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_a3319518909 _q(electronic bk.) |
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_a9783319518909 _q(electronic bk.) |
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| 050 | 4 |
_aRC280.B7 _b2017 EB |
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| 066 | _c(S | ||
| 245 | 0 | 0 |
_aBasic research and clinical aspects of adamantinomatous craniopharyngioma _cJuan Pedro Martinez-Barbera, Cynthia Lilian Andoniadou, editors. |
| 264 | 1 |
_aCham, Switzerland _bSpringer International Publishing _c2017 |
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| 300 |
_a1 recurso en línea (xii, 220 páginas) _bilustraciones (algunas a color) |
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| 336 |
_aTexto _btxt _2rdacontent |
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_aelectrónico _bc _2rdamedia |
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_arecurso electrónico _bcr _2rdacarrier |
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| 347 |
_atext file _bPDF _2rda |
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| 505 | 0 |
_6880-01 _aPathogenesis of human ACP -- Transcriptomic and Genomic Analyses of Human Craniopharyngioma -- Genetically Modified Mouse Models of Adamantinomatous Craniopharyngioma -- Clinical Diagnosis of Human ACP -- Endocrine Deficits in Patients with Human Craniopharyngioma -- Obesity and metabolic disturbances in Adamantinomatous Craniopharyngioma Patients -- Radiology and Radiotherapy of Craniopharyngioma -- Surgical Treatment of Human ACP -- Intracystic Administration of Interferon-Alpha for Reduction of Cystic Tumour Burden -- Long-term Management and Clinical Trials in Adamantinomatous Craniopharyngioma. |
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| 520 | 3 | _aThis astute volume brings together the latest expert research on adamantinomatous craniopharyngiomas (ACPs). ACPs are histologically benign but clinically aggressive tumors exhibiting a high propensity for local invasion into the hypothalamus, optic and vascular structures. These tumors, as well as the current treatments, may result in pan-hypopituitarism, diabetes insipidus, morbid obesity followed by type II diabetes mellitus, blindness, as well as serious behavioral and psychosocial impairments. Exploring in detail advances in both the understanding of tumor biology as well as clinical advances in patient management are explored in detail, this book will also look towards potential new treatment approaches. Basic Research and Clinical Aspects of Adamantinomatous Craniopharyngioma is the first book compiling all current research on ACPs. Mouse and human studies have unequivocally demonstrated that mutations in CTNNB1 encoding -catenin underlie the etiology of the majority, if not all ACP tumors. Genetic studies in mice have shown that ACPs are tumors of the pituitary gland and not of the hypothalamus as previously thought, and are derived from Rathke's pouch precursors. In addition, a role for tissue-specific adult pituitary stem cells has been revealed as causative of ACP. Together, these studies have provided novel insights into the molecular and cellular etiology as well as the pathogenesis of human ACP. Finally, this volume covers new treatment approaches that have been shown to be effective both in reducing ACP burden as well as reducing the morbidity associated with therapy. | |
| 650 | 7 |
_aCerebro _xTumors. _2embne _0(OCoLC)fst00837679 _0 _9139532 |
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| 700 | 1 |
_aAndoniadou, Cynthia Lilian, _eeditor literario |
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| 700 | 1 |
_aMartinez-Barbera, Juan Pedro, _eeditor literario |
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| 856 | 4 | 0 |
_uhttps://go.openathens.net/redirector/universidadeuropea.es?url=http://link.springer.com/10.1007/978-3-319-51890-9 _zAcceso a este recurso digital (usuarios Universidad Europea de Madrid) |
| 880 | 0 |
_6505-00/(S _aPreface; Contents; About the Editors; Contributors; Pathogenesis of Human ACP; Definition and Historical Notes; Variants; Epidemiology; Morphological and Histological Characteristics of CP Subtypes; Genetic Distinctions of CP Subtypes; β-catenin: A Multifunctional Protein and Key Component of the Canonical Wnt Signalling Pathway; Mutations in exon 3 (CTNNB1) are not Sufficient to Induce Nuclear β-Catenin Accumulation in ACP Per se; ACPs Show Activation of Wnt Signalling Target Genes in Cell Clusters with Nuclear β-Catenin Accumulation; Axin2; BMP4; Fascin; Activated EGFR; SHH. |
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| 880 | 8 |
_6505-00/(S _aImpact of Activated Signalling Pathways on Proliferation and Differentiation in ACPs Occurrence of Tumour Stem Cells in ACP; Wnt and EGFR Pathways were Identified as Being Involved in the Cellular Motility of ACP; References; Transcriptomic and Genomic Analyses of Human Craniopharyngioma; Introduction; Adamantinomatous Craniopharyngioma; β-Catenin and the WNT/Wingless Pathway; ACP Genome Analyses; CTNNB1 Mutation; Epidermal Growth Factor Receptor; SHH; Additional Potential Relevant Pathways; Papillary Craniopharyngioma; Distinction from ACP; BRAF; Summary; References. |
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| 880 | 8 |
_6505-01/(S _aGenetically Modified Mouse Models of Adamantinomatous Craniopharyngioma Normal Development of the Pituitary Gland; Pathology of Human ACP; Over-Activation of the WNT/β-Catenin Pathway Underlies the Molecular Aetiology of Human and Mouse ACP; Childhood-Onset ACP is Likely to be a Tumour of Embryonic Origin; Pituitary Stem Cells are Present in Mouse and Human Pituitaries; Contribution of Stem Cells in the Long-Term Maintenance of the Anterior Pituitary; Paracrine Contribution of Stem Cells to Tumourigenesis; Conclusions; References; Clinical Diagnosis of Human ACP; Introduction. |
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| 988 | _aSpringer_Medicine_2017 | ||
| 998 |
_b02/2018 _dz _e- _zSI |
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_c95849 _d95849 _x1 |
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