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Relevant bibliographies by topics / P53 Genes

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Academic literature on the topic 'P53 Genes'

Author: Grafiati

Published: 4 June 2021

Last updated: 8 February 2022

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Journal articles on the topic "P53 Genes"

1

Keegan, Lunec, and Neal. "p53 and p53-regulated genes in bladder cancer." BJU International 82, no. 5 (November 1998): 710–20. http://dx.doi.org/10.1046/j.1464-410x.1998.00822.x.

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Shu, Kun-Xian, Biao Li, and Li-Xiang Wu. "The p53 network: p53 and its downstream genes." Colloids and Surfaces B: Biointerfaces 55, no. 1 (March 2007): 10–18. http://dx.doi.org/10.1016/j.colsurfb.2006.11.003.

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Klingler, H. Christoph. "p53 and p53 regulated genes in bladder cancer [review]." Current Opinion in Urology 9, no. 2 (March 1999): 172. http://dx.doi.org/10.1097/00042307-199903000-00015.

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4

Li, Yuwen, Jiao Liu, Nathan McLaughlin, Dimcho Bachvarov, Zubaida Saifudeen, and Samir S. El-Dahr. "Genome-wide analysis of the p53 gene regulatory network in the developing mouse kidney." Physiological Genomics 45, no. 20 (October 15, 2013): 948–64. http://dx.doi.org/10.1152/physiolgenomics.00113.2013.

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Despite mounting evidence that p53 senses and responds to physiological cues in vivo, existing knowledge regarding p53 function and target genes is largely derived from studies in cancer or stressed cells. Herein we utilize p53 transcriptome and ChIP-Seq (chromatin immunoprecipitation-high throughput sequencing) analyses to identify p53 regulated pathways in the embryonic kidney, an organ that develops via mesenchymal-epithelial interactions. This integrated approach allowed identification of novel genes that are possible direct p53 targets during kidney development. We find the p53-regulated transcriptome in the embryonic kidney is largely composed of genes regulating developmental, morphogenesis, and metabolic pathways. Surprisingly, genes in cell cycle and apoptosis pathways account for <5% of differentially expressed transcripts. Of 7,893 p53-occupied genomic regions (peaks), the vast majority contain consensus p53 binding sites. Interestingly, 78% of p53 peaks in the developing kidney lie within proximal promoters of annotated genes compared with 7% in a representative cancer cell line; 25% of the differentially expressed p53-bound genes are present in nephron progenitors and nascent nephrons, including key transcriptional regulators, components of Fgf, Wnt, Bmp, and Notch pathways, and ciliogenesis genes. The results indicate widespread p53 binding to the genome in vivo and context-dependent differences in the p53 regulon between cancer, stress, and development. To our knowledge, this is the first comprehensive analysis of the p53 transcriptome and cistrome in a developing mammalian organ, substantiating the role of p53 as a bona fide developmental regulator. We conclude p53 targets transcriptional networks regulating nephrogenesis and cellular metabolism during kidney development.

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Xu, H., and M. R. El-Gewely. "P53 network — its downstream regulated genes." Biochemical Society Transactions 28, no. 5 (October 1, 2000): A227. http://dx.doi.org/10.1042/bst028a227a.

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BOONMARS, T., Z. WU, I. NAGANO, and Y. TAKAHASHI. "What is the role of p53 during the cyst formation of Trichinella spiralis? A comparable study between knockout mice and wild type mice." Parasitology 131, no. 5 (July 11, 2005): 705–12. http://dx.doi.org/10.1017/s0031182005008036.

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During the cyst formation of Trichinella spiralis, the infected muscle cell undergoes basophilic change and apoptosis, which results in nurse cell formation. This study revealed expression kinetics of some apoptosis genes such as p53 and its closely related genes (tumor suppressor genes p53, p53; mouse double minute 2, MDM2; cyclin-dependent kinase inhibitor p21, p21waf). RT-PCR (reverse transcription polymerase chain reaction) results showed that these genes were temporarily expressed in the infected muscles during the cyst formation period, but not in normal muscles (or very low if any), which suggested the involvement of these apoptosis genes in the nurse cell formation. Cysts and neighbouring muscle cells were separately collected and RT-PCR was performed, which suggested that p53 was expressed in the cysts. An immunocytochemical study showed that p53 was expressed in the nucleoplasm of basophilic cell in the cyst and Trichinella larvae, which suggested involvement of these apoptosis genes in the nurse cell formation. The same p53 expression kinetic study was performed on p53 knockout mice. The knockout mice did not express p53 genes, but expressed the other apoptosis genes in the same kinetics with only minor exceptions, suggesting that the expressions of these genes during the cyst formation were more or less p53-independent. There were no differences in the number and morphology of the cysts between the knockout mice and wild type mice. Thus apoptosis seen during the Trichinella cyst formation can be operated in the presence or absence of p53.

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Hannemann, Holger, Kyle Rosenke, John M. O'Dowd, and Elizabeth A. Fortunato. "The Presence of p53 Influences the Expression of Multiple Human Cytomegalovirus Genes at Early Times Postinfection." Journal of Virology 83, no. 9 (February 18, 2009): 4316–25. http://dx.doi.org/10.1128/jvi.02075-08.

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ABSTRACT Human cytomegalovirus (HCMV) is a common cause of morbidity and mortality in immunocompromised and immunosuppressed individuals. During infection, HCMV is known to employ host transcription factors to facilitate viral gene expression. To further understand the previously observed delay in viral replication and protein expression in p53 knockout cells, we conducted microarray analyses of p53+/+ and p53−/− immortalized fibroblast cell lines. At a multiplicity of infection (MOI) of 1 at 24 h postinfection (p.i.), the expression of 22 viral genes was affected by the absence of p53. Eleven of these 22 genes (group 1) were examined by real-time reverse transcriptase, or quantitative, PCR (q-PCR). Additionally, five genes previously determined to have p53 bound to their nearest p53-responsive elements (group 2) and three control genes without p53 binding sites in their upstream sequences (group 3) were also examined. At an MOI of 1, >3-fold regulation was found for five group 1 genes. The expression of group 2 and 3 genes was not changed. At an MOI of 5, all genes from group 1 and four of five genes from group 2 were found to be regulated. The expression of control genes from group 3 remained unchanged. A q-PCR time course of four genes revealed that p53 influences viral gene expression most at immediate-early and early times p.i., suggesting a mechanism for the reduced and delayed production of virions in p53−/− cells.

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Friedlander, P., Y. Haupt, C. Prives, and M. Oren. "A mutant p53 that discriminates between p53-responsive genes cannot induce apoptosis." Molecular and Cellular Biology 16, no. 9 (September 1996): 4961–71. http://dx.doi.org/10.1128/mcb.16.9.4961.

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Human wild-type (wt) p53 can induce apoptosis in transiently transfected H1299 cells maintained at 37 degrees C, whereas tumor-derived mutant forms of p53 (with the mutation Ala-143, His-175, or Trp-248) fail to do so. At 37 degrees C, p53 with a mutation to Ala at amino acid 143 (p53Ala143) was transcriptionally inactive. However, at 32 degrees C, p53Ala143 strongly activated transcription from several physiologically relevant p53-responsive promoters, to extents similar or greater than that of wt p53. Unexpectedly, p53Ala143 was defective in inducing apoptosis in H1299 cells at 32 degrees C. Concomitantly with the loss of apoptotic activity, p53Ala143 was found to be deficient in its ability to activate transcription from the p53-responsive portions of the Bax and insulin-like growth factor-binding protein 3 gene promoters. It is proposed that there may exist distinct classes of p53-responsive promoters, whose ability to be activated by p53 can be regulated differentially. Such differential regulation may have functional consequences for the effects of p53 on cell fate.

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Bruins, Wendy, Oskar Bruning, Martijs J. Jonker, Edwin Zwart, Tessa V. van der Hoeven, Jeroen L. A. Pennings, Han Rauwerda, Annemieke de Vries, and Timo M. Breit. "The Absence of Ser389 Phosphorylation in p53 Affects the Basal Gene Expression Level of Many p53-Dependent Genes and Alters the Biphasic Response to UV Exposure in Mouse Embryonic Fibroblasts." Molecular and Cellular Biology 28, no. 6 (January 14, 2008): 1974–87. http://dx.doi.org/10.1128/mcb.01610-07.

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ABSTRACT Phosphorylation is important in p53-mediated DNA damage responses. After UV irradiation, p53 is phosphorylated specifically at murine residue Ser389. Phosphorylation mutant p53.S389A cells and mice show reduced apoptosis and compromised tumor suppression after UV irradiation. We investigated the underlying cellular processes by time-series analysis of UV-induced gene expression responses in wild-type, p53.S389A, and p53−/− mouse embryonic fibroblasts. The absence of p53.S389 phosphorylation already causes small endogenous gene expression changes for 2,253, mostly p53-dependent, genes. These genes showed basal gene expression levels intermediate to the wild type and p53−/−, possibly to readjust the p53 network. Overall, the p53.S389A mutation lifts p53-dependent gene repression to a level similar to that of p53−/− but has lesser effect on p53-dependently induced genes. In the wild type, the response of 6,058 genes to UV irradiation was strictly biphasic. The early stress response, from 0 to 3 h, results in the activation of processes to prevent the accumulation of DNA damage in cells, whereas the late response, from 12 to 24 h, relates more to reentering the cell cycle. Although the p53.S389A UV gene response was only subtly changed, many cellular processes were significantly affected. The early response was affected the most, and many cellular processes were phase-specifically lost, gained, or altered, e.g., induction of apoptosis, cell division, and DNA repair, respectively. Altogether, p53.S389 phosphorylation seems essential for many p53 target genes and p53-dependent processes.

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Abramowitz, Julia, Tzahi Neuman, Riki Perlman, and Dina Ben-Yehuda. "The P53 Pathway Is Inactive in Acute Myeloid Leukemia." Blood 120, no. 21 (November 16, 2012): 5122. http://dx.doi.org/10.1182/blood.v120.21.5122.5122.

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Abstract Abstract 5122 The pathway controlled by the p53 tumor-suppressor protein is altered in most, if not all, human cancers and the TP53 gene is mutated in half of all human tumors. Such mutations are rare in human hematological malignancies, leading to the assumption that the p53 pathway is inactivated by alternative mechanisms. However, to date, the state of activity of the p53 pathway in hematological malignancies is not well understood. We investigated the functional status of the p53 pathway in Acute Myeloid Leukemia (AML) patients, particularly in patients with cytogenetically normal AML (CN-AML) and patients with Acute Promyelocytic Leukemia (APL). We performed bioinformatic analysis of p53 pathway-related gene expression. For this purpose, we first assembled a list that, to the best of our knowledge, is the most comprehensive list to date of genes related to the p53 pathway. The list consists of 1153 p53 pathway-related genes: 916 p53-related genes and 582 partially overlapping genes related to important components of the p53 pathway (Mdm2, Mdmx, Puma, Slug and Chk2). The list of p53 pathway-related genes was constructed based on gene and protein web databases and literature search. Only genes with proven biochemical relationships to the p53 pathway were included. Publically available Affymetrix gene expression array data was analyzed which included 290 CN-AML and 34 APL patients at diagnosis in comparison to 63 normal bone marrow (nBM) samples. Differentially expressed genes (DEGs) were identified out of 1153 p53 pathway-related genes using a linear statistical model that produced gene expression contrasts between leukemic samples and nBM. Study effect differences were also corrected by this model. One hundred forty seven DEGs were identified in CN-AML and 172 in APL (fold change>2. 8, p value<0. 01). We found a significant over-representation of p53 pathway related DEGs above the genomic background in both leukemias. Our analysis demonstrated homogeneity of gene expression in APL patients and discovered that CN-AML patients were further divided into 3 sub-groups by hierarchical clustering analysis. Most of the DEGs were down regulated both in CN-AML (108/147) and in APL (135/172) patients. We analyzed the DEGs and concluded that in both leukemias there was no p53-dependent induction of canonical cell cycle arrest genes, canonical pro-apoptotic genes, p53-related antioxidant defense genes, DNA damage repair genes and anti-glycolysis genes. We compared our bioinformatic results to gene expression signatures related to p53 activation by various stimuli from the literature. This analysis demonstrated that p53 protein did not exert transcriptional activation of the majority of its target genes in CN-AML and APL, implying that p53 pathway is not activated in these leukemias. We found downregulation of p300, PCAF and CARM1 genes in patient samples compared to nBM. Deregulation of these genes points to decreased acetylation and methylation of the p53 protein that can result in the inhibition of p53 transcriptional activity. We examined protein levels of p53 and its main inhibitors Mdmx and Mdm2 by immunohistochemistry in 25 CN-AML and 23 APL patients in comparison to 36 nBM biopsies. We found that the fraction of cells expressing p53, Mdmx and Mdm2 proteins was significantly higher in leukemias (70–90%) compared to nBM (10–30%). However, the intensity of Mdm2 staining was not elevated in leukemic blasts compared to nBM and p53 levels were similarly low in both nBM and leukemias. Importantly, Mdmx protein level was significantly upregulated in leukemia cells, offering an explanation for inhibition of p53 transcriptional activity in leukemia. The increased level of Mdmx protein together with low levels of p53 protein is in agreement with inhibition of p53 transcriptional activity in CN-AML and APL demonstrated by our bioinformatic analysis. Inactivation of p53 pathway shown here may be one of the important leukomogenic events in AML development. Importantly, gene expression and thus the functional status of p53 pathway is very similar in CN-AML and APL patients compared to nBM, despite the different underlying molecular etiology of these diseases. This finding may have important therapeutic implications in that similar reactivation of the p53 pathway may be a therapeutic modality applicable to these two biologically different types of leukemia. Disclosures: No relevant conflicts of interest to declare.

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Dissertations / Theses on the topic "P53 Genes"

1

Mpagi, Meldrick Daniel. "In Search For New p53 Regulated Genes." Wright State University / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=wright1227282714.

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Berggren, Petra. "Molecular changes in the tumour suppressor genes p53 and CDKN2A/ARF in human urinary bladder cancer /." Stockholm : [Karolinska institutets bibl.], 2002. http://diss.kib.ki.se/2002/91-7349-128-4.

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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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Gustafsson, Britt. "Prognostic and epidemiological factors in childhood leukaemia : studies of p53 and MDM2 expression and of space-time clustering /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4173-4/.

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Lane, Trevor. "The influence of p53 on mutagenicity." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.294357.

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Ayanga, Bernard Aguya. "IDENTIFICATION OF GENES THAT COOPERATE WITH P53 IN TUMORIGENESIS." Ohio University / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1161966086.

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Wang, Qian. "p53 functional loss by mutation and p53 antagonizing proteins during tumor development /." Stockholm, 2000. http://diss.kib.ki.se/2000/20000525wang/.

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Teixeira, Roberto Augusto Plaza. ""Fatores clínicos e biológicos para recidivas em tumores de Wilms localizados"." Universidade de São Paulo, 2005. http://www.teses.usp.br/teses/disponiveis/5/5141/tde-04012006-105538/.

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Apesar do excelente prognóstico dos tumores de Wilms (TW) localizados (estádios I e II) e de histologia favorável (HF), 10% deles recidivam. Em 122 pacientes com TW com essas características, diagnosticados de 1976 e 2001, analisamos alguns fatores clínicos, como a idade por ocasião do diagnóstico e peso do tumor, em todos os pacientes; fatores biológicos, como o TP53 e a glicoproteína-p, em 40 deles; e variáveis histológicas de microestadiamento (invasão de seio renal, cápsula tumoral, vasos intra-renais e pseudocápsula inflamatória) em 28 com TW em estádio I. Correlacionando todos esses fatores com a presença de recidiva, observamos que a chance maior de recidiva estatisticamente significativa somente foi verificada em pacientes com duas ou mais variáveis de microestadiamento e/ou peso tumoral maior que 550 g
In spite of the excellent prognosis of localized favorable histology (FH) of Wilms' tumor (WT), 10% of them will relapse. In 122 TW patients with these characteristics, diagnosed between 1976 and 2001, some clinical factors have been analyzed, such as age at diagnosis and tumor weight in all patients; biological factors, like TP53 and p-glycoprotein, in 40 of them; and microsubstaging histological variables (invasion of renal sinus, tumor capsule, intrarenal vessels, and inflammatory pseudocapsule). Correlating all of those factors with relapse, we have observed that only patients with the association of two or more microsubstaging variables and/or tumor weight over 550 g showed a statistically significant higher chance of relapse

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Melo, Vinicius André Morais Rocha. "Construção de ferramentas para estudo da possível interação entre interferon-beta e p53." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/87/87131/tde-17082009-121304/.

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Formação de tumores deve-se a combinações de fatores. A via de p53 tem um papel fundamental no controle de proliferação e apoptose. O interferon-beta (IFNb) é importante na modulação da resposta imunológica, no efeito antitumoral e no impacto apoptótico em células tumorais. Segundo a literatura, IFNb ativa a transcrição de p53 e componentes do sistema IFN efetuam sua função pela via p53/p14arf. Neste projeto, foi construída uma série de ferramentas para explorar interações entre p53 e IFNb. A primeira ferramenta, uma linhagem celular derivada de B16 com expressão de p53 reduzida por miRNA. Também construímos vetores plasmidiais e adenovirais portadores dos cDNAs para eGFP, Luciferase, p53 ou IFNb. Os vetores são utilizados para introduzir estes fatores, sozinho ou combinados, na célula alvo. Mesmo confirmando a atividade de p53 ou IFNb sozinho, não foi observado um efeito aditivo destes fatores em conjunto com este tipo de ensaio. Futuros estudos das possíveis interações entre as vias de p53 e IFNb terão o benefício das ferramentas construídas neste projeto.
Formation of tumors it must to combinations of factors. The p53 pathway has an essential role in proliferation control and apoptosis. The interferon-beta (IFNb) is important in modulation of the immunologic response, in the antitumoral effect and in the apoptotic impact in tumor cells. According to literature, IFNb activate the p53 transcription and components of IFN system effect its function to p53/p14arf pathway. In this project, a series of tools was constructed to explore interactions between p53 and IFNb. The first tool, a cellular lineage derivative of B16 with expression of p53 reduced by miRNA. We also construct plasmidial and adenoviral vectors carriers of cDNAs for eGFP, Luciferase, p53 or IFNb. The vectors are used to introduce these factors, alone or agreed, in the target cell. Even confirming the activity of p53 or IFNb alone, an additive effect of these factors combined was not observed with this type of assay. Future studies of the possible interactions between p53 and IFNb pathways will have the benefit of the tools constructed in this project.

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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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Books on the topic "P53 Genes"

1

p53. Austin, Texas, USA: Landes Bioscience, 2011.

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A, Maxwell Steven, and Roth Jack A, eds. p53 suppressor gene. New York: Springer-Verlag, 1995.

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The p53 family: A subject collection from Cold Spring Harbor Perspectives in biology. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory Press, 2010.

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Shartava, Tsisana. DNA research, genetics, and cell biology. Hauppauge, N.Y: Nova Science Publishers, 2011.

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Hainaut, Pierre, Magali Olivier, and Klas G. Wiman. p53 in the Clinics. Springer, 2014.

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Hainaut, Pierre, Magali Olivier, and Klas G. Wiman. p53 in the Clinics. Springer, 2012.

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Sumitra, Deb, and Deb Swati Palit, eds. p53 protocols. Totowa, N.J: Humana Press, 2003.

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Cheng, Ronshan. Ras oncogenes and p53 suppressor genes in fish carcinogenesis models. 1995.

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M, Klijn Jan G., and European School of Oncology, eds. Prognostic and predictive value of p53. Amsterdam: Elsevier, 1997.

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Al-Mohanna, Mai Abudullah Fahad. Roles of p53 and p16 tumor suppressor genes in the cellular response to ultraviolet light. 2003.

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Book chapters on the topic "P53 Genes"

1

Haupt, Ygal, Sheldon Rowan, Eitan Shaulian, Eyal Gottlieb, Elisheva Yonish-Rouach, Karen Vousden, and Moshe Oren. "P53-Mediated Apoptosis." In Cancer Genes, 83–101. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4615-5895-8_5.

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Murphy, Maureen, and Arnold J. Levine. "The role of p53 in apoptosis." In Apoptosis Genes, 5–35. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5287-1_2.

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Zamamiri-Davis, Faith A., and Gerard P. Zambetti. "p53 Tumor-Suppressor Genes." In Cell Cycle and Growth Control, 635–66. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2004. http://dx.doi.org/10.1002/0471656437.ch19.

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Sang, Nianli, and Antonio Giordano. "Cell Cycle Genes: pRb and p53." In When Cells Die II, 339–79. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2005. http://dx.doi.org/10.1002/0471476501.ch14.

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Finlay, Cathy A. "Normal and malignant growth control by p53." In Oncogenes and Tumor Suppressor Genes in Human Malignancies, 327–44. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3088-6_17.

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Zhang, Lifang, Weimin Gao, and Phouthone Keohavong. "Analysis of Mutations in K-ras and p53 Genes in Sputum and Plasma Samples." In Molecular Toxicology Protocols, 373–94. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0223-2_22.

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Mukhopadhyay, Tapas, Steven A. Maxwell, and Jack A. Roth. "Gene Structure." In p53 Suppressor Gene, 13–18. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22275-1_2.

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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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Mukhopadhyay, Tapas, Steven A. Maxwell, and Jack A. Roth. "Biophysical and Biochemical Properties of the p53 Protein." In p53 Suppressor Gene, 55–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22275-1_4.

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Mukhopadhyay, Tapas, Steven A. Maxwell, and Jack A. Roth. "Regulation and Modulation of the Function of p53." In p53 Suppressor Gene, 73–112. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22275-1_5.

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Conference papers on the topic "P53 Genes"

1

Kumar Das, Jayanta, Suvankar Ghosh, Ranjeet Kumar Rout, and Pabitra Pal Choudhury. "A Study of P53 Gene and its Regulatory Genes Network." In 2018 8th International Conference on Cloud Computing, Data Science & Engineering (Confluence). IEEE, 2018. http://dx.doi.org/10.1109/confluence.2018.8442820.

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Zaccara, Sara, Toma Tebaldi, Yari Ciribilli, Alessandra Bisio, and Alberto Inga. "Abstract 1408: p53-directed translational control can shape and expand the universe of p53 target genes." 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.am2014-1408.

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Jin, Zhe Xiong, and Bao Qing Wang. "Induction of P53 genes in human hepatoma cells by Geraniin." In 2010 3rd International Conference on Biomedical Engineering and Informatics (BMEI). IEEE, 2010. http://dx.doi.org/10.1109/bmei.2010.5639640.

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Idogawa, Masashi, Yasushi Sasaki, Kohzoh Imai, Yasuhisa Shinomura, and Takashi Tokino. "Abstract 595: Single adenovirus-mediated simultaneous expression of p53 and the artificial microRNAs targeting anti-apoptotic p53 target genes." 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.am10-595.

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DASHZEVEG, Nurmaa, Naoe TAIRA, Yoshio MIKI, and Kiyotsugu YOSHIDA. "Abstract 4950: Discovery of the pro-apoptotic genes induced by tumor suppressor p53." 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.am2012-4950.

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Mittal, Shilpi, Rama Kadamb, Nidhi Bansal, and Daman Saluja. "Abstract 747: p53 activation through stress induction mediates differential regulation of target genes." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-747.

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Idogawa, Masashi, Yasushi Sasaki, Yasuhisa Shinomura, Kohzoh Imai, and Takashi Tokino. "Abstract 1171: Identification of p53 target genes by ChIP-Seq and transcriptome analysis combined with genome-wide p53-binding motif analysisin silico." 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.am2012-1171.

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Azarnier, Ronak Ghanbari, Agatha Zuchelkowski, Philip E. Chung, Zhe Jiang, and Eldad Zacksenhaus. "Abstract 2801: Identification of oncogenic/metastatic driver genes that cooperate with p53 or p53/Rb-loss to induce triple-negative breast cancer." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2801.

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Aptullahoglu, E., JP Wallis, H. Marr, S. Marshall, E. Willmore, and J. Lunec. "PO-445 E7107 treatment results in aberrantly spliced transcripts and protein products of P53 pathway genes." 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-eacr25.468.

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Choi, Jinhyang, David M. Roy, Stephen J. Curtis, Andrea Flesken-Nikitin, Chang-il Hwang, Wei Wang, and Alexander Yu Nikitin. "Abstract 4183: Modeling soft tissue sarcomas by conditional inactivation of p53 and Rb tumor suppressor genes." 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.am10-4183.

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Reports on the topic "P53 Genes"

1

Thornborrow, Edward, and James Manfredi. Differential Activation of p53 Target Genes in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2002. http://dx.doi.org/10.21236/ada405348.

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Li, Hua. Identification of Pro-Differentiation p53 Target Genes and Evaluation of Expression in Normal and Malignant Mammary Gland. Fort Belvoir, VA: Defense Technical Information Center, April 2007. http://dx.doi.org/10.21236/ada471561.

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Connolly, Denise C. Modeling Human Epithelial Ovarian Cancer in Mice by Alteration of Expression of the BRCA1 and/or p53 Genes. Fort Belvoir, VA: Defense Technical Information Center, February 2008. http://dx.doi.org/10.21236/ada485053.

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Connolly, Denise C. Modeling Human Epithelial Ovarian Cancer in Mice by Alteration of Expression of the BRCA1 and/or P53 Genes. Fort Belvoir, VA: Defense Technical Information Center, February 2005. http://dx.doi.org/10.21236/ada436423.

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Niguidula, Nancy J. 4-Aminobiphenyl (4-ABP)-DNA Damage in Breast Tissue and Relationship to p53 Mutation and Polymorphisms of Metabolizing Genes. Fort Belvoir, VA: Defense Technical Information Center, September 2001. http://dx.doi.org/10.21236/ada403392.

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Niguidula, Nancy J., and Regina M. Santella. 4-Aminobiphenyl (4-ABP)-DNA Damage in Breast Tissue and Relationship to p53 Mutations and Polymorphisms of Metabolizing Genes. Fort Belvoir, VA: Defense Technical Information Center, September 2002. http://dx.doi.org/10.21236/ada412857.

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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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Blackburn, Anneke C., and Joseph Jerry. Development of Spontaneous Mammary Tumors in BALB/c-p53+-Mice: Detection of Early Genetic Alterations and the Mapping of BALB/c Susceptibility Genes. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada410279.

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Smith, Sallie, and Joseph Jerry. Development of Spontaneous Mammary Tumors in BALB/c-p53+/-Mice: Detection of Early Genetic Alterations and the Mapping of BALB/c Susceptibility Genes. Fort Belvoir, VA: Defense Technical Information Center, January 2004. http://dx.doi.org/10.21236/ada424523.

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Prabha, Swayam, Vinod D. Labhasetwar, and Jamboor K. Vishwanathan. Nanoparticle-Mediated p53 Gene Therapy for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2003. http://dx.doi.org/10.21236/ada415301.

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