In situ detection of telomeres by fluorescence in situ hybridization and telomerase activity in glioblastoma multiforme: Correlation with p53 status, EGFR, c-myc, MIB1, and Topoisomerase IIα protein expression

Miracco, Clelia; Santi, M. M. De; Luzi, Pietro; Lalinga, Anna Vittoria; Laurini, Lorella; Nisi, Maria Caterina De; Angeloni, Giuseppina; Brogi, Marco; Cardone, Concetta; Carducci, A; Arcuri, Felice; Tosi, Piero; Rubino, Giovanni; Pirtoli, Luigi

doi:10.3892/ijo.23.6.1529

Cited by 9 publications

(7 citation statements)

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“…MIF contributes to the migratory and proliferative functions of human melanoma cells, as well as the neovascularization of G361 melanoma cell‐induced tumors (30). In vivo , MIF is highly expressed in several melanocytic tumor types, including melanoma and melanoma metastases, as well as benign nevi (54). Similarly implicated in non‐melanoma skin cancer, MIF is highly expressed and hypoxia‐induced in squamous cell carcinoma cells (55).…”

Section: Mif and Cutaneous Pathologiesmentioning

confidence: 99%

MIF: a key player in cutaneous biology and wound healing

Gilliver

Emmerson

Bernhagen

et al. 2010

Experimental Dermatology

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Owing to its implication in a range of pathological conditions, including asthma, rheumatoid arthritis, atherosclerosis, inflammatory bowel disease and cancer, the pleiotropic cytokine macrophage migration inhibitory factor (MIF) has been the subject of intensive recent investigation. In the field of dermatology, MIF is believed to be a detrimental factor in diseases such as systemic sclerosis, atopic dermatitis, psoriasis, eczema and UV radiation damage. However, its contribution to other aspects of cutaneous biology is currently unclear. Although its expression in intact skin is well characterized, little is known about MIF's role in cutaneous homoeostasis. However, recent data do identify MIF as a key player in the immune privilege of hair follicles. Similarly, although MIF is rapidly released and its local expression significantly induced upon wounding, its primary role in the ensuing repair process remains a source of contention. MIF has been identified as being a key effector of the beneficial effects of estrogen on wound repair, yet studies employing Mif null mice, recombinant MIF, and neutralizing anti-MIF antibodies have failed to provide a consensus as to whether it benefits or inhibits healing. In fact MIF appears to be able to exert both positive and negative effects, with the cell-specific relevancy of MIF in wound healing still unclear. Thus, if MIF and ⁄ or its downstream targets are to be therapeutically useful in the context of cutaneous repair, more needs to be done to establish the nature and mechanism of action of MIF and its receptors in healing wounds.

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Section: Mif and Cutaneous Pathologiesmentioning

confidence: 99%

MIF: a key player in cutaneous biology and wound healing

Gilliver

Emmerson

Bernhagen

et al. 2010

Experimental Dermatology

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“…It has been reported that MYC expression is elevated in almost all cancers including both HCC and GBM [ 18 , 41 ]. As compared to a nearly undetectable level in normal brain tissues, MYC is expressed in 80.6% of primary glioblastoma samples [ 43 , 44 ], and in 73% of astrocytomas [ 45 ]. The wide spread repression of miRNAs including let-7 by MYC and its contribution to tumorigenesis has also been clearly demonstrated [ 46 ].…”

Section: Discussionmentioning

confidence: 99%

Loss of MYC and E-box3 binding contributes to defective MYC-mediated transcriptional suppression of human MC-let-7a-1~let-7d in glioblastoma

et al. 2016

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Previously, we reported that MYC oncoprotein down-regulates the transcription of human MC-let-7a-1~let-7d microRNA cluster in hepatocarcinoma (HCC). Surprisingly, in silico analysis indicated that let-7 miRNA expression levels are not reduced in glioblastoma (GBM). Here we investigated the molecular basis of this differential expression. Using human GBM U87 and U251 cells, we first demonstrated that forced over-expression of MYC indeed could not down-regulate the expression of human MC-let-7a-1~let-7d microRNA cluster in GBM. Furthermore, analysis of MC-let-7a-1~let-7d promoter in GBM indicated that MYC failed to inhibit the promoter activity. Pearson's correlation and Linear Regression analysis using the expression data from GSE55092 (HCC) and GSE4290 (GBM) demonstrated a converse relationship of MC-let-7a-1~let-7d and MYC only in HCC but not in GBM. To understand the underlying mechanisms, we examined whether MYC could bind to the non-canonical E-box 3 located in the promoter of MC-let-7a-1~let-7d. Results from both chromatin immune-precipitation (ChIP) and super-shift assays clearly demonstrated the loss of MYC and E-box 3 binding in GBM, suggesting for the first time that a defective MYC and E-box3 binding in GBM is responsible for the differential MYC mediated transcriptional inhibition of MC-let-7a-1~let-7d and potentially other tumor suppressors. MYC and let-7 are key oncoprotein and tumor suppressor, respectively. Understanding the molecular mechanisms of their regulations will provide new insight and have important implications in the therapeutics of GBM as well as other cancers.

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“…Loss or inactivation of PTEN has been described in solid tumours of various organs, and it is mutant in about 30% of GBM, but not in low-grade gliomas and very rarely in anaplastic gliomas (Duerr et al, 1998;Zhou et al, 1999). EGFR is the main oncogene identified in brain tumours, but its prognostic value is controversial (Chakravarti et al, 2001;Muracciole et al, 2002;Miracco et al, 2003;Shinojima et al, 2003;Heimberger et al 2005a, b;Kleinschmidt-DeMasters et al, 2005;Lopes-Gines et al, 2005;Quan et al, 2005;Rich et al, 2005), although a fairly strong correlation with OS was observed in the present study. PDGF is often overexpressed in gliomas, with an elevation correlated with tumour grade (Shih and Holland, 2006) and was considered to be predictive of poor prognosis in a study on grade II tumours (Varela et al, 2004).…”

Section: Expressionsmentioning

confidence: 99%

Prognostic molecular markers with no impact on decision-making: the paradox of gliomas based on a prospective study

et al. 2008

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This study assessed the prognostic value of several markers involved in gliomagenesis, and compared it with that of other clinical and imaging markers already used. Four-hundred and sixteen adult patients with newly diagnosed glioma were included over a 3-year period and tumour suppressor genes, oncogenes, MGMT and hTERT expressions, losses of heterozygosity, as well as relevant clinical and imaging information were recorded. This prospective study was based on all adult gliomas. Analyses were performed on patient groups selected according to World Health Organization histoprognostic criteria and on the entire cohort. The endpoint was overall survival, estimated by the Kaplan -Meier method. Univariate analysis was followed by multivariate analysis according to a Cox model. p14 ARF , p16 INK4A and PTEN expressions, and 10p 10q23, 10q26 and 13q LOH for the entire cohort, hTERT expression for high-grade tumours, EGFR for glioblastomas, 10q26 LOH for grade III tumours and anaplastic oligodendrogliomas were found to be correlated with overall survival on univariate analysis and age and grade on multivariate analysis only. This study confirms the prognostic value of several markers. However, the scattering of the values explained by tumour heterogeneity prevents their use in individual decision-making.

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In situ detection of telomeres by fluorescence in situ hybridization and telomerase activity in glioblastoma multiforme: Correlation with p53 status, EGFR, c-myc, MIB1, and Topoisomerase IIα protein expression

Cited by 9 publications

References 0 publications

MIF: a key player in cutaneous biology and wound healing

MIF: a key player in cutaneous biology and wound healing

Loss of MYC and E-box3 binding contributes to defective MYC-mediated transcriptional suppression of human MC-let-7a-1~let-7d in glioblastoma

Prognostic molecular markers with no impact on decision-making: the paradox of gliomas based on a prospective study

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