anti-cancer drugs and the toxicity of high doses of drug to normal tissues. 3 In addition, only few chemotherapeutic agents, such as nitrosureas, are lipid-soluble and can penetrate into the central nervous system.…”

Section: Introductionmentioning

confidence: 99%

Increase of BCNU sensitivity by wt-p53 gene therapy in glioblastoma lines depends on the administration schedule

Biroccio¹,

Bufalo²,

Ricca³

et al. 1999

Gene Ther

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In this article, we investigated the effect induced by the ify the cell cycle profile in respect of Ad-p53 infected cells. reintroduction of wild-type p53 (wt-p53) protein on BCNU In contrast, BCNU→Ad-p53 sequence provoked G2-M sensitivity in the ADF glioblastoma line. Using a wt-p53 rearrest similar to that observed after treatment with BCNU combinant adenovirus (Ad-p53), we demonstrated that alone, but prevented the later recovery of the cells through exogenous wt-p53 expression was able to increase the the cell cycle, by driving the cells to apoptotic death. These sensitivity to BCNU in ADF cells. Interestingly, this effect results demonstrate that the administration sequence is was more evident when Ad-p53 infection was performed important to increase drug sensitivity. To generalize the after BCNU treatment compared with the opposite phenomenon observed on ADF line, the antiproliferative sequence. To understand the biological basis of these difeffect of the two different schedules was analyzed on other ferent behaviors, we analyzed the cell cycle of the differglioblastoma lines (A172, CRS-A2, U373MG) with different ently treated cells. We found that Ad-p53 infection induced BCNU sensitivity and p53 status. The data obtained a persistent accumulation of cells in the G0/G1 phase confirm that the wt-p53 gene transfer enhances BCNU while, as expected, BCNU induced a block in the G2-M sensitivity in glioblastoma cells depending on the phase. Ad-p53→BCNU sequence did not significantly modadministration sequence.

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“…One of the important factors that consist of this phenomenon is the autocrine signalling of growth factors (Vassbotn et al, 1993). The coexpression of platelet-derived growth factor (PDGF) and its receptor (PDGFR) is frequently detected in a variety of tumours including malignant glioma (Maxwell et al, 1990;Hermanson et al, 1992;Guha et al, 1995), lung cancer (Antoniades et al, 1992), and sarcoma (Smits et al, 1992), suggesting the existence of PDGF autocrine loop. Platelet-derived growth factor, a potent mitogen for glial cells, vascular smooth muscle cells, and fibroblasts, exists as disulphide-linked dimers of four homologous polypeptide chains, PDGF-A and -B, and the recently identified PDGF-C and PDGF-D (Ross et al, 1986;Deuel, 1987;Li et al, 2000;Bergsten et al, 2001;Gilbertson et al, 2001;LaRochelle et al, 2001).…”

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confidence: 99%

Inhibition of platelet-derived growth factor signalling induces autophagy in malignant glioma cells

et al. 2004

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Malignant gliomas highly coexpress platelet-derived growth factor (PDGF) and its receptor, suggesting the presence of an autocrine loop. Therefore, disruption of PDGF ligand/receptor complex represents a promising strategy for the treatment of malignant gliomas. However, the mechanisms of the antitumour effect exerted by the inhibition of PDGF-mediated cell growth remain unclear. In the present study, using anti-PDGF neutralising antibody, we investigated the effect of the inhibition of PDGF signalling on malignant glioma U87-MG, D54, and T98G cells with high levels of PDGF-A and -B. As a control, normal fibroblast MRC5 cells expressing low levels of PDGF-A and -B were used. Treatment with anti-PDGF neutralising antibody did not affect the expressions of PDGF-A, PDGF-B, and Akt, but suppressed the level of phosphorylated Akt in tumour cells, indicating the inhibition of PDGF signalling. The cell viability of all malignant glioma cells tested in this study was significantly inhibited in a time-dependent manner following the treatment compared to that of fibroblast cells (Po0.02 to o0.05). The antitumour effect of anti-PDGF antibody was suppressed by the activation of Akt and enhanced by the downregulation of Akt. Interestingly, the inhibition of PDGF signalling induced the development of acidic vesicular organelles and the autophagosome membrane association of the microtubule-associated protein light chain 3, which are characteristic of autophagy, in malignant glioma cells, while apoptotic cell death was not observed. Together these findings imply a new concept of autophagy for PDGF autocrine inhibition in malignant gliomas.

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Coexpression of platelet-derived growth factor (PDGF) and PDGF-receptor genes by primary human astrocytomas may contribute to their development and maintenance.

Abstract: The present studies investigated the expression of the two

Cited by 190 publications

References 36 publications

Expression of RECK in endothelial cells of glioma: comparison with CD34 and VEGF expressions

Expression of RECK in endothelial cells of glioma: comparison with CD34 and VEGF expressions

Increase of BCNU sensitivity by wt-p53 gene therapy in glioblastoma lines depends on the administration schedule

Inhibition of platelet-derived growth factor signalling induces autophagy in malignant glioma cells

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