Relevant bibliographies by topics / Tumour suppressor

Academic literature on the topic 'Tumour suppressor'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Tumour suppressor"

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Wagner, K. J., and S. G. E. Roberts. "Transcriptional regulation by the Wilms' tumour suppressor protein WT1." Biochemical Society Transactions 32, no. 6 (October 26, 2004): 932–35. http://dx.doi.org/10.1042/bst0320932.

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Wilms' tumour is a paediatric malignancy of the kidneys and is the most common solid tumour found in children. The Wilms' tumour suppressor protein WT1 is mutated in approx. 15% of Wilms' tumours, and is aberrantly expressed in many others. WT1 can manifest both tumour suppressor and oncogenic activities, but the reasons for this are not yet clear. The Wilms' tumour suppressor protein WT1 is a transcriptional activator, the function of which is under cell-context-specific control. We have previously described a small region at the N-terminus of WT1 (suppression domain) that inhibits the transcriptional activation domain by contacting a co-suppressor protein. We recently identified BASP1 as one of the components of the co-suppressor. Here, we analyse the mechanism of action of the WT1 suppression domain, and discuss its function in the context of the role of WT1 as a regulator of development.
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Swale, V. J., and A. G. Quinn. "Tumour suppressor genes." Clinical and Experimental Dermatology 25, no. 3 (May 2000): 231–35. http://dx.doi.org/10.1046/j.1365-2230.2000.00620.x.

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Cowell, J. K. "Tumour suppressor genes." Annals of Oncology 3, no. 9 (November 1992): 693–98. http://dx.doi.org/10.1093/oxfordjournals.annonc.a058319.

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KLEIN, G. "Tumour suppressor genes." Journal of Cell Science 1988, Supplement 10 (February 1, 1988): 171–80. http://dx.doi.org/10.1242/jcs.1988.supplement_10.13.

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Vile, R. "Tumour suppressor genes." BMJ 298, no. 6684 (May 20, 1989): 1335–36. http://dx.doi.org/10.1136/bmj.298.6684.1335.

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Maehama, T., F. Okahara, and Y. Kanaho. "The tumour suppressor PTEN: involvement of a tumour suppressor candidate protein in PTEN turnover." Biochemical Society Transactions 32, no. 2 (April 1, 2004): 343–47. http://dx.doi.org/10.1042/bst0320343.

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The tumour suppressor PTEN (phosphatase and tensin homologue deleted on chromosome 10) plays essential roles in regulating signalling pathways involved in cell growth and apoptosis, and is inactivated in a wide variety of tumours. The role of PTEN as a tumour suppressor has been firmly established; however, the mechanism(s) by which its function and activity are regulated remains elusive. Here, we summarize recent progress in research directed towards trying to understand the molecular basis of regulatory mechanisms for PTEN. We also describe our novel finding that a tumour suppressor candidate protein binds to extreme C-terminal region of PTEN and regulates PTEN protein turnover.
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Clurman, Bruce, and Mark Groudine. "Defining tumour-suppressor genes." Nature 389, no. 6647 (September 1997): 123. http://dx.doi.org/10.1038/38119.

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McCarthy, Nicola. "Surviving the tumour suppressor." Nature Reviews Molecular Cell Biology 8, no. 7 (July 2007): 516. http://dx.doi.org/10.1038/nrm2214.

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Bangham, Jenny. "Tumour-suppressor super models." Nature Reviews Cancer 5, no. 2 (January 20, 2005): 84. http://dx.doi.org/10.1038/nrc1554.

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Bangham, Jenny. "Tumour suppressor super models." Nature Reviews Genetics 6, no. 2 (February 2005): 91. http://dx.doi.org/10.1038/nrg1546.

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Dissertations / Theses on the topic "Tumour suppressor"

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de, Foy K. "Analysis of candidate tumour suppressor genes in sporadic ovarian tumours." Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.598448.

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The aim of this thesis was to identify genes which are important in the initiation and/or progression of sporadic ovarian cancer. A series of ovarian teratomas and carcinomas was collected and three candidate tumour suppressor genes were analysed. The c-mos gene is an ovarian teratoma susceptibility gene in mice; its absence causes the growth of these tumours. Twenty human ovarian teratomas were collected and the coding region of the c-mos gene was analysed for somatic and germline mutations. No disease-causing alterations were found. Germline mutations of the BRCA2 gene predispose individuals to breast and ovarian cancer. To determine whether mutations in BRCA2 are important in sporadic ovarian cancer, loss of heterozygosity studies and mutation analysis were carried out on BRCA2 in a series of sporadic epithelial ovarian tumours. Loss of heterozygosity was identified in 46% of tumours. Four truncating mutations were identified in 50 tumours, two of which were germline and two somatic. All four mutations were accompanied by loss of the second allele. These results suggest that BRCA2 behaves as a tumour suppressor gene but that somatic mutations are not a common even in sporadic ovarian cancer. The insulin-like growth factor II receptor gene (IGF2R) on chromosome 6q is in a region which is frequently lost in ovarian tumours. A loss of heterozygosity analysis of the IGF2R locus in 38 informative epithelial ovarian tumours demonstrated 55% with loss of one allele. To perform mutation analysis of IGF2R, the technique of fluorescent chemical cleavage of mismatch was established in the laboratory and used to analyse IGF2R cDNA from 18 tumours. No disease-causing alterations were identified. Antibodies were used to examine the expression of the IGF2R protein through immunohistochemical studies of 53 ovarian tumour tissue sections. Seven tumours were identified in which epithelial tumour cells stained negatively for IGF2R. No correlation could be found between immunohistochemical results and LOH and mutation analysis results, suggesting that IGF2R is probably down-regulated at the level of transcription or translation in those samples which showed negative staining.
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Liu, Lu. "Oncogenes and tumour suppressor genes in human central nervous system tumours /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3532-7/.

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Discenza, Maria Teresa. "Regulation of expression of the Wilms' tumour 1 tumour suppressor gene." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=82855.

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Wilms' tumour, a pediatric kidney cancer that affects 1 in 10 000 children, is an excellent paradigm for studying the relationship between cancer and development. The Wilms' tumour suppressor 1 ( WT1) gene was identified through the study of hereditary cases of Wilms' tumour showing cytogenetic deletions at chromosome position 11p13. The WT1 gene encodes a zinc finger transcription factor necessary for the development of the genitourinary system. WT1 functions as an activator or a repressor, interacts with a number of different protein partners and regulates the expression of several genes important for cellular growth and differentiation. WT1 mRNA is present in tissues of mesodermal origin that undergo a mesenchymal to epithelial transition. Expression of WT1 is tightly regulated both temporally and spatially during development of the urogenital system.
We have identified a novel trans-acting factor, named complex D, which shows sequence specific binding to the WT1 promoter. By electrophoretic mobility shift assays (EMSA), we demonstrate that the transcription factor Sp1 binds the WT1 promoter at a site overlapping the complex D binding site. Molecular mass determination experiments and in situ UV crosslinking indicate that complex D is approximately 130 kDa and consists of at least two proteins. Transient transfection assays show that the integrity of the complex D binding site is necessary for maximal activation of a reporter gene, suggesting that complex D may function as an activator.
Similar to WT1, the ETS-domain transcription factor Pea3 is expressed in tissues where mesenchymal-epithelial interactions occur and both gene products are implicated in regulating the expression of genes necessary for the epithelialization of common organs. Transient transfection assays using WT1 promoter-reporter gene constructs identified a Pea3 responsive element in the WT1 promoter. Overexpression of Pea3 transactivates the WT1 promoter and the presence of the intact Pea3 responsive element is necessary for the transactivation. We demonstrate, by EMSA, the sequence specific binding of Pea3 to the responsive element.
WT1 and the paired box domain transcription factor Paired box 2 (Pax2) are expressed at the initial stages of metanephric kidney development and are critical for the initiation of nephrogenesis. We generated WT1/Pax2 compound heterozygous mutant mice to provide an in vivo model for studying the interplay between WT1 and Pax2 during nephrogenesis. WT1+/-/Pax2 1Neu/+ kidneys were 50% smaller that wild type kidneys and displayed a more severe underdevelopment of the medulla, renal calyces and renal pelvis compared to Pax21Neu/+ kidneys. We demonstrate that WT1 and Pax2 proteins physically interact in vitro and in vivo. Our data suggest that WT1 is a modifier of the Pax2 mutant phenotype and that both proteins may be implicated in a common pathway in the transcriptional network governing metanephric development.
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Judson, Hannah. "Investigation of candidate imprinted tumour suppressor genes." Thesis, University of Edinburgh, 2001. http://hdl.handle.net/1842/28316.

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Imprinting is an epigenetic phenomenon that silences one allele of a gene, so that expression in one or more cell types is exclusively monoallelic, and dependent on parental origin. Approaches used to identify novel imprinted genes rely on characteristic features such as the clustering of imprinted genes, or their association with differentially methylated CpG islands. An imprinted tumour suppressor gene involved in pathogenesis of neuroblastoma is believed to lie within chromosome 1p36. In this region, a search was initiated for imprinted genes in the vicinity of the imprinted gene TP73. The DFFB gene, encoding the apoptotic nuclease DNA fragmentation factor, was identified, and its intron-exon structure was elucidated. A pseudogene was also identified on chromosome 9. The tumour suppressor candidacy of DFFB was assessed through a comprehensive mutation screen of 42 neuroblastoma DNAs. No tumour-specific mutations were identified. Imprinting was then assessed by RT-PCR, which revealed biallelic expression of DFFB. It is unlikely that DFFB acts as a tumour suppressor in neuroblastoma. During a systematic screen, a differentially methylated CpG island, NV149, had been identified. In the present study, this locus was mapped to 6q24. The nearest gene was found to be the cell-cycle control gene, ZAC. Monallelic expression of ZAC from the paternal allele only was demonstrated in a range of fetal tissues. ZAC may possess a dual role in disease, such that upregulation by paternal duplication or paternal uniparental disomy of chromosome 6 results in transient neonatal diabetes mellitus (TNDM), whereas loss or down regulation of ZAC results in a loss of cell cycle control, and hence tumorigenesis. Through analysis of a panel of B cell lymphomas, evidence was found for hypermethylation of the NV149 CpG island, which may be one mechanism through which expression of ZAC is lost in tumours.
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Mancini, DiNardo Debora. "Methylation-mediated inactivation of tumour suppressor genes." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0021/NQ58149.pdf.

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Patel, Anjla Chhotubhai. "The role of fat tumour suppressor gene." Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.619808.

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Marcar, Lynnette Nongkynrih. "Inhibition of p53 tumour suppressor function by tumour associated MAGE-A proteins." Thesis, University of Dundee, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.521696.

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Burns, Alice Sin Ying Wai. "The role of the p53 tumour suppressor pathway in central primitive neuroectodermal tumours." Thesis, University of Newcastle Upon Tyne, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300357.

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Wang, Yemin. "Role of tumour suppressor ING3 in melanoma pathogenesis." Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/3850.

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The type II tumour suppressor ING3 has been shown to modulate transcription, cell cycle control, and apoptosis. To investigate the putative role of ING3 in melanoma development, we examined the expression of ING3 in 58 dysplastic nevi, 114 primary melanomas, and 50 metastatic melanomas with tissue microarray and immunohistochemistry. Overall ING3 was reduced in metastatic melanomas compared with dyslastic nevi and primary melanomas. Reduced nuclear ING3 staining also correlated with melanoma progression, increased cytoplasmic ING3 level, tumour location at sun-exposed sites, and a poorer disease-specific 5-year survival of patients with primary melanoma. Multivariate analysis revealed that nuclear ING3 staining can independently predict patient outcome in primary melanomas. In melanoma cells, ING3 expression was rapidly induced by UV irradiation. Using stable clones of melanoma cells overexpressing ING3, we showed that ING3 significantly promoted UV-induced apoptosis. Unlike its homologues ING1b and ING2, ING3-enhanced apoptosis upon UV irradiation was independent of functional p53. Furthermore, ING3 did not affect the expression of mitochondrial proteins but increased the cleavage of Bid and caspases. Moreover, ING3 upregulated Fas expression and ING3-mediated apoptosis was blocked by inhibiting caspase-8 or Fas activation. Knockdown of ING3 expression decreased UV-induced apoptosis remarkably, suggesting that ING3 plays a crucial role in cellular response to UV radiation. To explore how ING3 is deregulated in advanced melanomas, we examined ING3 expression in metastatic melanoma cells and found that ING3 was downregulated due to a rapid protein turnover in these cells. Further studies demonstrated that ING3 undergoes degradation via the ubiquitin-proteasome pathway. We also demonstrate that ING3 interacts with the SCF (Skp1/Cul1/Roc1/Skp2) E3 ligase complex. Knockdown of Cul1 or Skp2 significantly stabilized ING3 in melanoma cells. In addition, lysine residue 96 is essential for ING3 ubiquitination as its mutation to arginine completely abrogated ING3 turnover and enhanced ING3-stimulatd apoptosis upon UV irradiation. Taken together, ING3 is deregulated in melanomas as a result of both nucleus-to-cytoplasm shift and rapid degradation. The level of ING3 in the nucleus may be an important marker for human melanoma progression and prognosis. Restoration of ING3 expression significantly sensitizes melanoma cells to UV radiation through the activation of Fas/caspase-8 pathway.
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Marston, Nicola Jane. "Mutational analysis of the tumour suppressor protein, p53." Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387679.

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Books on the topic "Tumour suppressor"

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The oncogene and tumour suppressor gene factsbook. 2nd ed. San Diego, Calif: Academic Press, 1997.

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Phillips, Stewart Mark Anthony. The loss of tumour suppressor genes in prostate cancer. Birmingham: University of Birmingham, 1995.

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Lecane, Philip Sidney. A study of the p53 tumour suppressor gene in adenovirus transformed human cells. Birmingham: University of Birmingham, 1995.

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Tammemagi, Martin Carl. Tobacco smoking, p53 tumour suppressor gene alterations, and clinicopathologic features and prognosis in non-small cell lung cancer. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1998.

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El-Deiry, Wafik S. Tumor Suppressor Genes. New Jersey: Humana Press, 2003. http://dx.doi.org/10.1385/1592593283.

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El-Deiry, Wafik S. Tumor Suppressor Genes. New Jersey: Humana Press, 2003. http://dx.doi.org/10.1385/1592593291.

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S, El-Deiry Wafik, ed. Tumor suppressor genes. Totowa, N.J: Humana Press, 2003.

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Rangnekar, Vivek M., ed. Tumor Suppressor Par-4. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-80558-6.

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Rangnekar, Vivek M., ed. Tumor Suppressor Par-4. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-73572-2.

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Macdonald, F. Oncogenes and tumor suppressor genes. Oxford: Bios Scientific Publishers, 1991.

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Book chapters on the topic "Tumour suppressor"

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Lane, D. P., C. Midgley, and T. Hupp. "Tumour suppressor genes and molecular chaperones." In Molecular Chaperones, 113–17. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-2108-8_14.

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Piris, Miguel A., Juan C. Martinez, Margarita Sanchez-Beato, Juan F. Garcia, Carmen Bellas, Javier Menarguez, Raquel Villuendas, and Emilia Lloret. "Tumour Suppressor Genes in Hodgkin’s Disease." In Etiology of Hodgkin’s Disease, 209–22. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4613-0339-8_17.

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Hollywood, D. P., and N. R. Lemoine. "Growth Factors, Oncogenes and Tumour Suppressor Genes." In Assessment of Cell Proliferation in Clinical Practice, 27–43. Tokyo: Springer Japan, 1992. http://dx.doi.org/10.1007/978-4-431-68287-5_2.

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Evan, Gerard, Trevor Littlewood, David Hancock, Martin Bennett, Elizabeth Harrington, and Abdallah Fanidi. "C-MYC: Oncogene and Tumour Suppressor Gene." In Apoptosis, 63–84. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4757-9217-1_5.

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Hollywood, D. P., and N. R. Lemoine. "Growth Factors, Oncogenes and Tumour Suppressor Genes." In Assessment of Cell Proliferation in Clinical Practice, 27–43. London: Springer London, 1992. http://dx.doi.org/10.1007/978-1-4471-3190-8_2.

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Lefebvre, Karen J., Sarah Assadian, Wissal El-Assaad, and Jose G. Teodoro. "Regulation of Angiogenesis by Tumour Suppressor Pathways." In Experimental and Clinical Metastasis, 79–99. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-3685-0_8.

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Sherbet, G. V., and M. S. Lakshmi. "Tumour suppressor genes." In The Genetics of Cancer, 171–82. Elsevier, 1997. http://dx.doi.org/10.1016/b978-012639875-5/50013-3.

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Hesketh, Robin. "Tumour Suppressor Genes." In The Oncogene & Tumour Suppressor Gene Factsbook, 26–30. Elsevier, 1997. http://dx.doi.org/10.1016/b978-012344548-3/50005-4.

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Tavassoli, Mahvash, and Francesco Pezzella. "Oncogenesis and tumour suppression." In Oxford Textbook of Cancer Biology, edited by Francesco Pezzella, Mahvash Tavassoli, and David J. Kerr, 136–54. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198779452.003.0011.

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Two sets of genes are among the major driver of tumours, both malignant and benign: the oncogenes and the tumour suppressor genes. Oncogene refers to a gene that encodes for a protein (oncoprotein) in which excessive and unregulated activity can transform a normal cell into a cancer cell. As it is necessary for just one of the two gene copies to be abnormal, oncogenesis is defined as dominant. Tumour suppressor genes are known for their roles in inhibiting cell growth and have antitumour effects. According to the classic model, growth suppressor genes are recessive and therefore both copies have to be inactivated in order for an effect to be seen. Exception however occurs! Recently also non-coding mRNAs (i.e. an mRNA that is not translated into a protein) have been found to be able to induce oncogenic and suppressive effects. Finally, both some genes and some non-coding mRNA are able, in certain cellular contexts, to behave both as both an oncogenic and a suppressive factor.
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Hesketh, Robin. "Tumour Suppressor Genes Detected in Human Tumours." In The Oncogene & Tumour Suppressor Gene Factsbook, 83–85. Elsevier, 1997. http://dx.doi.org/10.1016/b978-012344548-3/50015-7.

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Conference papers on the topic "Tumour suppressor"

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Dawoud, M., M. Dawoud, D. Jones, K. Hodivala-Dilke, S. Dreger, C. Chelala, N. Asaad, and L. Jones. "Microenvironmental Changes in DCIS: Myoepithelial Cells Change from Tumour Suppressor to Tumour Promoter." 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-09-4161.

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Blagih, J., A. Hock, S. Mason, F. Zani, K. Blyth, and K. Vousden. "PO-403 The tumour suppressor P53 as a guardian of immune tolerance and suppression." 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-eacr25.914.

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Bazzichetto, C., F. Conciatori, I. Falcone, F. Cognetti, L. Ciuffreda, and M. Milella. "PO-293 Tumour/stroma interactions in colorectal cancer (CRC) models: role of the tumour suppressor PTEN." 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-eacr25.807.

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Orság, Petr, Hana Pivoňková, Medard Plucnara, Petra Horáková, and Miroslav Fojta. "Recognition of 7-deazapurine-substituted binding sites by tumour suppressor p53 protein." In XVth Symposium on Chemistry of Nucleic Acid Components. Prague: Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2011. http://dx.doi.org/10.1135/css201112427.

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Künzler, P., CA Seemayer, S. Kuchen, M. Neidhart, M. Pruschy, BA Michel, RE Gay, and S. Gay. "THU0104 In vivoandin vitroinvestigations of the tumour suppressor p16 in rheumatoid arthritis." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.981.

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Russell, RA, E. Dunlop, and A. Tee. "PO-102 Understanding the role of the tumour suppressor, FLCN, in renal tumorigenesis." 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-eacr25.143.

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Furlan, T., K. Sana, J. Guenther, AV Nguyen, and J. Troppmair. "PO-217 Tumour suppressor function of the oxidoreductase p66Shc in BRAFV600E-transformed cells." 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-eacr25.252.

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Janiszewska, J., M. Bodnar, M. Kostrzewska-Poczekaj, K. Bednarek, J. Paczkowska, R. Greenam, K. Szyfter, M. Wierzbicka, M. Jarmuz-Szymczak, and M. Giefing. "PO-380 Epigenetically regulated MAF is a new potential tumour suppressor gene in LSCC." 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-eacr25.408.

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Imoto, Issei, Shigeo Haruki, Ken-ich Kozaki, Takeshi Matsui, Hiroshi Kawachi, Shuhei Komatsu, Tomoki Muramatsu, Yutaka Shimada, Tatsuyuki Kawano, and Johji Inazawa. "Abstract 3071: Frequent silencing ofprotocadherin 17, a candidate tumour suppressor for esophageal squamous-cell carcinoma." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3071.

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Youness, R., R. Assal, M. Gad, and A. Abdel Motaal. "PO-352 Hijacking hepatocellular carcinoma (HCC) tumour progression through restoring TP53/miR-15a/miR-16 tumour suppressor axis by a novel quercetin glycoside." 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-eacr25.382.

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Reports on the topic "Tumour suppressor"

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Swafford, D. S., J. Tesfaigzi, and S. A. Belinsky. Expression of the p16{sup INK4a} tumor suppressor gene in rodent lung tumors. Office of Scientific and Technical Information (OSTI), December 1995. http://dx.doi.org/10.2172/381388.

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Shyam, E., and P. Reddy. Tumor Suppressors and Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2001. http://dx.doi.org/10.21236/ada403397.

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Shyam, E., and P. Reddy. Tumor Suppressors and Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2002. http://dx.doi.org/10.21236/ada412779.

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Zeremski, Marija. Use of Genetic Suppressor Elements to Identify Potential Breast Tumor Suppressor Genes. Fort Belvoir, VA: Defense Technical Information Center, October 1999. http://dx.doi.org/10.21236/ada384064.

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Freeman, Michael. SIRT3 is a Mitochondrial Tumor Suppressor and Genetic Loss Results in a Murine Model for ER/PR-Positive Mammary Tumors Connecting Metabolism and Carcinogenesis Mitochondrial Tumor Suppressor. Revision. Fort Belvoir, VA: Defense Technical Information Center, November 2013. http://dx.doi.org/10.21236/ada604003.

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Yu, Xiaochun. Characterize RAP80, a Potential Tumor Suppressor Gene. Fort Belvoir, VA: Defense Technical Information Center, April 2008. http://dx.doi.org/10.21236/ada485136.

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Yu, Xiaochun. Characterize RAP80, a Potential Tumor Suppressor Gene. Fort Belvoir, VA: Defense Technical Information Center, April 2009. http://dx.doi.org/10.21236/ada520785.

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Tomoda, Toshifumi, and Michael E. Barish. Novel Role of Merlin Tumor Suppressor in Autophagy and its Implication in Treating NF2-Associated Tumors. Fort Belvoir, VA: Defense Technical Information Center, April 2014. http://dx.doi.org/10.21236/ada608945.

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Tomoda, Toshifumi, Jr Jhung, Hirota Donald, and Yuki. Novel Role of Merlin Tumor Suppressor in Autophagy and its Implication in Treating NF2-Associated Tumors. Fort Belvoir, VA: Defense Technical Information Center, April 2012. http://dx.doi.org/10.21236/ada563285.

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Barish, Michael E., Toshifumi Tomoda, Akiko Sumitomo, and Yuki Hirota. Novel Role of Merlin Tumor Suppressor in Autophagy and its Implication in Treating NF2-Associated Tumors. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada592192.

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