Готові списки джерел за темами / P53; tumour suppressor; cancer

Добірка наукової літератури з теми "P53; tumour suppressor; cancer"

Автор: Grafiati
Опубліковано: 10 грудня 2022
Оновлено: 28 січня 2023

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Статті в журналах з теми "P53; tumour suppressor; cancer"

1

S Patil, Priya, Jaydeep N Pol, and Ashalata D Patil. "ROLE OF TUMOUR SUPPRESSOR GENE P53 IN TRIPLE NEGATIVE BREAST CANCER." International Journal of Anatomy and Research 5, no. 4.2 (November 1, 2017): 4585–89. http://dx.doi.org/10.16965/ijar.2017.402.

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2

HUPP, Ted R., David P. LANE, and Kathryn L. BALL. "Strategies for manipulating the p53 pathway in the treatment of human cancer." Biochemical Journal 352, no. 1 (November 7, 2000): 1–17. http://dx.doi.org/10.1042/bj3520001.

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Human cancer progression is driven in part by the mutation of oncogenes and tumour-suppressor genes which, under selective environmental pressures, give rise to evolving populations of biochemically altered cells with enhanced tumorigenic and metastatic potential. Given that human cancers are biologically and pathologically quite distinct, it has been quite surprising that a common event, perturbation of the p53 pathway, occurs in most if not all types of human cancers. The central role of p53 as a tumour-suppressor protein has fuelled interest in defining its mechanism of function and regulation, determining how its inactivation facilitates cancer progression, and exploring the possibility of restoring p53 function for therapeutic benefit. This review will highlight the key biochemical properties of p53 protein that affect its tumour-suppressor function and the experimental strategies that have been developed for the re-activation of the p53 pathway in cancers.
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3

Nishikawa, Shigeto, and Tomoo Iwakuma. "Drugs Targeting p53 Mutations with FDA Approval and in Clinical Trials." Cancers 15, no. 2 (January 9, 2023): 429. http://dx.doi.org/10.3390/cancers15020429.

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Mutations in the tumor suppressor p53 (p53) promote cancer progression. This is mainly due to loss of function (LOS) as a tumor suppressor, dominant-negative (DN) activities of missense mutant p53 (mutp53) over wild-type p53 (wtp53), and wtp53-independent oncogenic activities of missense mutp53 by interacting with other tumor suppressors or oncogenes (gain of function: GOF). Since p53 mutations occur in ~50% of human cancers and rarely occur in normal tissues, p53 mutations are cancer-specific and ideal therapeutic targets. Approaches to target p53 mutations include (1) restoration or stabilization of wtp53 conformation from missense mutp53, (2) rescue of p53 nonsense mutations, (3) depletion or degradation of mutp53 proteins, and (4) induction of p53 synthetic lethality or targeting of vulnerabilities imposed by p53 mutations (enhanced YAP/TAZ activities) or deletions (hyperactivated retrotransposons). This review article focuses on clinically available FDA-approved drugs and drugs in clinical trials that target p53 mutations and summarizes their mechanisms of action and activities to suppress cancer progression.
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4

Steffens Reinhardt, Luiza, Kira Groen, Brianna C. Morten, Jean-Christophe Bourdon та Kelly A. Avery-Kiejda. "Cytoplasmic p53β Isoforms Are Associated with Worse Disease-Free Survival in Breast Cancer". International Journal of Molecular Sciences 23, № 12 (15 червня 2022): 6670. http://dx.doi.org/10.3390/ijms23126670.

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TP53 mutations are associated with tumour progression, resistance to therapy and poor prognosis. However, in breast cancer, TP53′s overall mutation frequency is lower than expected (~25%), suggesting that other mechanisms may be responsible for the disruption of this critical tumour suppressor. p53 isoforms are known to enhance or disrupt p53 pathway activity in cell- and context-specific manners. Our previous study revealed that p53 isoform mRNA expression correlates with clinicopathological features and survival in breast cancer and may account for the dysregulation of the p53 pathway in the absence of TP53 mutations. Hence, in this study, the protein expression of p53 isoforms, transactivation domain p53 (TAp53), p53β, Δ40p53, Δ133p53 and Δ160p53 was analysed using immunohistochemistry in a cohort of invasive ductal carcinomas (n = 108). p53 isoforms presented distinct cellular localisation, with some isoforms being expressed in tumour cells and others in infiltrating immune cells. Moreover, high levels of p53β, most likely to be N-terminally truncated β variants, were significantly associated with worse disease-free survival, especially in tumours with wild-type TP53. To the best of our knowledge, this is the first study that analysed the endogenous protein levels of p53 isoforms in a breast cancer cohort. Our findings suggest that p53β may be a useful prognostic marker.
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5

Lee, Jonathan M., and Alan Bernstein. "Apoptosis, cancer and the p53 tumour suppressor gene." Cancer and Metastasis Reviews 14, no. 2 (June 1995): 149–61. http://dx.doi.org/10.1007/bf00665797.

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6

Bui, Tung, Yu Gu, Frédéric Ancot, Virginie Sanguin-Gendreau, Dongmei Zuo та William J. Muller. "Emergence of β1 integrin-deficient breast tumours from dormancy involves both inactivation of p53 and generation of a permissive tumour microenvironment". Oncogene 41, № 4 (15 листопада 2021): 527–37. http://dx.doi.org/10.1038/s41388-021-02107-7.

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AbstractThe molecular and cellular mechanisms underlying mammary tumour dormancy and cancer recurrence are unclear and remain to be elucidated. Here, we report that mammary epithelial-specific disruption of β1 integrin in a murine model of Luminal B human breast cancer drastically impairs tumour growth with proliferation block, apoptosis induction and cellular senescence. β1 integrin-deficient dormant lesions show activation of the tumour suppressor p53, and tumours that circumvent dormancy possess p53 mutation analogous to those in human disease. We further demonstrate that mammary epithelial deletion of p53 in β1 integrin-deficient mice fully rescues tumour dormancy and bypasses cellular senescence. Additionally, recurrent β1 integrin-deficient tumours exhibit fibrosis with increased cancer-associated fibroblast infiltration and extracellular matrix deposition, absent in fast-growing β1 integrin/p53-deficient lesions. Taken together, these observations argue that β1 integrin modulates p53-dependent cellular senescence resulting in tumour dormancy and that pro-tumourigenic stromal cues and intrinsic genetic mutation are required for dormancy exit.
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7

Ghosh, Anirban, Deborah Stewart, and Greg Matlashewski. "Regulation of Human p53 Activity and Cell Localization by Alternative Splicing." Molecular and Cellular Biology 24, no. 18 (September 15, 2004): 7987–97. http://dx.doi.org/10.1128/mcb.24.18.7987-7997.2004.

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ABSTRACT The development of cancer is a multistep process involving mutations in proto-oncogenes, tumor suppressor genes, and other genes which control cell proliferation, telomere stability, angiogenesis, and other complex traits. Despite this complexity, the cellular pathways controlled by the p53 tumor suppressor protein are compromised in most, if not all, cancers. In normal cells, p53 controls cell proliferation, senescence, and/or mediates apoptosis in response to stress, cell damage, or ectopic oncogene expression, properties which make p53 the prototype tumor suppressor gene. Defining the mechanisms of regulation of p53 activity in normal and tumor cells has therefore been a major priority in cell biology and cancer research. The present study reveals a novel and potent mechanism of p53 regulation originating through alternative splicing of the human p53 gene resulting in the expression of a novel p53 mRNA. This novel p53 mRNA encodes an N-terminally deleted isoform of p53 termed p47. As demonstrated within, p47 was able to effectively suppress p53-mediated transcriptional activity and impair p53-mediated growth suppression. It was possible to select for p53-null cells expressing p47 alone or coexpressing p53 in the presence of p47 but not cells expressing p53 alone. This showed that p47 itself does not suppress cell viability but could control p53-mediated growth suppression. Interestingly, p47 was monoubiquitinated in an Mdm2-independent manner, and this was associated with its export out of the nucleus. In the presence of p47, there was a reduction in Mdm2-mediated polyubiquitination and degradation of p53, and this was also associated with increased monoubiquitination and nuclear export of p53. The expression of p47 through alternative splicing of the p53 gene thus has a major influence over p53 activity at least in part through controlling p53 ubiquitination and cell localization.
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8

Alhebshi, Hasen, Kun Tian, Lipsita Patnaik, Rebecca Taylor, Pavel Bezecny, Callum Hall, Patricia Anthonia Johanna Muller, et al. "Evaluation of the Role of p53 Tumour Suppressor Posttranslational Modifications and TTC5 Cofactor in Lung Cancer." International Journal of Molecular Sciences 22, no. 24 (December 7, 2021): 13198. http://dx.doi.org/10.3390/ijms222413198.

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Mutations in the p53 tumor suppressor are found in over 50% of cancers. p53 function is controlled through posttranslational modifications and cofactor interactions. In this study, we investigated the posttranslationally modified p53, including p53 acetylated at lysine 382 (K382), p53 phosphorylated at serine 46 (S46), and the p53 cofactor TTC5/STRAP (Tetratricopeptide repeat domain 5/ Stress-responsive activator of p300-TTC5) proteins in lung cancer. Immunohistochemical (IHC) analysis of lung cancer tissues from 250 patients was carried out and the results were correlated with clinicopathological features. Significant associations between total or modified p53 with a higher grade of the tumour and shorter overall survival (OS) probability were detected, suggesting that mutant and/or modified p53 acts as an oncoprotein in these patients. Acetylated at K382 p53 was predominantly nuclear in some samples and cytoplasmic in others. The localization of the K382 acetylated p53 was significantly associated with the gender and grade of the disease. The TTC5 protein levels were significantly associated with the grade, tumor size, and node involvement in a complex manner. SIRT1 expression was evaluated in 50 lung cancer patients and significant positive correlation was found with p53 S46 intensity, whereas negative TTC5 staining was associated with SIRT1 expression. Furthermore, p53 protein levels showed positive association with poor OS, whereas TTC5 protein levels showed positive association with better OS outcome. Overall, our results indicate that an analysis of p53 modified versions together with TTC5 expression, upon testing on a larger sample size of patients, could serve as useful prognostic factors or drug targets for lung cancer treatment.
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9

Vousden, Karen H. "Functions of p53 in metabolism and invasion." Biochemical Society Transactions 37, no. 3 (May 20, 2009): 511–17. http://dx.doi.org/10.1042/bst0370511.

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The p53 protein is an important tumour suppressor that is inactivated in many human cancers. Understanding how p53 is regulated and the downstream consequences of p53 function is helping us to devise novel therapies based on the reactivation of p53. Such approaches may be useful in the treatment of cancer, but a growing understanding of a role for p53 in other conditions suggests that modulation of p53 may have broader applications.
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10

Chang, F., S. Syrjänen, A. Tervahauta, and K. Syrjänen. "Tumourigenesis associated with the p53 tumour suppressor gene." British Journal of Cancer 68, no. 4 (October 1993): 653–61. http://dx.doi.org/10.1038/bjc.1993.404.

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Дисертації з теми "P53; tumour suppressor; cancer"

1

Webley, Katherine Mary. "p53 in colorectal cancer." Thesis, University of Sheffield, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286842.

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2

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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3

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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4

Scobie, Linda. "The role of p53 in cell transformation by BPV-4." Thesis, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360279.

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5

Stuart, Debra. "The role of p53 in mouse skin keratinocytes." Thesis, University of Glasgow, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.364083.

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6

Dowell, Stephanie Patricia. "Studies of the p53 tumour suppressor gene and related proteins in cytopathology." Thesis, King's College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336432.

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7

Froggatt, Nicola Jane. "Alterations to the tumour suppressor genes p53 and dcc in colorectal neplasia." Thesis, University of York, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385322.

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8

Mee, Trevor Richard. "Analysis of the proteolytic cleavage reaction of the tumour suppressor protein p53." Thesis, University of York, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310987.

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9

Zhu, Yong-Ming. "Studies on expression of tumour suppressor genes in acute myeloblastic leukaemia." Thesis, Nottingham Trent University, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297012.

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10

McArdle, Stephanie. "p53 epitopes as potential tumour targets for immunotherapy programmes against cancers." Thesis, University of Sheffield, 2000. http://etheses.whiterose.ac.uk/14459/.

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The tumour suppressor gene p53 is pivotal in the regulation of program cell death (apoptosis), and point mutations within the gene represent the most common genetic alterations in human cancers. This process can result in the overexpression and/or accumulation of mutated and/or wild-type p53 protein within the cell. Cytotoxic T lymphocytes (CTL) play a critical role in the immune defense by recognising peptide/MHC complexes on the surface of virally infected or tumour cells followed by lysis. Therefore, p53-derived peptides are potential candidates for immunisation strategies designed to induce anti-tumour CTL in patients.
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Книги з теми "P53; tumour suppressor; cancer"

1

The p53 tumor suppressor pathway and cancer. New York: Springer, 2005.

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2

Zambetti, Gerard P., ed. The p53 Tumor Suppressor Pathway and Cancer. Boston, MA: Springer US, 2005. http://dx.doi.org/10.1007/0-387-30127-5.

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3

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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4

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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5

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

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6

The p53 tumor suppressor pathway and cancer. New York, NY: Springer, 2005.

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7

Zambetti, Gerard P. The p53 Tumor Suppressor Pathway and Cancer. Springer, 2014.

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8

The p53 Tumor Suppressor Pathway and Cancer (Protein Reviews, Vol. 2). Springer, 2007.

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9

Quantification of the p53 tumor suppressor gene product in cell lines and serum of cancer patients: Development of new methodology and clinical studies. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1993.

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10

Hodgkiss, Andrew. Introduction to cancer biology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198759911.003.0001.

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A brief introduction to cancer biology, aimed at psychiatrists, is offered. Selective DNA transcription, the cell cycle, receptor tyrosine kinases, and cell signalling pathways are introduced, using the EGFR/RAS/MAPK pathway as an exemplar. The molecular pathology of oncogenesis is summarized, including discussion of oncogenes, tumour suppressor genes, and examples of driver mutations. The exploitation of such mutations in stratified medicine, using molecularly targeted agents, is mentioned. Finally, Hanahan and Weinberg’s six hallmarks of cancer are listed, adding angiogenesis and metastasis to the picture of oncogenesis.
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Частини книг з теми "P53; tumour suppressor; cancer"

1

Mukhopadhyay, Tapas, Steven A. Maxwell, and Jack A. Roth. "Potential Clinical Significance of the p53 Tumor Suppressor Gene in Cancer Patients." In p53 Suppressor Gene, 113–25. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22275-1_6.

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2

Deppert, W. "p53: Oncogene, Tumor Suppressor, or Both?" In Molecular Diagnostics of Cancer, 27–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77521-5_3.

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3

Corcoran, Chad A., Ying Huang, and M. Saeed Sheikh. "Energy Generating Pathways and the Tumor Suppressor p53." In Mitochondria and Cancer, 131–50. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-84835-8_8.

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4

Allred, D. Craig, Richard Elledge, Gary M. Clark, and Suzanne A. W. Fuqua. "The p53 tumor-suppressor gene in human breast cancer." In Cancer Treatment and Research, 63–77. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2592-9_4.

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5

Jia, Libin, Xin Wei Wang, Zongtang Sun, and Curtis C. Harris. "Interactive Effects of p53 Tumor Suppressor Gene and Hepatitis B Virus in Hepatocellular Carcinogenesis." In Molecular Pathology of Gastroenterological Cancer, 209–18. Tokyo: Springer Japan, 1997. http://dx.doi.org/10.1007/978-4-431-65915-0_15.

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6

Soussi, Thierry, Jean Tredaniel, Richard Lubin, Gerard Zalcman, and Albert Hirsh. "The p53 Tumor Suppressor Gene in Lung Cancer: From Molecular to Serological Diagnosis." In Clinical and Biological Basis of Lung Cancer Prevention, 221–30. Basel: Birkhäuser Basel, 1998. http://dx.doi.org/10.1007/978-3-0348-8924-7_19.

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7

Das, Gokul M. "Estrogen Receptor—Tumor Suppressor Protein p53 Signaling Crosstalk as Potential Targets of Xenoestrogens." In Mitochondria as Targets for Phytochemicals in Cancer Prevention and Therapy, 27–32. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-9326-6_2.

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8

Siddik, Zahid H. "Drug Resistance and the Tumor Suppressor p53: The Paradox of Wild-Type Genotype in Chemorefractory Cancers." In Drug Resistance in Cancer Cells, 209–31. New York, NY: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-89445-4_9.

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9

Feng, Zhaohui, and Arnold J. Levine. "The Regulation of the IGF-1/mTOR Pathway by the p53 Tumor Suppressor Gene Functions." In mTOR Pathway and mTOR Inhibitors in Cancer Therapy, 37–48. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-271-1_2.

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10

Sage, Julien, Laura Attardi, and Terry Van Dyke. "Roles of p53 and pRB Tumor Suppressor Networks in Human Cancer: Insight from Studies in the Engineered Mouse." In Genetically Engineered Mice for Cancer Research, 293–308. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-69805-2_14.

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Тези доповідей конференцій з теми "P53; tumour suppressor; cancer"

1

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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2

Khromova, N., M. Novikova, V. Dugina, B. Kopnin, and P. Kopnin. "PO-232 Actin-dependent effect of tumour suppressor P53 on human lung cancer cell malignant characteristics." 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-eacr25.749.

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3

Shin, Yong-Jun, Steven M. Lipkin, Brandon Hencey, and Xiling Shen. "Disturbance Rejection Helps Modulate the p53 Oscillation." In ASME 2011 Dynamic Systems and Control Conference and Bath/ASME Symposium on Fluid Power and Motion Control. ASMEDC, 2011. http://dx.doi.org/10.1115/dscc2011-6046.

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Designing a system that adequately processes the input and that rejects the effects of disturbance is a central theme in feedback control theory. In this paper, we use the concept of “disturbance rejection” to analyze the oscillatory behavior of p53, a well-known tumor suppressor protein. Our analysis reveals that the p53 oscillation is not completely dictated by the p53-MDM2 negative feedback loop—it is also modulated by periodic DNA repair-related fluctuations. According to our disturbance rejection model, the feedback loop normally filters the effects of noise and fluctuations on p53, but upon DNA damage, it stops performing the filtering function so that DNA repair-related fluctuations can modulate the p53 oscillation. Our analysis suggests that the overexpression of MDM2, observed in many types of cancer, can make the feedback mechanism less responsive to the modulating signals after DNA damage occurs.
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4

Flowers, Brittany M., Patty B. Garcia, Barbara M. Grüner, Monte M. Winslow, and Laura D. Attardi. "Abstract A28: Understanding the role of the tumor suppressor p53 in pancreatic cancer development." In Abstracts: AACR Special Conference: Advances in Modeling Cancer in Mice: Technology, Biology, and Beyond; September 24-27, 2017; Orlando, Florida. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.mousemodels17-a28.

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5

Forys, Jason T., Raleigh D. Kladney, and Jason D. Weber. "Abstract A40: Investigating the functional response of the ARF tumor suppressor to acute p53 loss." 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-a40.

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6

Bendor, Jordan, Jesse Zamudio, Tyler Jacks, and Nadva Dimitrova. "Abstract PR02: The diverse roles of long noncoding RNAs in the p53 tumor suppressor pathway." In Abstracts: AACR Special Conference on Noncoding RNAs and Cancer: Mechanisms to Medicines; December 4-7, 2015; Boston, MA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.nonrna15-pr02.

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7

Hori, Naoto, Hiroshi Tazawa, Masahiko Nishizaki, Satoru Kikuchi, Shuya Yano, Michihiro Ishida, Megumi Watanabe, Yasuo Urata, Shunsuke Kagawa, and Toshiyoshi Fujiwara. "Abstract 5338: Preclinical study of telomerase-specific p53 tumor suppressor gene overexpression in human scirrhous gastric cancer cells with different p53 status." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5338.

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8

Kulkarni, S., GJ Fetterly, CD Morrison, AA Adjei, C. Andrews, SP Edge, UK Mukhopadhyay, WM Swetzig, and GM Das. "OT1-03-03: Effect of Tamoxifen Therapy on Inhibition of Tumor Suppressor p53 by Estrogen Receptor." In Abstracts: Thirty-Fourth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 6‐10, 2011; San Antonio, TX. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/0008-5472.sabcs11-ot1-03-03.

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9

Jones, RA, JC Liu, J. Zhe, AA Schimmer, and Z. Eldad. "Abstract P1-04-05: Role of the Rb and p53 Tumor Suppressor Pathways in Mammary Tumorigenesis." In Abstracts: Thirty-Fifth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 4‐8, 2012; San Antonio, TX. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/0008-5472.sabcs12-p1-04-05.

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10

Chen, Xiaoxiang, and Shukui Wang. "IDDF2018-ABS-0183 P53-induced MIR-1249 suppresses tumour progression by targeting VEGFA and HMGA2 in colorectal cancer." In International Digestive Disease Forum (IDDF) 2018, Hong Kong, 9–10 June 2018. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2018. http://dx.doi.org/10.1136/gutjnl-2018-iddfabstracts.22.

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Звіти організацій з теми "P53; tumour suppressor; cancer"

1

Yang, Annie. Role of the p53 Tumor Suppressor Homolog, p63, in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2005. http://dx.doi.org/10.21236/ada437662.

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2

Yang, Annie. Role of the p53 Tumor Suppressor Homolog, p63, in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2006. http://dx.doi.org/10.21236/ada456200.

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3

Yang, Annie. Role of the p53 Tumor Suppressor Homolog, p63, in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2007. http://dx.doi.org/10.21236/ada471497.

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4

Liu, Jingwen. Negative Regulation of Tumor Suppressor p53 Transcription in Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada396148.

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5

Liu, Jingwen. Negative Regulation of Tumor Suppressor p53 Transcription in Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, July 2004. http://dx.doi.org/10.21236/ada431331.

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6

Manfredi, James. Regulation of the Tumor Suppressor Activity of p53 in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2000. http://dx.doi.org/10.21236/ada395583.

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7

Manfredi, James J. Regulation of The Tumor Suppressor Activity of P53 In Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 1999. http://dx.doi.org/10.21236/ada383030.

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8

Kulesz-Martin, Molly. The Tumor Suppressor Protein p53 and its Physiological Splicing Variant p53as in a Mouse Mammary Cancer Model. Fort Belvoir, VA: Defense Technical Information Center, October 1997. http://dx.doi.org/10.21236/ada340579.

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9

Baker, William C. Racial Differences in Prostate Cancer Molecular Biology: An Evaluation of Tumor Suppressor Genes in BCL2, P53 and RB in Black and Africans. Fort Belvoir, VA: Defense Technical Information Center, July 1999. http://dx.doi.org/10.21236/ada376157.

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10

Maltese, William A. Functional Analysis of the Beclin-1 Tumor Suppressor Interaction with hVps34 (Type-III P13'-kinase) in Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, June 2008. http://dx.doi.org/10.21236/ada486772.

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