Relevant bibliographies by topics / Oncogenic transformations

Academic literature on the topic 'Oncogenic transformations'

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Published: 4 June 2021
Last updated: 19 February 2023

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Journal articles on the topic "Oncogenic transformations"

1

Paterno, G. D., L. L. Gillespie, M. S. Dixon, J. M. Slack, and J. K. Heath. "Mesoderm-inducing properties of INT-2 and kFGF: two oncogene-encoded growth factors related to FGF." Development 106, no. 1 (May 1, 1989): 79–83. http://dx.doi.org/10.1242/dev.106.1.79.

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Many theories of neoplasia suggest that oncogenic transformations result from aberrations in the control mechanisms which normally regulate growth and differentiation during embryonic development. It has recently become clear that many proto-oncogenes are differentially expressed during embryonic development and may thus be important embryonic regulatory molecules. We report here that the products of two transforming oncogenes int-2 and hst/ks (now called kfgf) can, with different potencies, induce mesoderm formation in isolated Xenopus laevis animal pole explants and stimulate DNA synthesis in mammalian fibroblasts. The results suggest that these proteins may function as mesoderm inducers in mammalian embryogenesis and that similar receptor/signalling pathways may be utilized for developmental and oncogenic processes. Finally, we have shown that the Xenopus assay system used in this study provides a powerful screen for protein factors that are active in development.
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Ito, Reina E., Chitose Oneyama, and Kazuhiro Aoki. "Oncogenic mutation or overexpression of oncogenic KRAS or BRAF is not sufficient to confer oncogene addiction." PLOS ONE 16, no. 4 (April 1, 2021): e0249388. http://dx.doi.org/10.1371/journal.pone.0249388.

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Oncogene addiction is a cellular property by which cancer cells become highly dependent on the expression of oncogenes for their survival. Oncogene addiction can be exploited to design molecularly targeted drugs that kill only cancer cells by inhibiting the specific oncogenes. Genes and cell lines exhibiting oncogene addiction, as well as the mechanisms by which cell death is induced when addicted oncogenes are suppressed, have been extensively studied. However, it is still not fully understood how oncogene addiction is acquired in cancer cells. Here, we take a synthetic biology approach to investigate whether oncogenic mutation or oncogene expression suffices to confer the property of oncogene addiction to cancer cells. We employed human mammary epithelium-derived MCF-10A cells expressing the oncogenic KRAS or BRAF. MCF-10A cells harboring an oncogenic mutation in a single-allele of KRAS or BRAF showed weak transformation activity, but no characteristics of oncogene addiction. MCF-10A cells overexpressing oncogenic KRAS demonstrated the transformation activity, but MCF-10A cells overexpressing oncogenic BRAF did not. Neither cell line exhibited any oncogene addiction properties. These results indicate that the introduction of oncogenic mutation or the overexpression of oncogenes is not sufficient for cells to acquire oncogene addiction, and that oncogene addiction is not associated with transformation activity.
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Calabrese, Fiorella, Federica Pezzuto, Francesca Lunardi, Francesco Fortarezza, Sofia-Eleni Tzorakoleftheraki, Maria Vittoria Resi, Mariaenrica Tiné, Giulia Pasello, and Paul Hofman. "Morphologic-Molecular Transformation of Oncogene Addicted Non-Small Cell Lung Cancer." International Journal of Molecular Sciences 23, no. 8 (April 9, 2022): 4164. http://dx.doi.org/10.3390/ijms23084164.

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Patients with non-small cell lung cancer, especially adenocarcinomas, harbour at least one oncogenic driver mutation that can potentially be a target for therapy. Treatments of these oncogene-addicted tumours, such as the use of tyrosine kinase inhibitors (TKIs) of mutated epidermal growth factor receptor, have dramatically improved the outcome of patients. However, some patients may acquire resistance to treatment early on after starting a targeted therapy. Transformations to other histotypes—small cell lung carcinoma, large cell neuroendocrine carcinoma, squamous cell carcinoma, and sarcomatoid carcinoma—have been increasingly recognised as important mechanisms of resistance and are increasingly becoming a topic of interest for all specialists involved in the diagnosis, management, and care of these patients. This article, after examining the most used TKI agents and their main biological activities, discusses histological and molecular transformations with an up-to-date review of all previous cases published in the field. Liquid biopsy and future research directions are also briefly discussed to offer the reader a complete and up-to-date overview of the topic.
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Clark, SS, Y. Liang, CK Reedstrom, and SQ Wu. "Nonrandom cytogenetic changes accompany malignant progression in clonal lines abelson virus-infected lymphocytes." Blood 84, no. 12 (December 15, 1994): 4301–9. http://dx.doi.org/10.1182/blood.v84.12.4301.bloodjournal84124301.

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Initially, lymphoid cells transformed by v-abl or BCR/ABL oncogenes are poorly oncogenic but progress to full transformation over time. Although expression of the oncogene is necessary to initiate and maintain transformation, other molecular mechanisms are thought to be required for full transformation. To determine whether tumor progression in ABL oncogene-transformed lymphoid cells has a genetic basis, we examined whether progression of the malignant phenotype of transformed clones correlates with particular cytogenetic abnormalities. A modified in vitro bone marrow transformation model was used to obtain clonal Abelson murine leukemia virus-transformed B lymphoid cells that were poorly oncogenic. Multiple subclones were then derived from each clone and maintained over a marrow-derived stromal cell line for several weeks. Over time, clonally related Abelson murine leukemia virus-transformed subclones progressed asynchronously to full transformation. The data show that tumor progression can occur in the absence of detectable cytogenetic changes but, more importantly, that certain cytogenetic abnormalities appear reproducibly in highly malignant subclones. Therefore, three independent subclones showed deletion in a common region of chromosome 13. Other highly malignant cells carried a common breakpoint in the X chromosome, and, finally, two subclones carried an additional chromosome 5. These results are consistent with the hypothesis that ABL oncogenes are sufficient for the initial transformation of cells but that additional genetic events can drive oncogenic progression. These observations further suggest that diverse genetic mechanisms may be able to drive tumor progression in cells transformed with ABL oncogenes.
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Alkharam, A. S., and D. E. Watt. "Risk Scaling Factors from Inactivation to Chromosome Aberrations, Mutations and Oncogenic Transformations in Mammalian Cells." Radiation Protection Dosimetry 70, no. 1 (April 1, 1997): 537–40. http://dx.doi.org/10.1093/oxfordjournals.rpd.a032012.

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Julien, Sylvie, Mirjana Radosavljevic, Nathalie Labouret, Sophie Camilleri-Broet, Frederic Davi, Martine Raphael, Thierry Martin, and Jean-Louis Pasquali. "AIDS Primary Central Nervous System Lymphoma: Molecular Analysis of the Expressed VH Genes and Possible Implications for Lymphomagenesis." Journal of Immunology 162, no. 3 (February 1, 1999): 1551–58. http://dx.doi.org/10.4049/jimmunol.162.3.1551.

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Abstract AIDS-associated primary central nervous system lymphomas are late events that have an extremely poor prognosis. Despite different hypotheses, the brain localization of these B cell lymphomas remains an enigma. To better define the cell origin of the lymphomas and the possible role of the B cell receptor (BCR) in the brain localization and/or in the oncogenic transformation, we analyzed the V region genes of the Ig heavy chain expressed by lymphoma cells in five randomly selected patients. After amplifying the rearranged VHDJH DNA by PCR, cloning, and sequencing of the amplified products, we observed that: 1) of the five lymphomas analyzed, four were clearly monoclonal; 2) there was no preferential use of one peculiar VH family or one peculiar segment of gene; 3) the mutation analysis showed that an Ag-driven process occurred in at least two cases, probably before the oncogenic event; and 4) there was no intraclonal variability, suggesting that the hypermutation mechanism is no longer efficient in these lymphoma B cells. Taken together, our results suggest that distinct Ags could be recognized by the BCR of the lymphoma cells in different patients and that, if the Ags are responsible for the brain localization of these B cells bearing mutated BCR, other factors must be involved in B cell transformations in primary central nervous system lymphoma.
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de Oliveira, Guilherme A. P., Elaine C. Petronilho, Murilo M. Pedrote, Mayra A. Marques, Tuane C. R. G. Vieira, Elio A. Cino, and Jerson L. Silva. "The Status of p53 Oligomeric and Aggregation States in Cancer." Biomolecules 10, no. 4 (April 4, 2020): 548. http://dx.doi.org/10.3390/biom10040548.

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Despite being referred to as the guardian of the genome, when impacted by mutations, p53 can lose its protective functions and become a renegade. The malignant transformation of p53 occurs on multiple levels, such as altered DNA binding properties, acquisition of novel cellular partners, or associating into different oligomeric states. The consequences of these transformations can be catastrophic. Ongoing studies have implicated different oligomeric p53 species as having a central role in cancer biology; however, the correlation between p53 oligomerization status and oncogenic activities in cancer progression remains an open conundrum. In this review, we summarize the roles of different p53 oligomeric states in cancer and discuss potential research directions for overcoming aberrant p53 function associated with them. We address how misfolding and prion-like amyloid aggregation of p53 seem to play a crucial role in cancer development. The misfolded and aggregated states of mutant p53 are prospective targets for the development of novel therapeutic strategies against tumoral diseases.
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Neitzel, Carina, Philipp Demuth, Simon Wittmann, and Jörg Fahrer. "Targeting Altered Energy Metabolism in Colorectal Cancer: Oncogenic Reprogramming, the Central Role of the TCA Cycle and Therapeutic Opportunities." Cancers 12, no. 7 (June 29, 2020): 1731. http://dx.doi.org/10.3390/cancers12071731.

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Colorectal cancer (CRC) is among the most frequent cancer entities worldwide. Multiple factors are causally associated with CRC development, such as genetic and epigenetic alterations, inflammatory bowel disease, lifestyle and dietary factors. During malignant transformation, the cellular energy metabolism is reprogrammed in order to promote cancer cell growth and proliferation. In this review, we first describe the main alterations of the energy metabolism found in CRC, revealing the critical impact of oncogenic signaling and driver mutations in key metabolic enzymes. Then, the central role of mitochondria and the tricarboxylic acid (TCA) cycle in this process is highlighted, also considering the metabolic crosstalk between tumor and stromal cells in the tumor microenvironment. The identified cancer-specific metabolic transformations provided new therapeutic targets for the development of small molecule inhibitors. Promising agents are in clinical trials and are directed against enzymes of the TCA cycle, including isocitrate dehydrogenase, pyruvate dehydrogenase kinase, pyruvate dehydrogenase complex (PDC) and α-ketoglutarate dehydrogenase (KGDH). Finally, we focus on the α-lipoic acid derivative CPI-613, an inhibitor of both PDC and KGDH, and delineate its anti-tumor effects for targeted therapy.
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Shrivastava, Richa, and Smrati Bhadauria. "Role of Growth Factor Signaling in Cancer." Defence Life Science Journal 1, no. 1 (June 1, 2016): 34. http://dx.doi.org/10.14429/dlsj.1.10059.

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<div class="page" title="Page 1"><div class="layoutArea"><div class="column"><div class="page" title="Page 1"><div class="layoutArea"><div class="column"><p><span>Growth factors may be defined as any group of protein that stimulate the growth of specific tissues and play an important role in promoting cellular differentiation and cellular division. Growth factors impart one of the important hallmark of cancer i.e sustaining proliferative signaling. They may act through paracrine, autocrine and endocrine signaling to effect growth and proliferation of cancer cells. They may act through various signaling cascades like MAPK, PI3K/AKT, JAK/STAT etc to activate their downstream mediates affecting various pathlogical and physiological functions. Abrupt signaling patterns of growth factors can induce oncogenic transformations. An enhanced understanding of these pathways can help targeting neoplastic transformation at an early stage. This review summarizes various mechanisms for targeted therapeutics against growth factor in cancer and their future prospective.</span></p></div></div></div></div></div></div><p> </p>
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Aggarwal, Vaishali, Hardeep Singh Tuli, Jagjit Kaur, Diwakar Aggarwal, Gaurav Parashar, Nidarshana Chaturvedi Parashar, Samruddhi Kulkarni, et al. "Garcinol Exhibits Anti-Neoplastic Effects by Targeting Diverse Oncogenic Factors in Tumor Cells." Biomedicines 8, no. 5 (April 30, 2020): 103. http://dx.doi.org/10.3390/biomedicines8050103.

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Garcinol, a polyisoprenylated benzophenone, is the medicinal component obtained from fruits and leaves of Garcinia indica (G. indica) and has traditionally been extensively used for its antioxidant and anti-inflammatory properties. In addition, it has been also been experimentally illustrated to elicit anti-cancer properties. Several in vitro and in vivo studies have illustrated the potential therapeutic efficiency of garcinol in management of different malignancies. It mainly acts as an inhibitor of cellular processes via regulation of transcription factors NF-κB and JAK/STAT3 in tumor cells and have been demonstrated to effectively inhibit growth of malignant cell population. Numerous studies have highlighted the anti-neoplastic potential of garcinol in different oncological transformations including colon cancer, breast cancer, prostate cancer, head and neck cancer, hepatocellular carcinoma, etc. However, use of garcinol is still in its pre-clinical stage and this is mainly attributed to the limitations of conclusive evaluation of pharmacological parameters. This necessitates evaluation of garcinol pharmacokinetics to precisely identify an appropriate dose and route of administration, tolerability, and potency under physiological conditions along with characterization of a therapeutic index. Hence, the research is presently ongoing in the dimension of exploring the precise metabolic mechanism of garcinol. Despite various lacunae, garcinol has presented with promising anti-cancer effects. Hence, this review is motivated by the constantly emerging and promising positive anti-cancerous effects of garcinol. This review is the first effort to summarize the mechanism of action of garcinol in modulation of anti-cancer effect via regulation of different cellular processes.
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Dissertations / Theses on the topic "Oncogenic transformations"

1

Svingen, Terje, and n/a. "Hox Transcription Factors: Their Involvement in Human Cancer Cells and In Vitro Functional Specificity." Griffith University. School of Biomolecular and Biomedical Science, 2005. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20050830.135356.

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Hox genes are regulatory genes encoding small proteins containing a highly conserved 61-amino acid motif, the homeodomain, that enables Hox proteins to bind to DNA at specifically recognised binding sites and transcriptionally activate their target genes. In mammalian species there are 39 Hox genes and they are structural and functional homologs of the Drosophila homeotic complex (Horn-C). During embryogenesis and early development the Hox genes are expressed in a spatiotemporal fashion, where they operate as master transcriptional regulators. Hox genes are further expressed in fully differentiated adult cells, potentially in a tissue-specific manner involving maintenance of the normal phenotype. In selected oncogenic transformations, dysregulated Hox gene expression has been observed, indicating an involvement of these transcriptional regulators in carcinogenesis and metastasis. Utilising quantitative real-time PCR assays, these studies investigated the expression patterns of 20 Hox genes and two wellcharacterised Hox cofactors (Pbx and Meis) in malignant and non-malignant human breast and skin cancer cells. Dysregulated Hox expression was observed for all malignancies tested, of which some misexpressed Hox genes seemed random, whereas other Hox transcripts showed altered levels potentially corresponding with the invasive capacity of the cells. Also, the Hox cofactors Pbx and Meis showed no marked changes in expression levels from the non-malignant to the malignant phenotypes, indicating that it is dysregulated Hox gene expression rather than dysregulated gene expression of Hox cofactors that potentially commit the cell to redifferentiate and undergo oncogenic transformation. Although the Hox proteins are known to be key transcriptional regulators of development, the mechanisms by which they gain their in vivo functional specificity is still largely unknown. They all show strikingly similar transcriptional specificity in vitro, yet show unique specificity in their in vivo environment. This paradox has been the subject of intense scrutiny, however very few direct Hox target genes have been identified, making it a difficult task to decipher the exact manner in which Hox proteins exert their functional potential. Therefore, the studies presented herein were aimed at identifying further Hox target genes in the human system. Utilising differential display approaches, several potential downstream target genes were isolated. Substantiated with real-time PCR assays, one of these potential targets was selected as a likely direct Hox gene target, and as such subjected to further studies. By the combination of bioinformatic analyses, transfection protocols and luciferase assays, a gene encoding the SR-related protein SRrpl3O was shown to be trans-activated in vitro by HOXD4 via a putative Hox binding element within its promoter region. This is the first reported link between Hox transcription factors and the SR and SR-related family of pre-mRNA splicing proteins, offering a new and exciting insight into the complex nature of Hox functional specificity. Finally, this thesis also puts forward new ideas regarding how the Hox proteins gain their transcriptional and functional specificity. Utilising bioinformatic tools in conjunction with performing an extensive review of the disparate catalogue of Hox-related research reports, work herein offers the first comprehensive analysis of the mammalian Hox gene targets in relation to their promoter structures, as well as with respect to the expanded Hox DNA-binding elements. This work reports that identified Hox targets generally contain TATA-less core promoters, many of which have several GC-box elements. The Hox binding elements show no apparent preference regarding their location relative to the transcription start site (TSS), as they are found both upstream and downstream of the TSS, as well as being located close to proximal core promoter elements for some genes and at more distant positions in other gene promoters. Finally, the core Hox binding element TAAT/ATTA contains only part of the necessary recognition sequence involved in Hox-DNA binding, and the notion that flanking base pairs dictate trans-regulatory potential is further explored with the hypothesis that the immediate 3' base pair dictates an activator/repressor-switch of the Hox trans-regulatory effect.
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Svingen, Terje. "Hox Transcription Factors: Their Involvement in Human Cancer Cells and In Vitro Functional Specificity." Thesis, Griffith University, 2005. http://hdl.handle.net/10072/365774.

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Hox genes are regulatory genes encoding small proteins containing a highly conserved 61-amino acid motif, the homeodomain, that enables Hox proteins to bind to DNA at specifically recognised binding sites and transcriptionally activate their target genes. In mammalian species there are 39 Hox genes and they are structural and functional homologs of the Drosophila homeotic complex (Horn-C). During embryogenesis and early development the Hox genes are expressed in a spatiotemporal fashion, where they operate as master transcriptional regulators. Hox genes are further expressed in fully differentiated adult cells, potentially in a tissue-specific manner involving maintenance of the normal phenotype. In selected oncogenic transformations, dysregulated Hox gene expression has been observed, indicating an involvement of these transcriptional regulators in carcinogenesis and metastasis. Utilising quantitative real-time PCR assays, these studies investigated the expression patterns of 20 Hox genes and two wellcharacterised Hox cofactors (Pbx and Meis) in malignant and non-malignant human breast and skin cancer cells. Dysregulated Hox expression was observed for all malignancies tested, of which some misexpressed Hox genes seemed random, whereas other Hox transcripts showed altered levels potentially corresponding with the invasive capacity of the cells. Also, the Hox cofactors Pbx and Meis showed no marked changes in expression levels from the non-malignant to the malignant phenotypes, indicating that it is dysregulated Hox gene expression rather than dysregulated gene expression of Hox cofactors that potentially commit the cell to redifferentiate and undergo oncogenic transformation. Although the Hox proteins are known to be key transcriptional regulators of development, the mechanisms by which they gain their in vivo functional specificity is still largely unknown. They all show strikingly similar transcriptional specificity in vitro, yet show unique specificity in their in vivo environment. This paradox has been the subject of intense scrutiny, however very few direct Hox target genes have been identified, making it a difficult task to decipher the exact manner in which Hox proteins exert their functional potential. Therefore, the studies presented herein were aimed at identifying further Hox target genes in the human system. Utilising differential display approaches, several potential downstream target genes were isolated. Substantiated with real-time PCR assays, one of these potential targets was selected as a likely direct Hox gene target, and as such subjected to further studies. By the combination of bioinformatic analyses, transfection protocols and luciferase assays, a gene encoding the SR-related protein SRrpl3O was shown to be trans-activated in vitro by HOXD4 via a putative Hox binding element within its promoter region. This is the first reported link between Hox transcription factors and the SR and SR-related family of pre-mRNA splicing proteins, offering a new and exciting insight into the complex nature of Hox functional specificity. Finally, this thesis also puts forward new ideas regarding how the Hox proteins gain their transcriptional and functional specificity. Utilising bioinformatic tools in conjunction with performing an extensive review of the disparate catalogue of Hox-related research reports, work herein offers the first comprehensive analysis of the mammalian Hox gene targets in relation to their promoter structures, as well as with respect to the expanded Hox DNA-binding elements. This work reports that identified Hox targets generally contain TATA-less core promoters, many of which have several GC-box elements. The Hox binding elements show no apparent preference regarding their location relative to the transcription start site (TSS), as they are found both upstream and downstream of the TSS, as well as being located close to proximal core promoter elements for some genes and at more distant positions in other gene promoters. Finally, the core Hox binding element TAAT/ATTA contains only part of the necessary recognition sequence involved in Hox-DNA binding, and the notion that flanking base pairs dictate trans-regulatory potential is further explored with the hypothesis that the immediate 3' base pair dictates an activator/repressor-switch of the Hox trans-regulatory effect.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Physical Sciences
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CALVO, FERNANDA B. "Construcao e caracterizacao in vitro de um vetor retroviral bicistronico codificando endostatina e interleucina-2 para utilizacao em terapia genica." reponame:Repositório Institucional do IPEN, 2009. http://repositorio.ipen.br:8080/xmlui/handle/123456789/9487.

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Dissertacao (Mestrado)
IPEN/D
Instituto de Pesquisas Energeticas e Nucleares - IPEN-CNEN/SP
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Lehmann, Kerstin Elisabeth. "Regulation of epithelial cell transformation and survival by Raf activation." Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248242.

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Pierro, Cristina. "Remodelling of Ca2+ signalling mechanisms during K-RAS-driven oncogenic transformation." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610740.

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Ye, Fang. "PPARγ and Smad2 Mediate Ski Induced Energy Metabolism Shift and Oncogenic Transformation." Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1280930750.

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Kabbout, Mohamed Nazih. "ETS1 AND ETS2 ROLE IN RAS ONCOGENIC TRANSFORMATION IN MOUSE EMBRYONIC FIBROBLASTS." The Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1275408102.

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Shima, Yasuko. "In vitro transformation of mesenchymal stem cells by oncogenic H-ras[Val12]." Kyoto University, 2007. http://hdl.handle.net/2433/135685.

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Sumner, Evan T. "Characterizing the Oncogenic Properties of C-terminal Binding Protein." VCU Scholars Compass, 2016. http://scholarscompass.vcu.edu/etd/4153.

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The paralogous C-terminal binding proteins (CtBP) 1 and 2 are evolutionarily conserved transcriptional coregulators that target and disrupt the expression of several genes essential for multiple cellular processes critical to regulating tumor formation. CtBP’s ability to govern the transcription of genes necessary for apoptosis, tumor suppression, invasion/migration and EMT gives rise to its oncogenic activities. Both isoforms of CtBP are found to be overexpressed in cancers including colorectal, pancreatic, ovarian, and breast, with higher levels correlating to lower overall median survival. Although multiple lines of evidence suggest CtBP plays a role in tumorigenesis, it has never been formally characterized as an oncogene. For this reason, the goal of this dissertation was to design a set of experiments to determine the transforming ability of CtBP2 in vitro using both murine and human fibroblast and in vivo using the Apcmin/+ mouse model of cancer. Specifically, we demonstrate that overexpression of CtBP2 alone can drive transformation of NIH3T3 cells leading to loss of contact inhibition, increased x invasion/migration, and anchorage independent growth. In addition, CtBP2 was found to cooperate with the large T-antigen (LT) component of the simian virus 40 (SV40) to lead to transformation of murine embryonic fibroblasts (MEFs) and with both LT and small T-antigen (ST) to induce migration/invasion and anchorage-independent growth in BJ human foreskin fibroblasts. To confirm the role of Ctbp2 in a mouse tumor model with Ctbp overexpression, we bred Apcmin/+ mice to Ctbp2 heterozygous (Ctbp2+/-) mice, which otherwise live normal lifespans. CtBP is a known target of the APC tumor suppressor and is thus stabilized in APC mutated human colon cancers and is found in high levels in Apcmin/+ polyps. Remarkably, removing an allele of Ctbp2 doubled the median survival of Apcmin/+ mice (P <0.001) and reduced polyp formation to near undetectable levels. These data suggest the importance of CtBP2 in driving cellular transformation and identify it as a potential target for prevention or therapy in APC mutant backgrounds.
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Webster, Marc A. "Mechanisms of polyomavirus transformation of the mouse mammary gland /." *McMaster only, 1996.

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Books on the topic "Oncogenic transformations"

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Tatchell, Kelly. Selected abstracts on the ras oncogene family and cell transformation. Bethesda, MD: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, 1986.

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Gregory, Bock, Marsh Joan, and Symposium on Proto-oncogenes in Cell Development (1989 : Ciba Foundation), eds. Proto-oncogenes in cell development. Chichester: Wiley, 1990.

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1941-, Bradshaw Ralph A., and Prentis Steve, eds. Oncogenes and growth factors. Amsterdam: Elsevier Science, 1989.

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Oncogenes. Boca Raton, Fla: CRC Press, 1986.

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Oncogenes. 2nd ed. Boca Raton, Fla: CRC Press, 1989.

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E, Milo George, Casto Bruce C, and Shuler Charles Fredric 1953-, eds. Transformation of human epithelial cells: Molecular and oncogenetic mechanisms. Boca Raton: CRC Press, 1992.

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Ross, D. W. Introduction to oncogenes and molecular cancer medicine. New York: Springer, 1998.

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A, Sharp Phillip, and Bristol-Myers Squibb Symposium on Cancer Research (14th : 1990 : Massachusetts Institute of Technology), eds. Nuclear processes and oncogenes. San Diego: Academic Press, 1992.

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1951-, Cavennee Webster, Hastie Nicholas, Stanbridge Eric J, and Banbury Center, eds. Recessive oncogenes and tumor suppression. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory Press, 1989.

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Hormones, growth factors, and oncogenes. Boca Raton, Fla: CRC Press, 1987.

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Book chapters on the topic "Oncogenic transformations"

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Hynes, Richard O. "Oncogenic Transformation." In Fibronectins, 301–34. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3264-3_12.

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Hunter, Tony. "The Functions of Oncogene Products." In Cell Transformation, 79–95. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-5009-5_4.

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Brockhausen, Inka, and William Kuhns. "Glycosylation in Cancer and Oncogenic Transformation." In Glycoproteins and Human Disease, 157–73. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-662-21960-7_19.

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Jenuwein, Thomas, and Rolf Müller. "The fos Oncogene and Transformation." In Oncogenes and Growth Control, 278–83. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-73325-3_38.

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Bertaux-Skeirik, Nina, Jomaris Centeno, Jian Gao, Joel Gabre, and Yana Zavros. "Oncogenic Transformation of Human-Derived Gastric Organoids." In Methods in Molecular Biology, 205–13. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/7651_2016_4.

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Rogelj, Snezna, and Michael Klagsbrun. "Oncogenic Transformation by Basic Fibroblast Growth Factor." In Autocrine and Paracrine Mechanisms in Reproductive Endocrinology, 19–28. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5751-3_3.

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Cote, Gilbert J., Elizabeth G. Grubbs, and Marie-Claude Hofmann. "Thyroid C-Cell Biology and Oncogenic Transformation." In Medullary Thyroid Carcinoma, 1–39. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-22542-5_1.

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Nowell, Peter C., and Carlo M. Croce. "Immunoglobulin Genes, Oncogenes, and Human B-Cell Tumors." In Cell Transformation, 65–78. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-5009-5_3.

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Gebhardt, Angelika, and J. Gordon Foulkes. "Transformation by the v-abl Oncogene." In Oncogenes and Growth Control, 115–20. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-73325-3_16.

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Hunter, Tony. "Phosphorylation in Signal Transmission and Transformation." In Oncogenes and Growth Control, 138–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-73325-3_19.

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Conference papers on the topic "Oncogenic transformations"

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Garbe, James C., Lukas Vrba, Mark W. Jackson, Bernard Futscher, Mark LaBarge, and Martha R. Stampfer. "Abstract A41: Vulnerability of human mammary epithelial cells to oncogenic transformation." In Abstracts: Second AACR International Conference on Frontiers in Basic Cancer Research--Sep 14-18, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.fbcr11-a41.

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Nguyen, Hung Thanh, Lifang Chan, and Mathijs Voorhoeve. "Abstract A44: The role of ultraconserved noncoding RNAs in oncogenic transformation." In Abstracts: Third AACR International Conference on Frontiers in Basic Cancer Research - September 18-22, 2013; National Harbor, MD. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.fbcr13-a44.

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Koleci, N., Y. Wu, VR Mittapalli, S. Bohler, C. Molnar, JM Weiss, and M. Erlacher. "Analyzing the effects of oncogenic SHP2 on apoptosis signaling during malignant transformation." In 32. Jahrestagung der Kind-Philipp-Stiftung für pädiatrisch onkologische Forschung. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1687135.

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Mills, Lisa, Ronald Marler, Marta Herreros-Villanueva, Lizhi Zhang, Fergus Couch, Cynthia Wetmore, and Martin E. Fernandez-Zapico. "Abstract A58: GLI1 mediates oncogenic KRAS-induced transformation in pancreatic ductal adenocarcinoma." In Abstracts: AACR Special Conference on Pancreatic Cancer: Progress and Challenges; June 18-21, 2012; Lake Tahoe, NV. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.panca2012-a58.

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Wilson, Boris G., Xiaohua Shen, Elizabeth S. McKenna, Xi Wang, Yoon-Jae Cho, Edward C. Koellhoffer, Phuong T. L. Nguyen, Scott L. Pomeroy, Stuart H. Orkin, and Charles W. M. Roberts. "Abstract 4799: Epigenetic antagonism between Polycomb and SWI/SNF complexes during oncogenic transformation." 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.am10-4799.

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McKenzie, L., N. Martinez-Soria, HJ Blair, H. Issa, A. Isa, R. Tirtakusuma, C. Bonifer, and O. Heidenreich. "The oncogenic transcription factor RUNX1/ETO corrupts the cell cycle to drive leukaemic transformation." In 31. Jahrestagung der Kind-Philipp-Stiftung für pädiatrisch onkologische Forschung. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1645018.

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Tran, Anthony. "Abstract 535: The impact on transcriptome diversity after oncogenic transformation of human mammary epithelial cells." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-535.

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Deschênes-Simard, Xavier, Filippos Kottakis, Frédéric Lessard, Nabeel Bardeesy, and Gerardo Ferbeyre. "Abstract A09: Downregulation of PI3K signaling by high ERK activity prevents transformation by oncogenic RAS." In Abstracts: Third AACR International Conference on Frontiers in Basic Cancer Research - September 18-22, 2013; National Harbor, MD. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.fbcr13-a09.

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Bele, Aditya, Channabasavaiah Basavaraju Gurumurthy, Xiangshan Zhao, Jun Wang, Sameer Mirza, Shakur Mohibi, Hamid Band, and Vimla Band. "Abstract 4177: Synergistic role of ecdysoneless with oncogenic Ras in transformation of human mammary epithelial cells." 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.am2012-4177.

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Knarr, Matthew, Lily J. Kwiatkowski, Michele Dziubinski, Jessica McAnulty, Stephanie Skala, Stefanie Avril, Ronny Drapkin, and Analisa DiFeo. "Abstract B02: miR-181a initiates and perpetuates oncogenic transformation through the regulation of innate immune signaling." In Abstracts: AACR Special Conference on Advances in Ovarian Cancer Research; September 13-16, 2019; Atlanta, GA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3265.ovca19-b02.

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Reports on the topic "Oncogenic transformations"

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Garbe, James. Vulnerability of Normal Human Mammary Epithelial Cells to Oncogenic Transformation. Fort Belvoir, VA: Defense Technical Information Center, October 2008. http://dx.doi.org/10.21236/ada492855.

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Garbe, James C. Vulnerability of Normal Human Mammary Epithelial Cells to Oncogenic Transformation. Fort Belvoir, VA: Defense Technical Information Center, April 2012. http://dx.doi.org/10.21236/ada586809.

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McCormick, J. J. Malignant transformation of diploid human fibroblasts by transfection of oncogenes. Office of Scientific and Technical Information (OSTI), January 1992. http://dx.doi.org/10.2172/6852538.

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Scharer, Christopher. Identification of the Transformational Properties and Transcriptional Targets of the Oncogenic SRY Transcription Factor SOX4. Fort Belvoir, VA: Defense Technical Information Center, January 2009. http://dx.doi.org/10.21236/ada497252.

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Scharer, Christopher. Identification of the Transformational Properties and Transcriptional Targets of the Oncogenic SRY Transcription Factor SOX4. Fort Belvoir, VA: Defense Technical Information Center, January 2010. http://dx.doi.org/10.21236/ada524928.

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McCormick, J., and V. Maher. Malignant transformation of diploid human fibroblasts by transfection of oncogenes: Progress report, July 1986--June 1989. Office of Scientific and Technical Information (OSTI), January 1989. http://dx.doi.org/10.2172/6067022.

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McCormick, J. J. Malignant transformation of diploid human fibroblasts by transfection of oncogenes. Part 2, Progress report, July 1989--June 1992. Office of Scientific and Technical Information (OSTI), December 1992. http://dx.doi.org/10.2172/10107606.

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