Thematische Bibliographien / Tumourigenesis

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Auswahl der wissenschaftlichen Literatur zum Thema „Tumourigenesis“

Autor: Grafiati

Veröffentlicht am 4. Juni 2021

Zuletzt aktualisiert am 6. September 2023

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Zeitschriftenartikel zum Thema "Tumourigenesis"

Peiser, J., A. Smith, B. Bapat und H. Stern. „Colorectal tumourigenesis“. Surgical Oncology 3, Nr. 4 (August 1994): 195–201. http://dx.doi.org/10.1016/0960-7404(94)90034-5.

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Warfel, Noel A., und Wafik S. El-Deiry. „p21WAF1 and tumourigenesis“. Current Opinion in Oncology 25, Nr. 1 (Januar 2013): 52–58. http://dx.doi.org/10.1097/cco.0b013e32835b639e.

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Chang, Xiaotian, und Kehua Fang. „PADI4 and tumourigenesis“. Cancer Cell International 10, Nr. 1 (2010): 7. http://dx.doi.org/10.1186/1475-2867-10-7.

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Reincke, M., F. Beuschlein, M. Slawik und K. Borm. „Molecular adrenocortical tumourigenesis“. European Journal of Clinical Investigation 30 (Dezember 2000): 63–68. http://dx.doi.org/10.1046/j.1365-2362.2000.0300s3063.x.

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Hickman, J. „Apoptosis and tumourigenesis“. Current Opinion in Genetics & Development 12, Nr. 1 (01.02.2002): 67–72. http://dx.doi.org/10.1016/s0959-437x(01)00266-0.

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BUCKLEY, I. „Tumourigenesis: A malignant scenario“. Cell Biology International Reports 15, Nr. 7 (Juli 1991): 545–49. http://dx.doi.org/10.1016/0309-1651(91)90001-y.

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Heijmans, J., N. V. J. A. Büller, E. Hoff, A. A. Dihal, T. van der Poll, M. A. D. van Zoelen, A. Bierhaus et al. „Rage signalling promotes intestinal tumourigenesis“. Oncogene 32, Nr. 9 (02.04.2012): 1202–6. http://dx.doi.org/10.1038/onc.2012.119.

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Fu, K., F. Lloyd, C. Forrest, B. Klopcic und I. Lawrance. „P036 SPARC affects colorectal tumourigenesis“. Journal of Crohn's and Colitis 7 (Februar 2013): S24—S25. http://dx.doi.org/10.1016/s1873-9946(13)60059-8.

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Froldi, Francesca, Milán Szuperák und Louise Y. Cheng. „Neural stem cell derived tumourigenesis“. AIMS Genetics 2, Nr. 1 (2015): 13–24. http://dx.doi.org/10.3934/genet.2015.1.13.

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Kishida, S., und K. Kadomatsu. „Involvement of midkine in neuroblastoma tumourigenesis“. British Journal of Pharmacology 171, Nr. 4 (24.01.2014): 896–904. http://dx.doi.org/10.1111/bph.12442.

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Dissertationen zum Thema "Tumourigenesis"

Maharjan, Rajani. „New Insights in Adrenal Tumourigenesis“. Doctoral thesis, Uppsala universitet, Institutionen för kirurgiska vetenskaper, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-326149.

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Unilateral cortisol producing adenoma (CPA) is the most common cause of ACTH-independent Cushing’s syndrome and is surgically curable. On the other hand, adrenocortical carcinomas (ACCs) are rare and aggressive tumours. Although the overall survival of the patients with ACC is very poor, the outcome can be heterogeneous and vary significantly between the patients. This thesis comprises studies showing genetic and genomic events occurring in CPAs and ACCs, their functional impact and clinical correlations. The Wnt/β-catenin and cAMP/PKA signalling pathways are crucial in adrenal homeostasis and frequent mutations in members of these pathways (CTNNB1, GNAS, and PRKACA) are found in CPAs. Mutational analysis revealed that ~60% of the CPAs harboured mutations in either of these genes. Transcriptome signature exhibited increased expression of genes involved in steroidogenesis in PRKACA/GNAS mutated (Cluster1) tumours in comparison to CTNNB1 mutated /wildtype (Cluster2) tumours. In addition we have also observed that gain of chromosome arm 9q was the most frequent arm level copy number variation (CNV) occurring in CPAs and were exclusively present in Cluster2 tumours. We also discovered novel PRKACA mutations occurring in ACCs, causing activation of cAMP/signalling pathway. Comprehensive analysis of Wnt/β-catenin signalling pathway in ACCs revealed novel interstitial deletions occurring in CTNNB1 leading to deletion of the N-terminus of β-catenin. This is a novel and yet another frequent event leading to activated Wnt/β-catenin signalling and downstream targets in ACCs. Both, mutations occurring in CTNNB1 and nuclear expression of its protein were associated with poor overall survival. Through multiregional sampling approach we discovered intra-tumour heterogeneity in ACC tumours. Although all the multiregions within a tumour showed presence of shared basal CNVs, they encompassed private CNVs, different ploidy levels and private mutations in known driver genes. We found intra-tumour heterogeneity in CTNNB1, PRKACA, TERT promoter and TP53 mutations as well as ZNRF3 and CDKN2A/2B homozygous deletions.

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Oliver, Joseph James. „Characterizing ErbB2-induced mammary tumourigenesis“. Thesis, Kingston, Ont. : [s.n.], 2007. http://hdl.handle.net/1974/687.

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Tam, Kevin J. „Semaphorin 3C in prostate cancer tumourigenesis“. Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/61319.

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The full abstract for this thesis is available in the body of the thesis, and will be available when the embargo expires.
Medicine, Faculty of
Experimental Medicine, Division of
Medicine, Department of
Graduate

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Robinson, James Peter. „Tumourigenesis of Peutz-Jeghers Syndrome polyps“. Thesis, Queen Mary, University of London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.522321.

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Aimls, Mark Anthony Slevin. „The role of gangliosides in tumourigenesis“. Thesis, Manchester Metropolitan University, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.359140.

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Blyth, Karen. „A transgenic model to study the role of oncogenes and tumour suppression genes in T cell lymphoma“. Thesis, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321716.

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Johansson, Térèse A. „Pancreatic Endocrine Tumourigenesis : Genes of potential importance“. Doctoral thesis, Uppsala University, Department of Medical Sciences, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-9294.

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Understanding signalling pathways that control pancreatic endocrine tumour (PET) development and proliferation may reveal novel targets for therapeutic intervention. The pathogenesis for sporadic and hereditary PETs, apart from mutations of the MEN1 and VHL tumour suppressor genes, is still elusive. The protein product of the MEN1 gene, menin, regulates many genes. The aim of this thesis was to identify genes involved in pancreatic endocrine tumourigenesis, with special reference to Notch signalling.

Messenger RNA and protein expression of NOTCH1, HES1, HEY1, ASCL1, NEUROG3, NEUROD1, DLK1, POU3F4, PDX1, RPL10, DKK1 and TPH1 were studied in human PETs, sporadic and MEN 1, as well as in tumours from heterozygous Men1 mice. For comparison, normal and MEN1 non-tumourous human and mouse pancreatic specimens were used. Nuclear expression of HES1 was consistently absent in PETs. In mouse tumours this coincided with loss of menin expression, and there was a correlation between Men1 expression and several Notch signalling factors. A new phenotype consisting of numerous menin-expressing endocrine cell clusters, smaller than islets, was found in Men1 mice. Expression of NEUROG3 and NEUROD1 was predominantly localised to the cytoplasm in PETs and islets from MEN 1 patients and Men1 mice, whereas expression was solely nuclear in wt mice. Differences in expression levels of Pou3f4, Rpl10 and Dlk1 between islets of Men1 and wt mice were observed.

In addition, combined RNA interference and microarray expression analysis in the pancreatic endocrine cell line BON1 identified 158 target genes of ASCL1. For two of these, DKK1 (a negative regulator of the WNT/β-catenin signalling pathway) and TPH1, immunohistochemistry was performed on PETs. In concordance with the microarray finding, DKK1 expression showed an inverse relation to ASCL1 expression.

Altered subcellular localisation of HES1, NEUROD1 and NEUROG3 and down-regulation of DKK1 may contribute to tumourigenesis.

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Small, Donna. „The role of cathepsin S in tumourigenesis“. Thesis, Queen's University Belfast, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.580089.

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Recent studies have demonstrated that cysteine cathepsin S, predominantly from tumour- associated macrophages, promotes tumour development and progression. Conversely, previous work examining human colorectal and brain biopsies have shown that the tumour cells themselves are a major source of CatS. In order to clarify the contribution of stromal- derived versus tumour cell-derived CatS in colorectal tumourigenesis, investigations were carried out using the syngeneic MC38 coloadenocarcinoma cell line, which was found to expressed and produced CatS. Loss-of-function CatS experiments performed on the MC38 cells demonstrated a reduction in invasion, lower activity level and reduced proteolysis, signifying a role for CatS in various aspects of tumourigenesis. Investigations in vivo using CatS null mice revealed a role for both tumour cell and stromal-derived CatS in MC38 tumour development and highlighted that CatS derived from either sources partially compensated for each other, and that depletion from both sources was required for the most significant retardation of tumour growth, This noted anti-tumour effect was characterised by a reduction in tumour cell proliferation and increased apoptosis, which may be attributable, at least in part, to the significant diminution in tumour neo-angiogenesis. Mean vessel number and vessel area was significantly reduced in tumours which lacked both sources of CatS, were the vessels presented with increased leakiness; suggestive of more dysfunctional tumour vessel architecture, The observation of increased lung and liver metastases in the CatS null mice was unexpected, however, this may be due to the expression of tumour cell derived CatS, thereby promoting rnetastases. This may be a result of decreased immuno-protective and anti-tumour roles due to the loss of CatS. Taken together, these findings clearly highlight a functional role for CatS in several hallmarks of tumourigenesis, particularly angiogenesis. The data also demonstrates CatS as a valid anti-angiogenic target in the treatment of cancer, at least in solid tumours.

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Devlin, Andrea. „A study of CYP1B1 expression in tumourigenesis“. Thesis, University of Ulster, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.494336.

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Lynch, Catherine Anne. „Mechanisms of epigenetic gene silencing in tumourigenesis“. Thesis, University of Ulster, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.428611.

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Bücher zum Thema "Tumourigenesis"

Williams, Kaye Janine. Tumourigenesis mechanisms in Li-Fraumeni syndrome. Manchester: University of Manchester, 1996.

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Kotsopoulos, Joanne. The effects of dietary folate on MNU-induced mammary tumourigenesis. Ottawa: National Library of Canada, 2002.

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Thomas, David Peter. Studies on tumourigenesis in transgenic mice expressing the early region genes of human papillomavirus type 16 (HPV-16). Birmingham: University of Birmingham, 1996.

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Hojilla, Carlo Vincent. The role of TIMP3 in mammary gland morphogenesis, involution, inflammation, and tumourigenesis. 2006.

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Buchteile zum Thema "Tumourigenesis"

Alden, C. L. „Male Rat Specific Alpha2uGlobulin Nephropathy and Renal Tumourigenesis“. In Nephrotoxicity, 535–41. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-2040-2_82.

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Teh, Muy-Teck. „Initiation of Human Tumourigenesis: Upregulation of FOXM1 Transcription Factor“. In Stem Cells and Cancer Stem Cells,Volume 3, 149–54. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-2415-0_14.

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Fahey-Lozano, Natasha, John E. La Marca, Marta Portela und Helena E. Richardson. „Drosophila Models of Cell Polarity and Cell Competition in Tumourigenesis“. In Advances in Experimental Medicine and Biology, 37–64. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-23629-8_3.

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Oshima, Hiroko, Kanae Echizen, Yusuke Maeda und Masanobu Oshima. „The Role of Chronic Inflammation in the Promotion of Gastric Tumourigenesis“. In Chronic Inflammation, 173–86. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-56068-5_14.

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Bernheim, Jan L. „The ‘Des Syndrome’: A prototype of Human Teratogenesis and Tumourigenesis by Xenoestrogens?“ In Environmental Science and Technology Library, 81–118. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-015-9769-2_5.

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Cools, Martine, Leendert H. J. Looijenga, Katja P. Wolffenbuttel und Guy T'Sjoen. „Managing the Risk of Germ Cell Tumourigenesis in Disorders of Sex Development Patients“. In Understanding Differences and Disorders of Sex Development (DSD), 185–96. Basel: S. KARGER AG, 2014. http://dx.doi.org/10.1159/000363642.

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Hutson, John M., Marilyn L. Baker, Masaru Terada, Baiyun Zhou und Georgia Paxton. „Embryological Mechanisms of Maldescent and Tumourigenesis“. In Germ Cell Tumours III, 1–6. Elsevier, 1994. http://dx.doi.org/10.1016/b978-0-08-042198-8.50008-x.

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Maher, Eamonn R. „von Hippel–Lindau disease and succinate dehydrogenase subunit (SDHB, SDHC, and SDHD) genes“. In Oxford Textbook of Endocrinology and Diabetes, 954–59. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.0686.

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This chapter considers the clinical and molecular features of von Hippel–Lindau (VHL) disease (OMIM 193300) and mutations in succinate dehydrogenase subunit genes (SDHB (OMIM 115310), SDHC (OMIM 605373), and SDHD (OMIM 168000)). Both disorders are important causes of phaeochromocytoma and, in addition to having overlapping clinical phenotypes, also share some similarities in mechanisms of tumourigenesis.

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Ferletta, Maria. „The Role of Sox Transcription Factors in Brain Tumourigenesis“. In Molecular Targets of CNS Tumors. InTech, 2011. http://dx.doi.org/10.5772/23616.

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Eggert, Angelika, Garrett M. Brodeur und Gudrun Schleiermacher. „Neuroblastoma“. In Oxford Textbook of Cancer in Children, 241–52. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198797210.003.0028.

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Neuroblastoma, a malignant neoplasm of the sympathetic nervous system, is the most common extracranial solid tumour in childhood. Since its first description in the nineteenth century, its highly heterogeneous clinical presentation has challenged clinicians and fascinated basic researchers. Neuroblastoma serves as a paradigm for the prognostic utility of biological and clinical data and the potential to tailor therapy for patient cohorts at low, intermediate, and high risk for recurrence. This chapter presents an overview of the key genetic, molecular, histological, and clinical features of neuroblastoma, as well as current risk-stratification strategies and therapeutic approaches. It also highlights how our understanding of tumour pathogenesis, coupled with molecular analyses, has illuminated critical signal transduction pathways and key molecules involved in neuroblastoma tumourigenesis, pointing to novel therapeutic targets for clinical development. Future treatment avenues for relapsed neuroblastoma are discussed, including new drugs targeting ALK, MYC/MYCN, histone deacetylases, or MDM2/TP53.

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Konferenzberichte zum Thema "Tumourigenesis"

Jenkins, Brendan, Virginie Deswaerte, Alison West, Paul Nguyen und Tracy Putoczki. „Abstract 1462: Non-inflammatory role of ASC-dependent inflammasomes in promoting gastric tumourigenesis via IL-18“. In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1462.

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Giovino, Camilla, Frank Telfer, Nish Patel, Sangeetha Paramathas, Ran Kafri und David Malkin. „Abstract 2689: Investigating the molecular mechanisms linking disrupted growth homeostasis to tumourigenesis in Li-Fraumeni Syndrome“. In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2689.

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Campbell, C., und R. Moorehead. „Examining the Role of ErbB2 in a Mouse Model of Type I Insulin like Growth Factor Receptor-Induced Mammary Tumourigenesis.“ In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-3156.

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Mantamadiotis, T., P. Daniel, G. Filiz, M. Christie, P. Waring, Y. Zhang, C. Pouton, D. Flanagan, E. Vincan und W. Phillips. „PO-202 PI3K activation in neural stem cells drives tumourigenesis which can be ameliorated by targeting the cAMP response element binding (CREB) protein“. In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.720.

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