Genomes and Genes
Experts and Doctors on tumor suppressor protein p53 in New York, United States
Locale: New York, United States
Topic: tumor suppressor protein p53
Publications304 found, 100 shown here
- Moynahan M. The cancer connection: BRCA1 and BRCA2 tumor suppression in mice and humans. Oncogene. 2002;21:8994-9007 pubmed..Analysis of Brca1-associated mammary tumors reveals significant similarities to BRCA1-associated breast cancer in regard to high tumor grade, hormone receptor negativity, a high incidence of p53 mutations and genetic instability. ..
- Stoffel A, Chaurushiya M, Singh B, Levine A. Activation of NF-kappaB and inhibition of p53-mediated apoptosis by API2/mucosa-associated lymphoid tissue 1 fusions promote oncogenesis. Proc Natl Acad Sci U S A. 2004;101:9079-84 pubmed..Furthermore, they provide evidence underlying the emerging role of the NF-kappaB signaling pathway in the inhibition of apoptosis. ..
- Poyurovsky M, Priest C, Kentsis A, Borden K, Pan Z, Pavletich N, et al. The Mdm2 RING domain C-terminus is required for supramolecular assembly and ubiquitin ligase activity. EMBO J. 2007;26:90-101 pubmed..We further show that the Mdm2 C-terminus is involved in intramolecular interactions and can set up a platform for direct protein-protein interactions with the E2. ..
- Becker K, Marchenko N, Palacios G, Moll U. A role of HAUSP in tumor suppression in a human colon carcinoma xenograft model. Cell Cycle. 2008;7:1205-13 pubmed..Our data suggest that changes in HAUSP modulate tumor growth and apoptotic sensitivity in vivo. ..
- Schramek D, Sendoel A, Segal J, Beronja S, Heller E, Oristian D, et al. Direct in vivo RNAi screen unveils myosin IIa as a tumor suppressor of squamous cell carcinomas. Science. 2014;343:309-13 pubmed publisher..Myosin IIa is diminished in human SCCs with poor survival, which suggests that in vivo RNAi technology might be useful for identifying potent but low-penetrance tumor suppressors. ..
- Borazanci E, Dang C, Robey R, Bates S, Chabot J, Von Hoff D. Pancreatic Cancer: "A Riddle Wrapped in a Mystery inside an Enigma". Clin Cancer Res. 2017;23:1629-1637 pubmed publisher..i>Clin Cancer Res; 23(7); 1629-37. ©2017 AACRSee all articles in this CCR Focus section, "Pancreatic Cancer: Challenge and Inspiration." ..
- Jiang H, Lin J, Su Z, Herlyn M, Kerbel R, Weissman B, et al. The melanoma differentiation-associated gene mda-6, which encodes the cyclin-dependent kinase inhibitor p21, is differentially expressed during growth, differentiation and progression in human melanoma cells. Oncogene. 1995;10:1855-64 pubmed..Taken together, these studies indicate that mda-6 (p21) may function as a negative regulator of melanoma growth, progression and metastasis. ..
- Relaix F, Wei X, Li W, Pan J, Lin Y, Bowtell D, et al. Pw1/Peg3 is a potential cell death mediator and cooperates with Siah1a in p53-mediated apoptosis. Proc Natl Acad Sci U S A. 2000;97:2105-10 pubmed..The observation that Pw1/Peg3 is necessary for the p53 apoptotic response suggests a pivotal role for this gene in determining cell death versus survival. ..
- Doughty M, De Jager P, Korsmeyer S, Heintz N. Neurodegeneration in Lurcher mice occurs via multiple cell death pathways. J Neurosci. 2000;20:3687-94 pubmed..Our results demonstrate that target deprivation induces a Bax-dependent, p53-independent cell death response in cerebellar granule cells in vivo. In contrast, Bax plays a minor role in GRID2(Lc)-mediated Purkinje cell death. ..
- Marchenko N, Zaika A, Moll U. Death signal-induced localization of p53 protein to mitochondria. A potential role in apoptotic signaling. J Biol Chem. 2000;275:16202-12 pubmed..We propose a model where p53 can contribute to apoptosis by direct signaling at the mitochondria, thereby amplifying the transcription-dependent apoptosis of p53. ..
- Li Y, Raffo A, Drew L, Mao Y, Tran A, Petrylak D, et al. Fas-mediated apoptosis is dependent on wild-type p53 status in human cancer cells expressing a temperature-sensitive p53 mutant alanine-143. Cancer Res. 2003;63:1527-33 pubmed..This model may be a useful tool for dissecting the specific interactions between wild-type p53 and the Fas signal transduction pathway in human cancer cells. ..
- McCarthy E, Celebi J, Baer R, Ludwig T. Loss of Bard1, the heterodimeric partner of the Brca1 tumor suppressor, results in early embryonic lethality and chromosomal instability. Mol Cell Biol. 2003;23:5056-63 pubmed
- Gottifredi V, McKinney K, Poyurovsky M, Prives C. Decreased p21 levels are required for efficient restart of DNA synthesis after S phase block. J Biol Chem. 2004;279:5802-10 pubmed..Thus, p21 down-regulation is multiply determined and is required for the reversibility of the arrest in S phase. ..
- Salazar G, Joshi A, Liu D, Wei H, Persson J, Wolgemuth D. Induction of apoptosis involving multiple pathways is a primary response to cyclin A1-deficiency in male meiosis. Dev Dyn. 2005;234:114-23 pubmed..This finding suggested that p53 may be involved in the process by which the arrested germ cells are removed from the seminiferous tubules but that other pathways function as well to ensure removal of the arrested spermatocytes. ..
- Wells B, Yoshida E, Johnston L. Compensatory proliferation in Drosophila imaginal discs requires Dronc-dependent p53 activity. Curr Biol. 2006;16:1606-15 pubmed..Our data suggest that dp53 may carry out an ancestral function that promotes animal survival through the coordination of responses leading to compensatory growth after tissue damage. ..
- Gamper A, Roeder R. Multivalent binding of p53 to the STAGA complex mediates coactivator recruitment after UV damage. Mol Cell Biol. 2008;28:2517-27 pubmed publisher..Based on our data, we propose a cooperative and modular binding mode for the recruitment of coactivator complexes to promoters. ..
- Borah J, Mujtaba S, Karakikes I, Zeng L, Muller M, Patel J, et al. A small molecule binding to the coactivator CREB-binding protein blocks apoptosis in cardiomyocytes. Chem Biol. 2011;18:531-41 pubmed publisher..Our study suggests small molecule modulation of acetylation-mediated interactions in gene transcription as a new approach to therapeutic interventions of human disorders such as myocardial ischemia. ..
- Paris F, Fuks Z, Kang A, Capodieci P, Juan G, Ehleiter D, et al. Endothelial apoptosis as the primary lesion initiating intestinal radiation damage in mice. Science. 2001;293:293-7 pubmed..This study provides a basis for new approaches to prevent radiation damage to the bowel. ..
- Bernardi R, Scaglioni P, Bergmann S, Horn H, Vousden K, Pandolfi P. PML regulates p53 stability by sequestering Mdm2 to the nucleolus. Nat Cell Biol. 2004;6:665-72 pubmed..These findings demonstrate an unexpected role of PML in the nucleolar network for tumour suppression. ..
- Arva N, Gopen T, Talbott K, Campbell L, Chicas A, White D, et al. A chromatin-associated and transcriptionally inactive p53-Mdm2 complex occurs in mdm2 SNP309 homozygous cells. J Biol Chem. 2005;280:26776-87 pubmed..Our data suggest that overproduction of Mdm2, resulting from a naturally occurring SNP, inhibits chromatin-bound p53 from activating the transcription of its target genes. ..
- Nair V. Activation of p53 signaling initiates apoptotic death in a cellular model of Parkinson's disease. Apoptosis. 2006;11:955-66 pubmed..Thus, these data suggest that activation of p53 signaling immediately after neurotoxin exposure acts as an initiating factor to mediate apoptosis in dopaminergic cells. ..
- Brooks C, Li M, Hu M, Shi Y, Gu W. The p53--Mdm2--HAUSP complex is involved in p53 stabilization by HAUSP. Oncogene. 2007;26:7262-6 pubmed..These findings reveal the complication of HAUSP-mediated effects in the p53-Mdm2 interplay. It also has important implications for the development of novel chemotherapeutic compounds aimed at blocking this protein-protein interaction. ..
- Yee H, Yie T, Goldberg J, Wong K, Rom W. Immunohistochemical study of fibrosis and adenocarcinoma in dominant-negative p53 transgenic mice exposed to chrysotile asbestos and benzo(a)pyrene. J Environ Pathol Toxicol Oncol. 2008;27:267-76 pubmed
- Sun X, Mittal K. MIB-1 (Ki-67), estrogen receptor, progesterone receptor, and p53 expression in atypical cells in uterine symplastic leiomyomas. Int J Gynecol Pathol. 2010;29:51-4 pubmed publisher..3+/-3.9%). Therefore, rather than being degenerative in nature, the atypical cells are actively proliferating. ..
- Kon N, Zhong J, Qiang L, Accili D, Gu W. Inactivation of arf-bp1 induces p53 activation and diabetic phenotypes in mice. J Biol Chem. 2012;287:5102-11 pubmed publisher..These findings underscore an important role of ARF-BP1 in maintaining ?-cell homeostasis in aging mice and reveal that the stability of p53 is critically regulated by ARF-BP1 in vivo. ..
- Cotignola J, Chou J, Roy P, Mitra N, Busam K, Halpern A, et al. Investigation of the effect of MDM2 SNP309 and TP53 Arg72Pro polymorphisms on the age of onset of cutaneous melanoma. J Invest Dermatol. 2012;132:1471-8 pubmed publisher..Further studies are needed to determine whether a nearby functional polymorphism is responsible for this effect in premenopausal women. ..
- Aksoy O, Chicas A, Zeng T, Zhao Z, McCurrach M, Wang X, et al. The atypical E2F family member E2F7 couples the p53 and RB pathways during cellular senescence. Genes Dev. 2012;26:1546-57 pubmed publisher..Mechanistically, E2F7 compensates for the loss of RB in repressing mitotic E2F target genes. Together, our results identify a causal role for E2F7 in cellular senescence and uncover a novel link between the RB and p53 pathways. ..
- Amengual J, Clark Garvey S, Kalac M, Scotto L, Marchi E, Neylon E, et al. Sirtuin and pan-class I/II deacetylase (DAC) inhibition is synergistic in preclinical models and clinical studies of lymphoma. Blood. 2013;122:2104-13 pubmed publisher..We report herein on the preclinical and clinical activity of this targeted strategy in aggressive lymphomas. This trial was registered at www.clinicaltrials.gov as #NCT00691210. ..
- Cong F, Zou X, Hinrichs K, Calame K, Goff S. Inhibition of v-Abl transformation by p53 and p19ARF. Oncogene. 1999;18:7731-9 pubmed..We also show that p53 is not the mediator of v-Abl toxicity in immortal fibroblasts and does not determine the susceptibility of immortal fibroblasts to v-Abl transformation. ..
- Li M, Luo J, Brooks C, Gu W. Acetylation of p53 inhibits its ubiquitination by Mdm2. J Biol Chem. 2002;277:50607-11 pubmed..This study has significant implications regarding a general mechanism by which protein acetylation modulates ubiquitination-dependent proteasome proteolysis. ..
- Murray J, Morgello S. Polyomaviruses and primary central nervous system lymphomas. Neurology. 2004;63:1299-301 pubmed..The authors conclude that polyomaviruses are unlikely to be related to the pathogenesis of most PCNSL. ..
- Perez de Castro I, Benet M, Jimenez M, Alzabin S, Malumbres M, Pellicer A. Mouse p10, an alternative spliced form of p15INK4b, inhibits cell cycle progression and malignant transformation. Cancer Res. 2005;65:3249-56 pubmed
- Parhar P, Ezer R, Shao Y, Allen J, Miller D, Newcomb E. Possible association of p53 codon 72 polymorphism with susceptibility to adult and pediatric high-grade astrocytomas. Brain Res Mol Brain Res. 2005;137:98-103 pubmed..002). Our results suggest a possible association between P53 Arg72Pro polymorphisms and susceptibility to brain tumors, particularly high-grade astrocytomas. ..
- Gao Z, Shao Y, Jiang X. Essential roles of the Bcl-2 family of proteins in caspase-2-induced apoptosis. J Biol Chem. 2005;280:38271-5 pubmed..Collectively, these results indicate that proteolytic activation of Bid and the subsequent induction of the mitochondrial apoptotic pathway through Bax/Bak is essential for apoptosis triggered by caspase-2. ..
- Talos F, Petrenko O, Mena P, Moll U. Mitochondrially targeted p53 has tumor suppressor activities in vivo. Cancer Res. 2005;65:9971-81 pubmed..Our in vivo data on the direct mitochondrial apoptotic p53 program lays the groundwork to further investigate its efficacy and safety and to address its possible therapeutic value in the future. ..
- Shakya R, Szabolcs M, McCarthy E, Ospina E, Basso K, Nandula S, et al. The basal-like mammary carcinomas induced by Brca1 or Bard1 inactivation implicate the BRCA1/BARD1 heterodimer in tumor suppression. Proc Natl Acad Sci U S A. 2008;105:7040-5 pubmed publisher..The remarkable similarities between the mammary carcinomas of Bard1-, Brca1-, and Bard1/Brca1-mutant mice indicate that the tumor suppressor activities of both genes are mediated through the BRCA1/BARD1 heterodimer. ..
- Zhao H, Traganos F, Dobrucki J, Wlodkowic D, Darzynkiewicz Z. Induction of DNA damage response by the supravital probes of nucleic acids. Cytometry A. 2009;75:510-9 pubmed publisher..The data indicate that supravital use of Ho 42, DRAQ5, and DCV induces various degrees of DDR, including activation of ATM, Chk2 and p53, which may have significant consequences on regulatory cell cycle pathways and apoptosis. ..
- Song T, Fong Y, Cho S, Gonen M, Hezel M, Tuorto S, et al. Comparison of hepatocellular carcinoma in American and Asian patients by tissue array analysis. J Surg Oncol. 2012;106:84-8 pubmed publisher..These data likely correlate with differences in molecular pathogenesis of HCC based on racial and regional differences. These findings may have implications in choice of molecular targeted therapies based on patient ethnicity. ..
- Madka V, Mohammed A, Li Q, Zhang Y, Biddick L, Patlolla J, et al. Targeting mTOR and p53 Signaling Inhibits Muscle Invasive Bladder Cancer In Vivo. Cancer Prev Res (Phila). 2016;9:53-62 pubmed publisher..A combination of CP and rapamycin may be a promising method of inhibiting muscle-invasive urothelial transitional cell carcinoma. ..
- Mai W, Gosa L, Daniëls V, Ta L, Tsang J, Higgins B, et al. Cytoplasmic p53 couples oncogene-driven glucose metabolism to apoptosis and is a therapeutic target in glioblastoma. Nat Med. 2017;23:1342-1351 pubmed publisher..Together, these studies identify a crucial link among oncogene signaling, glucose metabolism, and cytoplasmic p53, which may potentially be exploited for combination therapy in GBM and possibly other malignancies. ..
- Gorina S, Pavletich N. Structure of the p53 tumor suppressor bound to the ankyrin and SH3 domains of 53BP2. Science. 1996;274:1001-5 pubmed..The six most frequently observed p53 mutations disrupt 53BP2 binding in vitro. The structure provides evidence that the 53BP2-p53 complex forms in vivo and may have a critical role in the p53 pathway of tumor suppression. ..
- Ferbeyre G, de Stanchina E, Querido E, Baptiste N, Prives C, Lowe S. PML is induced by oncogenic ras and promotes premature senescence. Genes Dev. 2000;14:2015-27 pubmed..These results imply that PML acts with Rb and p53 to promote ras-induced senescence and provide new insights into PML regulation and activity. ..
- Chitale D, Jungbluth A, Marshall D, Leitao M, Hedvat C, Kolb D, et al. Expression of cancer-testis antigens in endometrial carcinomas using a tissue microarray. Mod Pathol. 2005;18:119-26 pubmed..CT antigens CT7, MAGE-A3 and MAGE-A4, but not NY-ESO-1, are expressed in high-grade endometrial carcinomas, and expression of MAGE-A4 is correlated with the presence of overexpressed p53. ..
- Cheng K, Grisendi S, Clohessy J, Majid S, Bernardi R, Sportoletti P, et al. The leukemia-associated cytoplasmic nucleophosmin mutant is an oncogene with paradoxical functions: Arf inactivation and induction of cellular senescence. Oncogene. 2007;26:7391-400 pubmed..These findings identify for the first time NPMc+ as an oncogene and shed new unexpected light on its mechanism of action. ..
- Kang H, Feng Z, Sun Y, Atwal G, Murphy M, Rebbeck T, et al. Single-nucleotide polymorphisms in the p53 pathway regulate fertility in humans. Proc Natl Acad Sci U S A. 2009;106:9761-6 pubmed publisher..These results also provide a plausible explanation for the evolutionary positive selection of some alleles in the p53 pathway and demonstrate the alleles in the p53 pathway as a good example of antagonistic pleiotropy. ..
- Osman A, Neskey D, Katsonis P, Patel A, Ward A, Hsu T, et al. Evolutionary Action Score of TP53 Coding Variants Is Predictive of Platinum Response in Head and Neck Cancer Patients. Cancer Res. 2015;75:1205-15 pubmed publisher..Prospective evaluation of this novel scoring system should enable more precise treatment selection for patients with HNSCC. ..
- Shieh S, Ahn J, Tamai K, Taya Y, Prives C. The human homologs of checkpoint kinases Chk1 and Cds1 (Chk2) phosphorylate p53 at multiple DNA damage-inducible sites. Genes Dev. 2000;14:289-300 pubmed
- Luo J, Nikolaev A, Imai S, Chen D, Su F, Shiloh A, et al. Negative control of p53 by Sir2alpha promotes cell survival under stress. Cell. 2001;107:137-48 pubmed..These results have significant implications regarding an important role for Sir2alpha in modulating the sensitivity of cells in p53-dependent apoptotic response and the possible effect in cancer therapy. ..
- Zhang Y, Ahsan H, Chen Y, Lunn R, Wang L, Chen S, et al. High frequency of promoter hypermethylation of RASSF1A and p16 and its relationship to aflatoxin B1-DNA adduct levels in human hepatocellular carcinoma. Mol Carcinog. 2002;35:85-92 pubmed..No association was found between methylation status and p53 status. These results suggest the hypothesis that exposure to environmental carcinogens may be involved in altered methylation of genes involved in cancer development. ..
- Yalcin S, Zhang X, Luciano J, Mungamuri S, Marinkovic D, Vercherat C, et al. Foxo3 is essential for the regulation of ataxia telangiectasia mutated and oxidative stress-mediated homeostasis of hematopoietic stem cells. J Biol Chem. 2008;283:25692-705 pubmed publisher..Our studies demonstrate that Foxo3 represses ROS in part via regulation of ATM and that this repression is required for maintenance of the hematopoietic stem cell pool. ..
- Kon N, Kobayashi Y, Li M, Brooks C, Ludwig T, Gu W. Inactivation of HAUSP in vivo modulates p53 function. Oncogene. 2010;29:1270-9 pubmed publisher..These data show that Hausp has a critical role in regulating the p53-Mdm2 pathway. ..
- Chen D, Shan J, Zhu W, Qin J, Gu W. Transcription-independent ARF regulation in oncogenic stress-mediated p53 responses. Nature. 2010;464:624-7 pubmed publisher..These findings reveal the dynamic feature of the ARF-p53 pathway and suggest that transcription-independent mechanisms are critically involved in ARF regulation during responses to oncogenic stress. ..
- Okamoto K, Li H, Jensen M, Zhang T, Taya Y, Thorgeirsson S, et al. Cyclin G recruits PP2A to dephosphorylate Mdm2. Mol Cell. 2002;9:761-71 pubmed..Cyclin G expression also results in reduced phosphorylation of human Hdm2 at S166. Thus, our data suggest that cyclin G recruits PP2A in order to modulate the phosphorylation of Mdm2 and thereby to regulate both Mdm2 and p53. ..
- St Clair S, Giono L, Varmeh Ziaie S, Resnick Silverman L, Liu W, Padi A, et al. DNA damage-induced downregulation of Cdc25C is mediated by p53 via two independent mechanisms: one involves direct binding to the cdc25C promoter. Mol Cell. 2004;16:725-36 pubmed..Importantly, this is a clear demonstration of p53-mediated transcriptional downregulation that is dependent on sequence-specific DNA binding by p53. ..
- Ryer E, Sakakibara K, Wang C, Sarkar D, Fisher P, Faries P, et al. Protein kinase C delta induces apoptosis of vascular smooth muscle cells through induction of the tumor suppressor p53 by both p38-dependent and p38-independent mechanisms. J Biol Chem. 2005;280:35310-7 pubmed..Together, our data suggest that SMC apoptosis proceeds through a pathway that involves PKCdelta, the intermediary p38 MAPK, and the downstream target tumor suppressor p53. ..
- Kim J, Hake S, Roeder R. The human homolog of yeast BRE1 functions as a transcriptional coactivator through direct activator interactions. Mol Cell. 2005;20:759-70 pubmed..Importantly, they thus provide a paradigm for BRE1 recruitment and function in both yeast and higher eukaryotes. ..
- Ohkubo S, Tanaka T, Taya Y, Kitazato K, Prives C. Excess HDM2 impacts cell cycle and apoptosis and has a selective effect on p53-dependent transcription. J Biol Chem. 2006;281:16943-50 pubmed..Thus, HDM2 can selectively down-regulate the transcription function of p53 without either degrading p53 or affecting the interaction of p53 with target promoters. ..
- Nguyen M, Kraft R, Aubert M, Goodwin E, DiMaio D, Blaho J. p53 and hTERT determine sensitivity to viral apoptosis. J Virol. 2007;81:12985-95 pubmed..Given the universality of the apoptotic antiviral response, p53 and telomerase regulation will likely be important for counteracting host defenses in many other viral infections. ..
- Stracker T, Couto S, Cordon Cardo C, Matos T, Petrini J. Chk2 suppresses the oncogenic potential of DNA replication-associated DNA damage. Mol Cell. 2008;31:21-32 pubmed publisher..These data suggest that Chk2 suppresses the oncogenic potential of DNA damage arising during S and G2 phases of the cell cycle. ..
- Ding J, He G, Gong W, Wen W, Sun W, Ning B, et al. Effects of nickel on cyclin expression, cell cycle progression and cell proliferation in human pulmonary cells. Cancer Epidemiol Biomarkers Prev. 2009;18:1720-9 pubmed publisher..These results will not only deepen our understanding of the molecular mechanism involved in nickel carcinogenecity, but also lead to the further study on chemoprevention of nickel-associated human cancer. ..
- Inoue H, Giannakopoulos S, Parkhurst C, Matsumura T, Kono E, Furukawa T, et al. Target genes of the largest human SWI/SNF complex subunit control cell growth. Biochem J. 2011;434:83-92 pubmed publisher..Chromatin immunoprecipitation and reporter assays suggested that hOsa2 had a direct effect on c-myc and p21 promoter activity. Thus hOsa2 plays an important role in controlling genes regulating the cell cycle. ..
- Laptenko O, Prives C. p53: master of life, death, and the epigenome. Genes Dev. 2017;31:955-956 pubmed publisher..Their findings indicate that p53 may exert its "guardian of genome" duties at least in part via safeguarding the epigenome of ESCs. ..
- Zaika A, Marchenko N, Moll U. Cytoplasmically "sequestered" wild type p53 protein is resistant to Mdm2-mediated degradation. J Biol Chem. 1999;274:27474-80 pubmed..This system provides evidence for an important level of regulation of Mdm2-directed p53 destruction in vivo that is linked to p53 modification. ..
- Jiang J, Denner L, Ling Y, Li J, Davis A, Wang Y, et al. Double blockade of cell cycle at g(1)-s transition and m phase by 3-iodoacetamido benzoyl ethyl ester, a new type of tubulin ligand. Cancer Res. 2002;62:6080-8 pubmed..Besides being a novel lead for the design of new anticancer tubulin ligands, the activity of 3-IAABE in the cell cycle may also help us to understand the molecular pharmacology of microtubule-active drugs...
- Shieh S, Ikeda M, Taya Y, Prives C. DNA damage-induced phosphorylation of p53 alleviates inhibition by MDM2. Cell. 1997;91:325-34 pubmed..Our studies provide a plausible mechanism by which the induction of p53 can be modulated by DNA-PK (or other protein kinases with similar specificity) in response to DNA damage. ..
- Raffo A, Kim A, Fine R. Formation of nuclear Bax/p53 complexes is associated with chemotherapy induced apoptosis. Oncogene. 2000;19:6216-28 pubmed..Additionally, the human prostate cancer cell line, LNCaP, also formed nuclear Bax/p53 complexes only after apoptosis was induced by paclitaxel. ..
- Li M, Chen D, Shiloh A, Luo J, Nikolaev A, Qin J, et al. Deubiquitination of p53 by HAUSP is an important pathway for p53 stabilization. Nature. 2002;416:648-53 pubmed..These findings reveal an important mechanism by which p53 can be stabilized by direct deubiquitination and also imply that HAUSP might function as a tumour suppressor in vivo through the stabilization of p53. ..
- Xie S, Wu H, Wang Q, Kunicki J, Thomas R, Hollingsworth R, et al. Genotoxic stress-induced activation of Plk3 is partly mediated by Chk2. Cell Cycle. 2002;1:424-9 pubmed..Furthermore, ectopic expression Chk2 activates cellular Plk3. Together, our studies suggest Chk2 may mediate direct activation of Plk3 in response to genotoxic stresses. ..
- Mathur M, Das S, Samuels H. PSF-TFE3 oncoprotein in papillary renal cell carcinoma inactivates TFE3 and p53 through cytoplasmic sequestration. Oncogene. 2003;22:5031-44 pubmed..Thus, PSF-TFE3 is a promising target for the treatment for a subset of renal cell carcinomas. ..
- Chen D, Kon N, Li M, Zhang W, Qin J, Gu W. ARF-BP1/Mule is a critical mediator of the ARF tumor suppressor. Cell. 2005;121:1071-83 pubmed..As such, ARF-BP1 may serve as a potential target for therapeutic intervention in tumors regardless of p53 status. ..
- Ackerman A, Mones J. Solar (actinic) keratosis is squamous cell carcinoma. Br J Dermatol. 2006;155:9-22 pubmed
- Yamamoto K, Nihrane A, Aglipay J, Sironi J, ARKIN S, Lipton J, et al. Upregulated ATM gene expression and activated DNA crosslink-induced damage response checkpoint in Fanconi anemia: implications for carcinogenesis. Mol Med. 2008;14:167-74 pubmed publisher..Our results suggest that cancer in FA may arise from selection for cells that escape from a chronically activated DDR checkpoint. ..
- Ranuncolo S, Wang L, Polo J, Dell Oso T, Dierov J, Gaymes T, et al. BCL6-mediated attenuation of DNA damage sensing triggers growth arrest and senescence through a p53-dependent pathway in a cell context-dependent manner. J Biol Chem. 2008;283:22565-72 pubmed publisher..The data suggest that targeted re-activation of TP53 could be of therapeutic value in centroblast-derived lymphomas. ..
- Li H, Balajee A, Su T, Cen B, Hei T, Weinstein I. The HINT1 tumor suppressor regulates both gamma-H2AX and ATM in response to DNA damage. J Cell Biol. 2008;183:253-65 pubmed publisher..Our findings suggest that the tumor suppressor function of HINT1 is caused by, at least in part, its normal role in enhancing cellular responses to DNA damage by regulating the functions of both gamma-H2AX and ATM. ..
- Mezentsev A, Amundson S. Global gene expression responses to low- or high-dose radiation in a human three-dimensional tissue model. Radiat Res. 2011;175:677-88 pubmed publisher..HNF4A protein levels and phosphorylation were found to increase in tissues and cells after low- but not high-dose irradiation. ..
- Marmorstein L, Ouchi T, Aaronson S. The BRCA2 gene product functionally interacts with p53 and RAD51. Proc Natl Acad Sci U S A. 1998;95:13869-74 pubmed..These findings demonstrate that BRCA2 physically and functionally interacts with two key components of cell cycle control and DNA repair pathways. Thus, BRCA2 likely participates with p53 and RAD51 in maintaining genome integrity. ..
- Mujtaba S, He Y, Zeng L, Yan S, Plotnikova O, Sachchidanand -, et al. Structural mechanism of the bromodomain of the coactivator CBP in p53 transcriptional activation. Mol Cell. 2004;13:251-63 pubmed..Using structural and biochemical analyses, we define the molecular determinants for the specificity of this molecular recognition. ..
- Su Z, Emdad L, Sarkar D, Randolph A, Valerie K, Yacoub A, et al. Potential molecular mechanism for rodent tumorigenesis: mutational generation of Progression Elevated Gene-3 (PEG-3). Oncogene. 2005;24:2247-55 pubmed..The inherent property of PEG-3 to function as a dominant negative of the growth inhibitory property of GADD34 might rescue cells from DNA damage-induced apoptosis leading to growth independence and tumorigenesis. ..
- Ouchi M, Ouchi T. Role of IFI16 in DNA damage and checkpoint. Front Biosci. 2008;13:236-9 pubmed..More recently, it has been shown that levels of IFI16 are increased by oxidative stress. Together, these results illustrate that IFI16 is involved in DNA damage signaling and cell cycle checkpoint. ..
- Manfredi J. The Mdm2-p53 relationship evolves: Mdm2 swings both ways as an oncogene and a tumor suppressor. Genes Dev. 2010;24:1580-9 pubmed publisher..Hence, Mdm2 is proving to be a key player in human cancer in its own right, and thus an important target for therapeutic intervention. ..
- Pasqualucci L, Dominguez Sola D, Chiarenza A, Fabbri G, Grunn A, Trifonov V, et al. Inactivating mutations of acetyltransferase genes in B-cell lymphoma. Nature. 2011;471:189-95 pubmed publisher..These results identify CREBBP/EP300 mutations as a major pathogenetic mechanism shared by common forms of B-cell non-Hodgkin's lymphoma, with direct implications for the use of drugs targeting acetylation/deacetylation mechanisms. ..
- Pires M, Hopkins B, Saal L, PARSONS R. Alterations of EGFR, p53 and PTEN that mimic changes found in basal-like breast cancer promote transformation of human mammary epithelial cells. Cancer Biol Ther. 2013;14:246-53 pubmed publisher..Consideration should be given to targeting EGFR and restoring p53 and PTEN signaling simultaneously as a strategy for treatment of this subtype of breast cancer. ..
- Rickman D, Beltran H, Demichelis F, Rubin M. Biology and evolution of poorly differentiated neuroendocrine tumors. Nat Med. 2017;23:1-10 pubmed publisher..We discuss the shared genomic alterations of these tumors independently of their site of origin, and we explore potential therapeutic strategies on the basis of recent biological findings. ..
- Jayaraman L, Murthy K, Zhu C, Curran T, Xanthoudakis S, Prives C. Identification of redox/repair protein Ref-1 as a potent activator of p53. Genes Dev. 1997;11:558-70 pubmed..Importantly, we have also determined that Ref-1 can stimulate p53 transactivation in vivo. This is the first example of a noncovalent protein modifier of p53 function identified in cells. ..
- Prives C, Hall P. The p53 pathway. J Pathol. 1999;187:112-26 pubmed..The need for bridging the gap between reductionist, biochemical and biophysical studies and biological and genetic analysis is emphasized. Only this will provide the needed framework for utilizing the information in clinical care. ..
- Jin S, Martinek S, Joo W, Wortman J, Mirkovic N, Sali A, et al. Identification and characterization of a p53 homologue in Drosophila melanogaster. Proc Natl Acad Sci U S A. 2000;97:7301-6 pubmed..It appears that p53 is structurally and functionally conserved from flies to mammals. Drosophila will provide a useful genetic system to the further study of the p53 network. ..
- Idrees M, Schlosshauer P, Li G, Burstein D. GLUT1 and p63 expression in endometrial intraepithelial and uterine serous papillary carcinoma. Histopathology. 2006;49:75-81 pubmed..GLUT1 expression may be induced by hypoxia-related as well as other mechanisms. ..
- Momota H, Shih A, Edgar M, Holland E. c-Myc and beta-catenin cooperate with loss of p53 to generate multiple members of the primitive neuroectodermal tumor family in mice. Oncogene. 2008;27:4392-401 pubmed publisher..These data provide insights into the biology and classification of human PNETs and suggest that multiple tumor types or variants can be generated from a fixed set of genetic abnormalities. ..