Relevant bibliographies by topics / Tumour suppressor gene pten

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Academic literature on the topic 'Tumour suppressor gene pten'

Author: Grafiati
Published: 4 June 2021
Last updated: 5 February 2022

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Journal articles on the topic "Tumour suppressor gene pten"

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B??ni, R., A. O. Vortmeyer, G. Burg, G. Hofbauer, and Z. Zhuang. "The PTEN tumour suppressor gene and malignant melanoma." Melanoma Research 8, no. 4 (August 1998): 300–302. http://dx.doi.org/10.1097/00008390-199808000-00002.

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Kaufmann, J., G. Pronk, K. Giese, and A. Klippel. "Identification of novel effectors of invasive cell growth downstream of phosphoinositide 3-kinase." Biochemical Society Transactions 32, no. 2 (April 1, 2004): 355–59. http://dx.doi.org/10.1042/bst0320355.

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Conventional approaches to identifying cancer targets are complicated by the chromosomal instability of tumour cells, and typically result in a large number of differentially expressed candidate genes with uncertain disease relevance. Here we present a novel approach which aims to elucidate the molecular changes that are induced after loss of tumour suppressor function. Using gene silencing tools, we mimic the loss of tumour suppressor function to identify key regulators of tumour initiation and progression. Loss of function of the tumour suppressor PTEN (phosphatase and tensin homologue deleted on chromosome 10) correlates with increased invasive cell growth due to the resulting chronic activation of the PI 3-kinase (phosphoinositide 3-kinase) pathway. Induced activation of PI 3-kinase either by inhibiting PTEN expression or by using p110*, a constitutively active PI 3-kinase, increased signalling and the invasive growth potential of cells. Using this unbiased approach we have identified novel downstream effectors of PI 3-kinase/PTEN signalling that mediate the behaviour of cells with a hyperactive PI 3-kinase pathway. These molecules represent candidate targets for therapeutic intervention in patients with PTEN-deficient tumours.
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Pereiro, Patricia, Antonio Figueras, and Beatriz Novoa. "Zebrafish pten Genes Play Relevant but Distinct Roles in Antiviral Immunity." Vaccines 8, no. 2 (April 26, 2020): 199. http://dx.doi.org/10.3390/vaccines8020199.

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The PTEN (phosphatase and TENsin homolog on chromosome 10) gene encodes a bifunctional phosphatase that acts as a tumor suppressor. However, PTEN has been implicated in different immune processes, including autophagy, inflammation, regulation of natural killer (NK) cell cytolytic activity and type I interferon responses. Unlike mammals, zebrafish possess two pten genes (ptena and ptenb). This study explores the involvement of both zebrafish pten genes in antiviral defense. Although ptena−/− and ptenb−/− larvae were more susceptible to Spring viremia of carp virus (SVCV), the viral replication rate was lower in the mutant larvae than in the wild-type larvae. We observed that both mutant lines showed alterations in the transcription of numerous genes, including those related to the type I interferon (IFN) system, cytolytic activity, autophagy and inflammation, and some of these genes were regulated in opposite ways depending on which pten gene was mutated. Even though the lower replication rate of SVCV could be associated with impaired autophagy in the mutant lines, the higher mortality observed in the ptena−/− and ptenb−/− larvae does not seem to be associated with an uncontrolled inflammatory response.
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Marino, Silvia, Paul Krimpenfort, Carly Leung, Hetty A. G. M. van der Korput, Jan Trapman, Isabelle Camenisch, Anton Berns, and Sebastian Brandner. "PTEN is essential for cell migration but not for fate determination and tumourigenesis in the cerebellum." Development 129, no. 14 (July 15, 2002): 3513–22. http://dx.doi.org/10.1242/dev.129.14.3513.

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PTEN is a tumour suppressor gene involved in cell cycle control, apoptosis and mediation of adhesion and migration signalling. Germline mutations of PTEN in humans are associated with familial tumour syndromes, among them Cowden disease. Glioblastomas, highly malignant glial tumours of the central nervous system frequently show loss of PTEN. Recent reports have outlined some aspects of PTEN function in central nervous system development. Using a conditional gene disruption approach, we inactivated Pten in mice early during embryogenesis locally in a region specific fashion and later during postnatal development in a cell-specific manner, to study the role of PTEN in differentiation, migration and neoplastic transformation. We show that PTEN is required for the realisation of normal cerebellar architecture, for regulation of cell and organ size, and for proper neuronal and glial migration. However, PTEN is not required for cell differentiation and lack of PTEN is not sufficient to induce neoplastic transformation of neuronal or glial cells
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Islam, Mohammad Ariful, Yingjie Xu, Harshal Zope, Wuji Cao, Morteza Mahmoudi, Robert Langer, Philip W. Kantoff, Jinjun Shi, Bruce R. Zetter, and Omid C. Farokhzad. "Restoration of tumor suppression in vivo by systemic delivery of chemically-modified PTEN mRNA nanoparticles." Journal of Clinical Oncology 35, no. 15_suppl (May 20, 2017): 11582. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.11582.

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11582 Background: The onset and maintenance of cancer frequently involves gain of oncogenic function along with loss of tumor suppression. PTEN is a well-characterized tumor suppressor gene that is lost or mutated in many human cancers including ~50% of metastatic castration-resistant prostate cancer (mCRPC). Reintroduction of functional PTEN for mCRPC treatment has proven difficult. Methods: PTEN mRNA was synthesized by in vitro transcription method and modified with ARCA capping and enzymatic polyadenylation, and then substituted with Pseudo-UTP, 5’-Methyl-CTP. A robust self-assembly approach was employed to prepare PTEN mRNA nanoparticles (NPs) using cationic lipid-like compound G0-C14 and PLGA polymer coated with lipid-PEG shell. PTEN expression in tumors and PI3K-AKT pathway were confirmed by IHC and western blot, respectively. Apoptosis was checked by flow cytometry and Tunel assays. In vivo toxicity was studied by hematologic and histologic tests, and immune response. Results: We successfully restored PTEN mRNA to PTEN-null prostate cancer (PCa) cells via systemic delivery of mRNA NPs. These mRNA NPs are stable in serum, demonstrate minimal toxicity, and provide highly effective transfection in PCa cells (substantially higher HA-PTEN expression than plasmid PTEN transfection) and PCa xenograft tumors, leading to ~85% inhibition of tumor cell growth in vitro and in vivo. We also confirm mRNA NP-mediated systemic restoration of PTEN function in PTEN-null PCa and delineate its tumor suppression through inhibition of the PI3K-AKT pathway and enhancement of apoptosis. Conclusions: The work provides proof of principle for the systemic reintroduction of mRNA-based tumor suppressor genes to tumors in vivo. Because PTEN loss is frequent in late-stage PCa, this approach may have feasibility in this patient population. Considering the strong potential of mRNA therapy and the lack of systemic studies of in vivo mRNA transfection of tumors, this study sheds light on the useful application of NP-mediated mRNA delivery for validating tumor suppressors (e.g., PTEN) as a therapeutic target in cancer treatment where loss of a tumor suppressor contributes to the underlying genetic mechanism of cancer.
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Persad, Sujata, Armelle A.Troussard, Timothy R. McPhee, David J. Mulholland, and Shoukat Dedhar. "Tumor Suppressor Pten Inhibits Nuclear Accumulation of β-Catenin and T Cell/Lymphoid Enhancer Factor 1–Mediated Transcriptional Activation." Journal of Cell Biology 153, no. 6 (June 4, 2001): 1161–74. http://dx.doi.org/10.1083/jcb.153.6.1161.

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β-Catenin is a protein that plays a role in intercellular adhesion as well as in the regulation of gene expression. The latter role of β-catenin is associated with its oncogenic properties due to the loss of expression or inactivation of the tumor suppressor adenomatous polyposis coli (APC) or mutations in β-catenin itself. We now demonstrate that another tumor suppressor, PTEN, is also involved in the regulation of nuclear β-catenin accumulation and T cell factor (TCF) transcriptional activation in an APC-independent manner. We show that nuclear β-catenin expression is constitutively elevated in PTEN null cells and this elevated expression is reduced upon reexpression of PTEN. TCF promoter/luciferase reporter assays and gel mobility shift analysis demonstrate that PTEN also suppresses TCF transcriptional activity. Furthermore, the constitutively elevated expression of cyclin D1, a β-catenin/TCF–regulated gene, is also suppressed upon reexpression of PTEN. Mechanistically, PTEN increases the phosphorylation of β-catenin and enhances its rate of degradation. We define a pathway that involves mainly integrin-linked kinase and glycogen synthase kinase 3 in the PTEN-dependent regulation of β-catenin stability, nuclear β-catenin expression, and transcriptional activity. Our data indicate that β-catenin/TCF–mediated gene transcription is regulated by PTEN, and this may represent a key mechanism by which PTEN suppresses tumor progression.
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Ibnat, Nabilah, Rowshan Ara Islam, and Ezharul Hoque Chowdhury. "Inhibition of Breast Tumour Growth with Intravenously Administered PRKCA siRNA- and PTEN Tumour Suppressor Gene-Loaded Carbonate Apatite Nanoparticles." Applied Sciences 11, no. 17 (September 2, 2021): 8133. http://dx.doi.org/10.3390/app11178133.

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Gene therapy aims to silence an oncogene through RNA interference, or replace an abnormal tumour suppressor via gene augmentation. In this study, we intended RNA interference for PRKCA oncogene and gene augmentation for PTEN tumour suppressor with a view to reduce tumour growth in a mouse model of breast cancer. Inorganic carbonate apatite nanoparticles (CA NPs) were utilized to deliver the synthetic siRNA and the purified gene-carrying plasmid DNA both in vitro and in vivo. Effects of PRKCA siRNA- and PTEN plasmid-loaded NPs on viability of MCF-7, MDA-MB-231 and 4T1 breast cancer cells were assessed by MTT assay. The cell viability data in MCF-7 cell line demonstrated that combined delivery of PRKCA specific siRNA and PTEN plasmid with CA NPs had an additive effect to significantly decrease cellular growth compared to individual treatments. In addition, we observed a similar pattern of cumulative influence for combined treatment in triple negative MDA-MB-231 breast cancer cell line. Upon treatment with PRKCA siRNA+PTEN plasmid-loaded NPs, a remarkable decrease in the phosphorylated form of AKT protein of PI3K/AKT pathway was observed in Western blot, indicative of diminished proliferative signal. Moreover, in vivo study in MCF-7 xenograft breast cancer mouse model demonstrated that the rate of growth and final tumour volume were reduced significantly in the mouse group that received intravenous treatment of PRKCA siRNA+NPs, and PTEN plasmid+NPs. Our findings demonstrated that PRKCA siRNA and PTEN plasmid loaded into CA NPs attenuated breast tumour growth, suggesting their therapeutic potential in the treatment of breast cancer.
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de Sousa, Sílvia Ferreira, Marina Gonçalves Diniz, Josiane Alves França, Thaís dos Santos Fontes Pereira, Rennan Garcias Moreira, Jean Nunes dos Santos, Ricardo Santiago Gomez, and Carolina Cavalieri Gomes. "Cancer genes mutation profiling in calcifying epithelial odontogenic tumour." Journal of Clinical Pathology 71, no. 3 (November 10, 2017): 279–83. http://dx.doi.org/10.1136/jclinpath-2017-204813.

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AimsTo identify calcifying epithelial odontogenic tumour (CEOT) mutations in oncogenes and tumour suppressor genes.MethodsA panel of 50 genes commonly mutated in cancer was sequenced in CEOT by next-generation sequencing. Sanger sequencing was used to cover the region of the frameshift deletion identified in one sample.ResultsMissense single nucleotide variants (SNVs) with minor allele frequency (MAF) <1% were detected in PTEN, MET and JAK3. A frameshift deletion in CDKN2A occurred in association with a missense mutation in the same gene region, suggesting a second hit in the inactivation of this gene. APC, KDR, KIT, PIK3CA and TP53 missense SNVs were identified; however, these are common SNVs, showing MAF >1%.ConclusionCEOT harbours mutations in the tumour suppressor PTEN and CDKN2A and in the oncogenes JAK3 and MET. As these mutations occurred in only one case each, they are probably not driver mutations for these tumours.
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Hlobilkova, Alice, Jana Knillova, Jiri Bartek, Jiri Lukas, and Zdenek Kolar. "THE MECHANISM OF ACTION OF THE TUMOUR SUPPRESSOR GENE PTEN." Biomedical Papers 147, no. 1 (November 1, 2003): 19–25. http://dx.doi.org/10.5507/bp.2003.003.

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Inoue, Kazushi, Elizabeth A. Fry, and Pankaj Taneja. "Recent Progress in Mouse Models for Tumor Suppressor Genes and its Implications in Human Cancer." Clinical Medicine Insights: Oncology 7 (January 2013): CMO.S10358. http://dx.doi.org/10.4137/cmo.s10358.

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Gain-of-function mutations in oncogenes and loss-of-function mutations in tumor suppressor genes (TSG) lead to cancer. In most human cancers, these mutations occur in somatic tissues. However, hereditary forms of cancer exist for which individuals are heterozygous for a germline mutation in a TSG locus at birth. The second allele is frequently inactivated by gene deletion, point mutation, or promoter methylation in classical TSGs that meet Knudson's two-hit hypothesis. Conversely, the second allele remains as wild-type, even in tumors in which the gene is haplo-insufficient for tumor suppression. This article highlights the importance of PTEN, APC, and other tumor suppressors for counteracting aberrant PI3K, β-catenin, and other oncogenic signaling pathways. We discuss the use of gene-engineered mouse models (GEMM) of human cancer focusing on Pten and Apc knockout mice that recapitulate key genetic events involved in initiation and progression of human neoplasia. Finally, the therapeutic potential of targeting these tumor suppressor and oncogene signaling networks is discussed.
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Dissertations / Theses on the topic "Tumour suppressor gene pten"

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Vlachogiannis, G. "Investigation of unique dependencies of cells lacking the PTEN tumour suppressor gene." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1395122/.

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Over the past ten years significant effort has been put in the identification of pharmacological targets that facilitate the selective targeting of cancer cells. The concept of synthetic lethality in combination with RNA interference (RNAi) technology provides an attractive platform for the identification of such drug targets. With this in mind I designed, set up, and executed a large-scale siRNA screen aiming at identifying genes that exhibit a synthetic lethal relationship with loss of the PI3K/AKT signalling cascade negative regulator PTEN. A PTEN-isogenic cell system derived from the breast epithelial cell line MCF10A was employed in this study, and screened with a siRNA library against the “Druggable genome”. Putative hits exhibiting a potential synthetic lethal relationship with loss of PTEN were identified by differential Z-score analysis, and validated in a panel of breast cancer cell lines segregated based on their PTEN status. This analysis identified several PTEN-loss synthetic lethal candidate genes whose further evaluation may reveal new insights in the biology of PTEN null cancer cells. The functional mechanism underlying one of the identified PTEN-loss synthetic lethal putative hits (CYTH1/PSCD1) was investigated in detail. Knockdown of CYTH1 selectively induced apoptosis in the PTEN-/- MCF10A cells, and biochemical and genetic evidence supported a potential synthetic lethal relationship with PI3K/AKT pathway activation due to loss of PTEN. Although definite confirmation that CYTH1 was the sole target mediating the identified PTEN-loss synthetic lethal interaction was not obtained, further investigation on the exact nature of the described PTEN-loss synthetic lethal relationship may have the potential to uncover previously unknown vulnerabilities of PTEN-deficient cancer cells that could be pharmacologically exploited.
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Snaddon, Jennifer A. M. "Molecular analysis of the tumour suppressor genes MXI1 and PTEN in human squamous cell carcinoma of the head and neck." Thesis, Glasgow Caledonian University, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.340609.

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Crosland, Rachel. "Studies of the PTEN tumour suppressor in endometrial cancer." Thesis, Sheffield Hallam University, 2004. http://shura.shu.ac.uk/19515/.

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Somatic mutations in the PTEN gene (Phosphatase and Tensin Homologue Deleted on Chromosome Ten) have been found in many types of cancer, but most frequently in cancer of the endometrium. The PTEN gene encodes a D3 lipid phosphatase of the second messenger phosphatidylinositol 3,4,5-trisphosphate (PIP3), which activates protein kinase B/Akt. Constitutive activation of Akt has been found in cells that lack functional PTEN, thus by dephosphorylating PIP3, this enzyme modulates several cellular functions e.g. proliferation, differentiation and migration. The PTEN protein comprises a 403 amino acid, 55KDa protein which is present in the cytoplasm but has also been detected in the nucleus of some cells. The function of nuclear versus cytoplasmic PTEN has not yet been determined. Little is known about modulation of PTEN expression by molecules such as hormones and cytokines. It has been reported, however, that NGF, BDNF and vitamin D3 analogues can up-regulate PTEN. The steroid hormones oestrogen and progesterone have been proposed as mediators of PTEN transcription, since their expression in endometrium reflects the menstrual cycle. The role of TGF-beta1 in PTEN expression of PTEN in human cells has been also investigated, but the results are contradictory. Compounds which stimulate up-regulation of PTEN represent potential anti-tumour therapies and therefore merit investigation. To further investigate the role of PTEN in endometrial cancer the following approaches were taken. The effect of TGF-beta1 on two endometrial carcinoma cell lines, HEC-1B and Ishikawa were investigated. The cell lines were stimulated with TGF-beta1 in the presence or absence of serum, and changes in mRNA and protein levels of PTEN and other genes analysed by RT-PCR and Western blotting. The morphology, cell number and cell viability were also assessed. Modest up-regulation of PTEN mRNA was detected in both cell lines, but little change in protein levels was observed. In accordance with published data, TGF-beta1 suppressed the growth of, and changed the morphology of both cell lines. To study PTEN sub-cellular localisation, full-length human PTEN cDNA was used in RT-PCR to generate a 1.2Kb fragment which was cloned into a green fluorescent protein expression vector pEGFP-N1 to create pRC-2. Sequencing of pRC-2 confirmed the in-frame cloning of wild-type PTEN. Lipid-basedtransfection was used to transiently transfect HEC-1B, Ishikawa and Cos-7 cells. Strong perinuclear and cytoplasmic localisation was detected in these cell lines, and localisation to the endoplasmic reticulum was observed. Stimulation with TGF-beta and 17-beta-estradiol had no discernable effect on sub-cellular localisation of PTEN in either HEC-1B or Ishikawa cell lines. A mutational study was performed using a large repository of archival endometrial carcinomas and normal cervical controls. PCR was used to amplify PTEN exons 5 and 8 from extracted DNA and the fragments separated by single-strand conformation polymorphism (SSCP) analysis. A number of samples exhibiting bandshifts were detected in both exons.
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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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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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Zabkiewicz, Joanna. "In vivo modelling of tumour suppressor gene function." Thesis, Cardiff University, 2005. http://orca.cf.ac.uk/55388/.

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LKB1 has been implicated in a wide range of cellular functions and is associated with many potential substrates in in vitro studies, however the in vivo role of LKB1 remains unclear and its precise contribution to the prevention of intestinal tumours in the hereditary Peutz-Jegers syndrome is as yet uncharacterised. Conditional deletion of LKB1 in the murine small intestine resulted in significant disruption of intestinal homeostasis, particularly that of the differentiation process, suggesting LKB1 plays a key role in intestinal differentiation and it is loss of this function that predisposes to tumourigenesis
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Rohrig, A. E. "Role for tumour suppressor Merlin in gene expression." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1415770/.

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The tumour suppressor Merlin is mutated in the familial cancer syndrome Neurofibromatosis Type 2 (NF2) and in various sporadic tumours. Several lines of evidence show a role for Merlin in mediating contact-dependent inhibition of proliferation. Contact inhibition is essential for normal tissue homeostasis and its deregulation is a hallmark of cancer. Despite extensive efforts the mechanism underlying tumour suppression by Merlin remains elusive. A proteomics approach led to the identification of novel Merlin interacting proteins several of which are involved in gene expression, in particular transcription elongation, RNA processing and histone modifications, and are also deregulated in cancer. Among those are the RNA PolymeraseII-associated factor1 complex (Paf1C), CHD1, TAT-SF1 and spliceosome components. These interactions have been validated and mapped to Merlin’s FERM domain and loss-of-function Merlin mutations found in tumours invariably disrupt these interactions. The interaction of Merlin with the Paf1C is modulated by cell density and is required for Merlin’s tumour suppressor function. We find a remarkable case of tumour suppressor gene hypersensitivity in Merlin-deficient cells that correlates with Merlin’s ability to regulate gene expression. Using genome-wide expression profiling we identify a gene signature associated with growth arrest by Merlin expression that is consistent with Merlin’s role in mediating contact inhibition and suggests a role for Merlin in innate immunity and communication with the microenvironment. By integrating re-expression and knockdown gene signatures a core Merlin signature has been defined that correlates with NF2 mutational status and suggests differential drug sensitivities and potential therapeutic targets for treatment of NF2-related tumours. Using genome-wide occupancy analysis we identify a subset of genes where Merlin expression regulates association of the Paf1C with chromatin of coding regions. Some of these regulated genes are known target genes of YAP, the transcriptional co-activator of the Hippo tumour suppressor pathway. Although YAP expression rescues growth arrest by Merlin, Merlin can regulate expression independently of YAP. A model is proposed where Merlin functions parallel to YAP to regulate gene expression at the elongation level through the Paf1C.
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Woodward, Emma Roisin. "Molecular genetic studies of the VHL tumour suppressor gene." Thesis, University of Cambridge, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624312.

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Duarte, Antonio. "Regulation of gene expression by the Wilms' tumour suppressor, WT1." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.389178.

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Miranda, Alexandra de Sousa Montenegro. "Characterisation of LVI-1 (WDR76) as a candidate tumour suppressor gene." Thesis, University of Glasgow, 2006. http://theses.gla.ac.uk/4967/.

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The central aim of this study was to characterise the expression of the candidate tumour suppressor gene, LV/-J (lentivirus integration-I) and its products. The LVI-J gene (WDR76) was discovered as a target for disruption by proviral insertional mutagenesis in a case of pre-B cell lymphoma in a FIV infected cat {Beatty, 1998 5 lid; Beatty, 2002 7 lid}. As LV/-J is highly conserved, my work focused on the human and murine orthologues to take advantage of the superior resources available for these species. My work showed potentially important differences in expression of the human and mouse genes with respect to promoter use and length of 3' untranslated sequences. The murine gene is transcribed mainly from the distal PI promoter, which appears to be a bi-directional element shared with the adjacent MJapJ gene, while the human gene transcripts are derived exclusively from the proximal P2 promoter. Direct analysis by RT-PCR showed that the murine gene could also be expressed from the P2 promoter. These findings have significant implications for Lvi-l protein expression as the P2 transcripts are predicted to express larger proteins with a distinct N-terminal sequence. To characterise the LV/-J gene products, rabbit polyclonal antisera were raised to GST fusion proteins expressed in bacteria. Use of the murine anti-ml.vi-I antiserum in Western blotting identified a protein of the expected size (58 kDa) based on translation of the major mRNA species from the PI promoter. Immunofluorescence and confocal microscopy suggested that this protein is localised mainly in the cytoplasm. Although the function of LVI-I is unknown, its closest relative in the human genome is DDB2, a protein involved in repair of UV-induced DNA damage. Regulation of LVI-I expression was examined after UV irradiation, providing preliminary evidence of responses at transcriptional and post-transcriptional levels. Further leads were followed by analogy with the yeast orthologue of LVI-I, YDLI56W, but no evidence of a complex between LVI-I and MSH6 was found. In conclusion, while function of the LVI-I gene remains to be establishes, it provides the basis for future characterisation of this highly conserved and potentially important eukaryotic gene.
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Books on the topic "Tumour suppressor gene pten"

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

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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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Menon, Deepa U. Autism and Intellectual Disabilities. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0053.

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PTEN (phosphatase and tensin homologue) on chromosome 10q23.3 is a tumor suppressor gene that encodes for a dual specificity phosphatase that regulates the phosphatidylinositol 3- kinase pathway and has an important role in brain development by affecting neuronal survival, neurite outgrowth, synaptic plasticity, and learning memory. Germline mutations of the PTEN gene have been implicated in a group of related tumor syndromes with autosomal dominant inheritance and variable expression and include the Cowden syndrome, Bannayan-Riley-Ruvalcaba syndrome, Proteus syndrome, and Juvenile Polyposis syndrome. These syndromes are collectively called the PTEN hamartoma tumor syndromes (PHTS) because they have a predisposition to tumors and hamartomas. PTEN germ line mutations have also been recently linked to autism and macrocephaly and the prevalence of PTEN mutation in children with autism spectrum disorder, and macrocephaly is reported to range from 1.1% to 16.7%.
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The Oncogene & Tumour Suppressor Gene Factsbook. Elsevier, 1997. http://dx.doi.org/10.1016/b978-0-12-344548-3.x5000-6.

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Fabre, Aurélie. Immunostaining and DNA analysis of Wilms' tumour (WT1) suppressor gene in ductal carcinoma in situ (DCIS) of the breast: Thesis. 1998.

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Hastie, Nick, and Eve Miller-Hodges. WT1 and its disorders. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0329_update_001.

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Mutations in the Wilms tumour suppressor gene, WT1, are associated with Wilms tumour in childhood. However, in addition WT1 has a key role in renal development, emerging roles in podocyte function, and a potential role in tissue regeneration. An understanding of WT1 is of increasing importance to clinical practice. WT1 is a complex gene with multiple isoforms. It is crucial for normal embryonic development, especially kidney development, where it is necessary for mesenchymal-to-epithelial transition to form the nephron. WT1 mutations lead to abnormalities in renal and genitourinary development, causing diseases such as Denys–Drash syndrome and Frasier syndrome as well as Wilms tumour. Recently, WT1 mutations have been recognized as a significant cause of isolated steroid-resistant nephrotic syndrome in children and young adults, without other associated syndromic features. WT1 continues to be expressed in adult podocytes, where it acts as a transcriptional activator of many podocyte genes. However, the specific role of WT1 in adult podocyte function remains poorly understood.
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Connor, Thomas, and Patrick H. Maxwell. Von Hippel–Lindau disease. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0332.

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Von Hippel–Lindau (VHL) disease is a dominantly inherited familial cancer syndrome caused by germline mutations in the VHL tumour suppressor gene. The most frequent manifestations of VHL disease are retinal and central nervous system haemangioblastomas, clear cell renal cell carcinomas, and phaeochromocytomas. Genetic testing and active screening for clinical manifestations is now started in childhood and has greatly improved the prognosis for patients with VHL disease. The VHL protein plays a critical role in regulating the cellular response to changes in oxygen tension. Loss of VHL function results in constitutive activation of a range of angiogenic and metabolic pathways. New drug therapies have been developed that reverse some of the cellular consequences of VHL loss of function in kidney cancer.
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Book chapters on the topic "Tumour suppressor gene pten"

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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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Jaffrain-Rea, Marie-Lise, Liliya Rostomyan, and Albert Beckers. "Prognostic Factors: Molecular Pathway – Tumour Suppressor Gene (MEN1)." In Neuroendocrine Tumors in Real Life, 135–48. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-59024-0_8.

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Yehia, Lamis, Joanne Ngeow, and Charis Eng. "PTEN-Related Overgrowth Syndromes." In Overgrowth Syndromes, 163–86. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190944896.003.0009.

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Individuals carrying germline mutations in the tumor suppressor gene phosphatase and tensin homolog (PTEN) may present with diverse clinical phenotypes, grouped under the term of PTEN hamartoma tumor syndrome (PHTS). This chapter will focus on two PHTS conditions: Bannayan-Riley-Ruvalcaba syndrome and Cowden syndrome. The first condition is an autosomal dominant disorder characterized by macrocephaly, intestinal hamartomatous polyposis, vascular malformations, lipomas, hemangiomas, and genital freckling. Other features include developmental delay, hypotonia, and scoliosis. Cowden syndrome is also an autosomal dominant disorder, mainly characterized by multiple hamartomas and high risk of breast, thyroid, and other cancers. PTEN encodes the main inhibitor of the PI3K-AKT pathway, regulating cell growth and proliferation, and protein synthesis. Therefore, germline loss-of-function mutations in this gene lead to excessive growth, particularly affecting connective tissues. Detection of PTEN mutations is critical for clinical management and treatment strategies.
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Chen, Chun-Ming, Tsai-Ling Lu, Fang-Yi Su, and Li-Ru You. "Susceptibility of Epithelium to PTEN-Deficient Tumorigenesis." In Tumor Suppressor Genes. InTech, 2012. http://dx.doi.org/10.5772/26837.

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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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Bostjancic, Emanuela, and Damjan Glavac. "MicroRNAs and lncRNAs as Tumour Suppressors." In Future Aspects of Tumor Suppressor Gene. InTech, 2013. http://dx.doi.org/10.5772/54701.

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Hesketh, Robin. "Gene Therapy for Cancer." In The Oncogene & Tumour Suppressor Gene Factsbook, 61–69. Elsevier, 1997. http://dx.doi.org/10.1016/b978-012344548-3/50011-x.

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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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"Preface." In The Oncogene & Tumour Suppressor Gene Factsbook, VII. Elsevier, 1997. http://dx.doi.org/10.1016/b978-012344548-3/50000-5.

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"Abbreviations." In The Oncogene & Tumour Suppressor Gene Factsbook, IX—XI. Elsevier, 1997. http://dx.doi.org/10.1016/b978-012344548-3/50001-7.

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Conference papers on the topic "Tumour suppressor gene pten"

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Qureshi, Sabuhi. "Study of PTEN immunohistochemical expression in endometrial hyperplasia." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685337.

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Objective: The incidence of endometrial hyperplasia & carcinoma is increasing in developing nations. Newer techniques are being tried to recognise endometrial hyperplasia. One of these is tumor suppressor gene phosphatase & tensin homologue (PTEN). It is frequently inactivated i.e turned off in endometrial hyperplasia lesions. This is an early event in endometrial tumorigenesis that may occur in response to known endocrine risk factors & offers an informative immunohistochemical marker for premalignant disease. The present study was planned to study PTEN immunohistochemical expression in endometrial hyperplasia. Methods: Women of >40 years of age presenting with abnormal uterine bleeding in the OPD of OBGYN Department of KG Medical University underwent endometrial biopsy. The histopathology of the biopsy tissue was done in department of Pathology of KG Medical University. The cases of endometrial hyperplasia were studied for PTEN immunohistochemical expression. Results: 168 women of >40 years of age with abnormal uterine bleeding underwent endometrial biopsy. 50 women were diagnosed as endometrial hyperplasia. Of these, PTEN evaluation was done in 27 cases. Loss of PTEN expression was found in 11 cases (40.74%) of endometrial hyperplasia. Loss of PTEN expression was more in complex hyperplasia with atypia (66.66%) as compared to simple hyperplasia without atypia (29.4%). Conclusion: There is positive correlation between loss of PTEN expression and grade of morphological differentiation of hyperplasia.
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Benitez, Jorge A., Webster K. Cavenee, and Frank B. Furnari. "Abstract B05: The tumor suppressor gene pten regulates gene expression through histone H3.3 deposition and Daxx interaction." In Abstracts: AACR Special Conference on Chromatin and Epigenetics in Cancer - June 19-22, 2013; Atlanta, GA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.cec13-b05.

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Encina, Gonzalo, Karin Alvarez, Paulina Orellana, Ana María Wielandt, Cynthia Villarroel, Daniela Simian, Luis Contreras, Udo Kronberg, Francisco López, and Pilar Carvallo. "Abstract 2230: Gene mutations and deletions inactivates PTEN tumor suppressor in Chilean colon cancer patients." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2230.

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Kohnoh, Takashi, Naozumi Hashimoto, Kazuyoshi Imaizumi, Koji Sakamoto, Daisuke Aoyama, Tomomi Ogawa, and Yoshinori Hasegawa. "Gene Modulation Of Phosphorylation Sites In Tumor Suppressor Pten Inhibits? Hypoxia-Induced Phenotype Changes Through Epithelial-Mesenchymal Transition (EMT) In Lung Cancer." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3503.

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Aoyama, Daisuke, Naozumi Hashimoto, Kazuyoshi Imaizumi, Takashi Kohnoh, Koji Sakamoto, Tomomi Ogawa, and Yoshinori Hasegawa. "Inhibition Of TGF-Beta-Induced Phenotype Alterations Through Epithelial-Mesenchymal Transition (EMT) In Lung Cancer By Gene Modulation Of Phosphorylation Sites In Tumor Suppressor Pten." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3506.

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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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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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Stewart, David J., Maria I. Nunez, Jaroslav Jelinek, David Hong, Sanjay Gupta, C. Marcelo Aldaz, Jean-Pierre Issa, Razelle Kurzrock, and Ignacio I. Wistuba. "Abstract 2303: Decitabine impact on immunohistochemistry scores for tumor suppressor genes FHIT, WWOX, FUS1 and PTEN in human tumor samples." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2303.

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Morgan, Richard, Guy Simpson, Agnieszka Michael, and Hardev S. Pandha. "Abstract 1297: Engrailed-2 (EN2) represses the transcription of the CST6 tumour suppressor gene in prostate cancer." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1297.

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Chen, Muhan, Christopher P. Pratt, Martha E. Zeeman, Nicholaus Schultz, Barry S. Taylor, Audrey O'Neill, Mireia Castillo-Martin, et al. "Abstract 2405: Identification of PHLPP as a tumour suppressor reveals the role of pathway feedback compensation in PTEN-mutant prostate cancer progression." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2405.

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Reports on the topic "Tumour suppressor gene pten"

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Wu, Hong. The Function of PTEN Tumor Suppressor Gene in Prostate Cancer Development. Fort Belvoir, VA: Defense Technical Information Center, March 2001. http://dx.doi.org/10.21236/ada394962.

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Wu, Hong. The Function of PTEN Tumor Suppressor Gene in Prostate Cancer Development. Fort Belvoir, VA: Defense Technical Information Center, March 2002. http://dx.doi.org/10.21236/ada405326.

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