Mitogen-Activated Protein (MAP) Kinase/MAP Kinase Phosphatase Regulation: Roles in Cell Growth, Death, and Cancer

Boutros, Tarek; Chevet, Éric; Metrakos, Peter

doi:10.1124/pr.107.00106

Cited by 515 publications

(471 citation statements)

References 522 publications

(669 reference statements)

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“…This raises the possibility that other alterations in BRAF may drive the activation of p-MAPK1 and CDKN2A in pilocytic astrocytoma of the optic nerve. Alternatively, alterations in negative regulatory factors of the MAPK pathway, such as the Sprouty family of proteins, Raf kinase inhibitor protein, impedes mitogenic signal propagation, and the (7) 10 (16) dual-specificity MAPK phosphatase [29][30][31][32][33][34][35][36] may be found in pilocytic astrocytoma of the optic nerve. Studies are currently under way to test for these possibilities.…”

Section: Modern Pathology (2013) 26 1279-1287mentioning

confidence: 99%

Pilocytic astrocytomas of the optic nerve and their relation to pilocytic astrocytomas elsewhere in the central nervous system

et al. 2013

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Pilocytic astrocytoma is a low-grade glioma that affects mostly children and young adults and can occur anywhere in the central nervous system. Pilocytic astrocytoma of the optic nerve is an equally indolent subtype that is occasionally associated with neurofibromatosis type 1. In earlier studies, this subtype was considered within the larger category of 'optic pathway glioma,' which included infiltrating astrocytomas and other hypothalamic tumors. However, there have been suggestions that gliomas in the optic nerve, and especially pilocytic astrocytoma of the optic nerve, are biologically different from tumors within the hypothalamus and other parts of the optic tract. Furthermore, the recent discovery of BRAF duplication and fusion with the KIAA1549 gene is reported to be more typical for posterior fossa tumors, and the rate of this aberration is not well known in pilocytic astrocytoma of the optic nerve. To determine the distinction of pilocytic astrocytoma of the optic nerve from pilocytic astrocytoma of the posterior fossa and to investigate the prevalence of BRAF aberrations, we reviewed the clinicopathological and molecular features of all such patients in our institution. Our study demonstrates that BRAF duplication is more frequent in posterior fossa tumors compared with pilocytic astrocytoma of the optic nerve (P ¼ 0.011). However, the rates of phospho-MAPK1 and CDKN2A expression were high in both pilocytic astrocytoma of the optic nerve and posterior fossa pilocytic astrocytoma, suggesting that the MAPK pathway is active in these tumors. Our study supports the notion that BRAF duplication is more typical of posterior fossa pilocytic astrocytoma and that molecular alterations other than KIAA1549 fusion may underlie MAPK pathway activation in pilocytic astrocytoma of the optic nerve.

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Section: Modern Pathology (2013) 26 1279-1287mentioning

confidence: 99%

Pilocytic astrocytomas of the optic nerve and their relation to pilocytic astrocytomas elsewhere in the central nervous system

et al. 2013

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“…Nevertheless, all the above reports do not define the areas of peritumor tissue used for analysis, nor their distance from the tumor edge. In this regard, we recently showed in peritumor tissue, up to 3.5 cm from the tumor margin, the presence of phosphorylated (p) extracellular signal-regulated kinases (ERKs) and c-Jun NH 2 terminal kinases (JNKs) (12,13) regulating cell proliferation, differentiation, motility and apoptosis (14). The neural stem cell marker nestin was also expressed in the same tissue.…”

Section: Introductionmentioning

confidence: 99%

Assessment of angiogenesis by CD105 and nestin expression in peritumor tissue of glioblastoma

et al. 2010

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Abstract. Angiogenesis in the peritumor tissue of glioblastoma (GBM) is still an open field of research. This study investigates neovascularization in the tumor surrounding areas by examining CD105 and nestin expression along with microvessel density (MVD) with the aim of establishing their possible prognostic significance. Angiogenesis was also confirmed by investigating, in vessel walls, the presence of pericytes, which are multipotent stem cells, expressing ·-smooth muscle actin (·-SMA). In our study, including 40 GBM patients, tissue samples were obtained from tumors (first area) and white matter at a distance <1 cm (second area) and between 1 and 3.5 cm (third area) from the tumor margin. CD105 and nestin were detected by immunohistochemistry in hyperplastic endothelium of GBM and peritumor tissue, and occasionally coexpressed or colocalized. Pericytes encircling hyperplastic endothelium were evident in all three areas. Univariate analysis revealed that patients with a CD105-MVD value ≥8 in the third area have a significantly shorter survival time and Cox analysis indicated an about 3.5-fold increase in death risk in the same patients. These results demonstrate that a tumor neoangiogenesis occurs in GBM peritumor tissue with intimate involvement of pericytes. CD105-MVD in the area located at a greater distance from the tumor margin carries prognostic significance.

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“…The signaling transduction pathways of MAPKs have been highly conserved from yeast to multicellular organisms. In mammals, at least four subfamilies of MAPKs have been described, including the extracellular signal-regulated kinases (ERKs), the c-Jun NH2-terminal kinases (JNKs), the p38 isoforms (p38s), and ERK5 (Pearson et al, 2001;Boutros et al, 2008;Wagner and Nebreda, 2009) (Figure 1). MAPKs are mainly modulated by upstream MAPK kinases (MKKs) and MAPK phosphatases that modify the phosphorylation of the MAPK threonine and tyrosine (T-X-Y) motif.…”

Section: Introductionmentioning

confidence: 99%

MAPK signaling in inflammation-associated cancer development

2010

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Mitogen-activated protein (MAP) kinases comprise a family of protein-serine/threonine kinases, which are highly conserved in protein structures from unicellular eukaryotic organisms to multicellular organisms, including mammals. These kinases, including ERKs, JNKs and p38s, are regulated by a phosphorelay cascade, with a prototype of three protein kinases that sequentially phosphorylate one another. MAPKs transduce extracellular signals into a variety of cellular processes, such as cell proliferation, survival, death, and differentiation. Consistent with their essential cellular functions, MAPKs have been shown to play critical roles in embryonic development, adult tissue homeostasis and various pathologies. In this review, we discuss recent findings that reveal the profound impact of these pathways on chronic inflammation and, particularly, inflammation-associated cancer development.

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Mitogen-Activated Protein (MAP) Kinase/MAP Kinase Phosphatase Regulation: Roles in Cell Growth, Death, and Cancer

Cited by 515 publications

References 522 publications

Pilocytic astrocytomas of the optic nerve and their relation to pilocytic astrocytomas elsewhere in the central nervous system

Pilocytic astrocytomas of the optic nerve and their relation to pilocytic astrocytomas elsewhere in the central nervous system

Assessment of angiogenesis by CD105 and nestin expression in peritumor tissue of glioblastoma

MAPK signaling in inflammation-associated cancer development

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