Genomes and Genes
Gene Symbol: Trp53
Description: transformation related protein 53
Alias: Tp53, bbl, bfy, bhy, p44, p53, cellular tumor antigen p53, mutant p53, p53 cellular tumor antigen, tumor suppressor p53, tumor supressor p53
Publications224 found, 100 shown here
- Mdm2 promotes the rapid degradation of p53Y Haupt
Lautenberg Center for General and Tumor Immunology, The Hebrew University Haddassah Medical School, Jerusalem, Israel
Nature 387:296-9. 1997..Raised amounts of Mdm2 strongly repress mutant p53 accumulation in tumour-derived cells...
- Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4aM Serrano
Cold Spring Harbor Laboratory, New York 11724, USA
Cell 88:593-602. 1997..of primary cells by ras requires either a cooperating oncogene or the inactivation of tumor suppressors such as p53 or p16...
- Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumoursL A Donehower
Division of Molecular Virology, Baylor College of Medicine, Houston, Texas 77030
Nature 356:215-21. 1992Mutations in the p53 tumour-suppressor gene are the most frequently observed genetic lesions in human cancers...
- Tumor spectrum analysis in p53-mutant miceT Jacks
Center for Cancer Research, Massachusetts Institute of Technology, Cambridge 02139
Curr Biol 4:1-7. 1994The p53 tumor suppressor gene is mutated in a large percentage of human malignancies, including tumors of the colon, breast, lung and brain. Individuals who inherit one mutant allele of p53 are susceptible to a wide range of tumor types...
- Regulation of p53 stability by Mdm2M H Kubbutat
ABL Basic Research Program, NCI FCRDC, Frederick, Maryland 21702 1201, USA
Nature 387:299-303. 1997The tumour-suppressor p53 is a short-lived protein that is maintained at low, often undetectable, levels in normal cells...
- Oncogene-induced senescence as an initial barrier in lymphoma developmentMelanie Braig
Charité Universitätsmedizin Berlin Haematology Oncology, 13353 Berlin, Germany
Nature 436:660-5. 2005..Here we show that Emicro-N-Ras transgenic mice harbouring targeted heterozygous lesions at the Suv39h1, or the p53 locus for comparison, succumb to invasive T-cell lymphomas that lack expression of Suv39h1 or p53, respectively...
- The mdm-2 oncogene product forms a complex with the p53 protein and inhibits p53-mediated transactivationJ Momand
Department of Molecular Biology, Lewis Thomas Laboratory, Princeton University, New Jersey 08544 1014
Cell 69:1237-45. 1992..phosphoprotein with an apparent molecular mass of 90 kd (p90) that forms a complex with both mutant and wild-type p53 protein has been characterized, purified, and identified...
- p53 induces differentiation of mouse embryonic stem cells by suppressing Nanog expressionTongxiang Lin
Section of Molecular Biology, Division of Biological Sciences, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093 0322, USA
Nat Cell Biol 7:165-71. 2005The tumour suppressor p53 becomes activated in response to upstream stress signals, such as DNA damage, and causes cell-cycle arrest or apoptosis...
- p53 and Pten control neural and glioma stem/progenitor cell renewal and differentiationHongwu Zheng
Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts 02115, USA
Nature 455:1129-33. 2008..secondary GBM subtype evolves from the slow progression of a low-grade disease that classically possesses PDGF and TP53 events...
- Distinct p53 transcriptional programs dictate acute DNA-damage responses and tumor suppressionColleen A Brady
Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA
Cell 145:571-83. 2011The molecular basis for p53-mediated tumor suppression remains unclear. Here, to elucidate mechanisms of p53 tumor suppression, we use knockin mice expressing an allelic series of p53 transcriptional activation mutants...
- A model for p53-induced apoptosisK Polyak
The Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
Nature 389:300-5. 1997The inactivation of the p53 gene in a large proportion of human cancers has inspired an intense search for the encoded protein's physiological and biological properties...
- Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomasWen Xue
Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA
Nature 445:656-60. 2007..b>p53 is an important tumour suppressor that acts to restrict proliferation in response to DNA damage or deregulation of ..
- 53BP1 promotes non-homologous end joining of telomeres by increasing chromatin mobilityNadya Dimitrova
The Rockefeller University, 1230 York Avenue, New York, New York 10065, USA
Nature 456:524-8. 2008....
- Telomere dysfunction promotes non-reciprocal translocations and epithelial cancers in miceS E Artandi
Department of Adult Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
Nature 406:641-5. 2000..Here we provide evidence that telomere attrition in ageing telomerase-deficient p53 mutant mice promotes the development of epithelial cancers by a process of fusion-bridge breakage that leads to the ..
- Restoration of p53 function leads to tumour regression in vivoAndrea Ventura
Center for Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA
Nature 445:661-5. 2007..Although loss of p53 function is a common feature of human cancers, it is not known whether sustained inactivation of this or other ..
- Identification of conserved gene expression features between murine mammary carcinoma models and human breast tumorsJason I Herschkowitz
Lineberger Comprehensive Cancer Center
Genome Biol 8:R76. 2007..To address this need, we characterized mammary tumor gene expression profiles from 13 different murine models using DNA microarrays and compared the resulting data to those from human breast tumors...
- Trp53R172H and KrasG12D cooperate to promote chromosomal instability and widely metastatic pancreatic ductal adenocarcinoma in miceSunil R Hingorani
Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
Cancer Cell 7:469-83. 2005..requirements for pancreatic ductal adenocarcinoma (PDA), we have targeted concomitant endogenous expression of Trp53(R172H) and Kras(G12D) to the mouse pancreas, revealing the cooperative development of invasive and widely ..
- Mutant p53 gain of function in two mouse models of Li-Fraumeni syndromeKenneth P Olive
Center for Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139, USA
Cell 119:847-60. 2004..is commonly altered in human tumors, predominantly through missense mutations that result in accumulation of mutant p53 protein. These mutations may confer dominant-negative or gain-of-function properties to p53...
- Delayed ageing through damage protection by the Arf/p53 pathwayAnder Matheu
Tumor Suppression Group, Spanish National Cancer Research Centre CNIO, Madrid 28029, Spain
Nature 448:375-9. 2007..pathway formed by the alternative reading frame protein of the Cdkn2a locus (Arf) and by p53 (also called Trp53) plays a central part in the detection and elimination of cellular damage, and this constitutes the basis of its ..
- mdm2 expression is induced by wild type p53 activityY Barak
Department of Chemical Immunology, Weizmann Institute of Science, Rehovot, Israel
EMBO J 12:461-8. 1993We have recently characterized a 95 kDa protein, p95, which exhibits enhanced binding to temperature-sensitive p53 (ts-p53) when cells are shifted down to 32...
- High-frequency developmental abnormalities in p53-deficient miceJ F Armstrong
Department of Pathology, University Medical School, Edinburgh, UK
Curr Biol 5:931-6. 1995Several strains of mice carrying null mutations of the tumour suppressor gene p53 have been developed. It has been reported that homozygous mice from all of these strains develop normally to birth, but then succumb rapidly to neoplasia.
- Gain of function of a p53 hot spot mutation in a mouse model of Li-Fraumeni syndromeGene A Lang
Department of Molecular Genetics, Section of Cancer Genetics, The University of Texas MD Anderson Cancer Center and The University of Texas Graduate School of Biomedical Sciences, 1515 Holcombe Boulevard, Houston, TX 77030, USA
Cell 119:861-72. 2004Individuals with Li-Fraumeni syndrome carry inherited mutations in the p53 tumor suppressor gene and are predisposed to tumor development...
- Chronic cisplatin treatment promotes enhanced damage repair and tumor progression in a mouse model of lung cancerTrudy G Oliver
David H Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, 02139, USA
Genes Dev 24:837-52. 2010..Importantly, we demonstrate that this response does not depend on the tumor suppressor p53 or its transcriptional target, p21...
- p53, the cellular gatekeeper for growth and divisionA J Levine
Department of Molecular Biology, Lewis Thomas Laboratory, Princeton University, New Jersey 08544, USA
Cell 88:323-31. 1997
- p53 mutant mice that display early ageing-associated phenotypesStuart D Tyner
Cell and Molecular Biology Program, Baylor College of Medicine, Houston, TX 77030, USA
Nature 415:45-53. 2002The p53 tumour suppressor is activated by numerous stressors to induce apoptosis, cell cycle arrest, or senescence...
- The differential effects of mutant p53 alleles on advanced murine lung cancerErica L Jackson
Center for Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02141, USA
Cancer Res 65:10280-8. 2005..In contrast to the lung tumors, expression of the point-mutant p53 alleles strongly promoted the development of sinonasal adenocarcinomas compared with simple loss-of-function, ..
- Nuclear FAK promotes cell proliferation and survival through FERM-enhanced p53 degradationSsang Taek Lim
Department of Reproductive Medicine, Moores Cancer Center, University of California, San Diego, 3855 Health Sciences Drive, MC0803, La Jolla, CA 92093, USA
Mol Cell 29:9-22. 2008..Here we show that, during mouse development, FAK inactivation results in p53- and p21-dependent mesodermal cell growth arrest...
- Early inactivation of p53 tumor suppressor gene cooperating with NF1 loss induces malignant astrocytomaYuan Zhu
Center for Developmental Biology and Kent Waldrep Foundation Center for Basic Research on Nerve Growth and Regeneration, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA
Cancer Cell 8:119-30. 2005..prevalent primary brain tumor, is resistant to all known therapies and frequently harbors mutations that inactivate p53 and activate Ras signaling...
- Nucleolar protein NPM interacts with HDM2 and protects tumor suppressor protein p53 from HDM2-mediated degradationSari Kurki
Haartman Institute and Molecular Cancer Biology Research Program, Biomedicum Helsinki, University of Helsinki, P O Box 63, FIN 00014 Helsinki, Helsinki, Finland
Cancer Cell 5:465-75. 2004..an abundant nucleolar phosphoprotein involved in ribosome biogenesis, and interacts with tumor suppressor proteins p53 and Rb...
- p53 suppresses the self-renewal of adult neural stem cellsKonstantinos Meletis
Department of Cell and Molecular Biology, Medical Nobel Institute, Karolinska Institute, SE 171 77 Stockholm, Sweden
Development 133:363-9. 2006..We show here that the prototypical tumor suppressor p53, which plays an important role in brain tumor initiation and growth, is expressed in the neural stem cell ..
- A subset of p53-deficient embryos exhibit exencephalyV P Sah
Department of Biology, Massachusetts Institute of Technology, Cambridge 02139, USA
Nat Genet 10:175-80. 1995..Mice lacking the p53 tumour suppressor gene are predisposed to tumours, but the viability of these animals indicates that p53 function ..
- Functional and physical interactions of the ARF tumor suppressor with p53 and Mdm2T Kamijo
Howard Hughes Medical Institute, St Jude Children s Research Hospital, 332 North Lauderdale, Memphis, TN 38105, USA
Proc Natl Acad Sci U S A 95:8292-7. 1998..p16(INK4a) and p19(ARF), that restrain cell growth by affecting the functions of the retinoblastoma protein and p53, respectively...
- Chk1 is an essential kinase that is regulated by Atr and required for the G(2)/M DNA damage checkpointQ Liu
Howard Hughes Medical Institute, Baylor College of Medicine, Houston, Texas 77030, USA
Genes Dev 14:1448-59. 2000..Taken together, these data indicate that Chk1 plays an essential role in the mammalian DNA damage checkpoint, embryonic development, and tumor suppression, and that Atr regulates Chk1...
- Rescue of early embryonic lethality in mdm2-deficient mice by deletion of p53R Montes de Oca Luna
Department of Molecular Genetics, University of Texas, M D Anderson Cancer Center, Houston 77030, USA
Nature 378:203-6. 1995The gene p53 encodes a transcriptional activator of genes involved in growth arrest, DNA repair and apoptosis. Loss of p53 function contributes to tumour development in vivo...
- Somatic activation of the K-ras oncogene causes early onset lung cancer in miceL Johnson
Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA
Nature 410:1111-6. 2001..This model was further characterized by examining the effects of germline mutations in the tumour suppressor gene p53, which is known to be mutated along with K-ras in human tumours...
- A spatially and temporally restricted mouse model of soft tissue sarcomaDavid G Kirsch
Center for Cancer Research, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, Massachusetts 02139, USA
Nat Med 13:992-7. 2007..Intramuscular delivery of an adenovirus expressing Cre recombinase in mice with conditional mutations in Kras and Trp53 was sufficient to initiate high-grade sarcomas with myofibroblastic differentiation...
- Spontaneous squamous cell carcinoma induced by the somatic inactivation of retinoblastoma and Trp53 tumor suppressorsAna Belén Martínez-Cruz
Molecular Oncology Unit, Division of Biomedicine, Centro de Investigaciones Energeticas, Medioambientales y Tecnologicas, Madrid, Spain
Cancer Res 68:683-92. 2008..Here, we report the functional consequences of the simultaneous elimination of Trp53 and retinoblastoma (Rb) genes in epidermis using Cre-loxP system...
- Loss of p53 induces changes in the behavior of subventricular zone cells: implication for the genesis of glial tumorsSara Gil-Perotin
Department Neuroscience and Cell Biology, Robert Wood Johnson Medical School, Piscataway, New Jersey 08854, USA
J Neurosci 26:1107-16. 2006..This study addresses these questions in mice carrying the deletion of p53, a tumor-suppressor gene expressed in the SVZ...
- Apoptosis in small intestinal epithelial from p53-null mice: evidence for a delayed, p53-independent G2/M-associated cell death after gamma-irradiationA J Merritt
Cancer Research Campaign Department of Epithelial Biology, Christie Hospital Trust, School of Biological Sciences, The University of Manchester, UK
Oncogene 14:2759-66. 1997..cells has been characterized and quantitated after irradiation of mice rendered homozygously null for the p53 gene. In wild-type animals homozygous for p53 a rapid (4...
- Disruption of the ARF-Mdm2-p53 tumor suppressor pathway in Myc-induced lymphomagenesisC M Eischen
Department of Biochemistry, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
Genes Dev 13:2658-69. 1999..The protracted latent period before the onset of frank disease likely reflects the ability of c-Myc to induce a p53-dependent apoptotic program that initially protects animals against tumor formation but is disabled when overtly ..
- Medulloblastoma growth inhibition by hedgehog pathway blockadeDavid M Berman
Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Science 297:1559-61. 2002....
- Integration of interferon-alpha/beta signalling to p53 responses in tumour suppression and antiviral defenceAkinori Takaoka
Department of Immunology, Faculty of Medicine and Graduate School of Medicine, University of Tokyo, Hongo 7 3 1, Bunkyo ku, Tokyo 113 0033, Japan
Nature 424:516-23. 2003..The tumour suppressor p53 and interferon-alpha and -beta (IFN-alpha/beta) are essential for the induction of apoptosis in cancerous cells and ..
- Deregulation of DNA methyltransferases and loss of parental methylation at the insulin-like growth factor II (Igf2)/H19 loci in p53 knockout mice prior to tumor developmentIn Young Park
Department of Biological Sciences, 373 1 Gusung Dong, Korea Advanced Institute of Science and Technology, Yusung Gu, Taejon 305 701, Republic of Korea
J Cell Biochem 94:585-96. 2005To ascertain whether p53 deficiency in vivo leads to the deregulation of DNA methylation machinery prior to tumor development, we investigated the expression profile of DNA methyltransferases in the thymus and the liver of p53(+/+), p53(+..
- DNA processing is not required for ATM-mediated telomere damage response after TRF2 deletionGiulia B Celli
Laboratory for Cell Biology and Genetic, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA
Nat Cell Biol 7:712-8. 2005..Upon removal of TRF2 from TRF2(F/-) p53-/- mouse embryo fibroblasts, a telomere damage response is observed at most chromosome ends...
- p53 regulates metanephric developmentZubaida Saifudeen
Section of Pediatric Nephrology, Department of Pediatrics, and the Hypertension and Renal Center of Excellence, Tulane University Health Sciences Center, New Orleans, LA 70112, USA
J Am Soc Nephrol 20:2328-37. 2009b>p53 is best known as a tumor suppressor that regulates cell-cycle, differentiation, and apoptosis pathways, but its potential role in embryonic development and organogenesis remains controversial...
- A genomewide study identifies the Wnt signaling pathway as a major target of p53 in murine embryonic stem cellsKyoung Hwa Lee
Laboratory of Cancer Biology and Genetics, National Cancer Institute, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 107:69-74. 2010Both p53 and the Wnt signaling pathway play important roles in regulating the differentiation of mouse embryonic stem cells (mESCs). However, it is not known whether they directly and/or functionally crosstalk in mESCs...
- Evidence for type II cells as cells of origin of K-Ras-induced distal lung adenocarcinomaXia Xu
Department of Surgery, Duke University, Durham, NC 27710, USA
Proc Natl Acad Sci U S A 109:4910-5. 2012..However, only type II cells appear to progress to adenocarcinoma...
- EMT and induction of miR-21 mediate metastasis development in Trp53-deficient tumoursOlga Bornachea
Molecular Oncology Unit, CIEMAT, Ave Complutense 40, E 28040 Madrid, Spain
Sci Rep 2:434. 2012..Here we show that squamous cell carcinomas generated by the specific ablation of Trp53 gene in mouse epidermis are highly metastatic...
- Retention of wild-type p53 in tumors from p53 heterozygous mice: reduction of p53 dosage can promote cancer formationS Venkatachalam
Division of Molecular Virology and Department of Cell Biology, Baylor College of Medicine, Houston, TX 77030, USA
EMBO J 17:4657-67. 1998..The tumor suppressor gene, p53, is mutated in approximately 50% of human sporadic cancers and in an inherited cancer predisposition (Li-Fraumeni ..
- The non-apoptotic role of p53 in neuronal biology: enlightening the dark side of the moonAndrea Tedeschi
Laboratory for NeuroRegeneration and Repair, Department of Neurology, Hertie Institute for Clinical Brain Research, University of Tuebingen, Otfried Mueller Strasse 27, Tuebingen D 72076, Germany
EMBO Rep 10:576-83. 2009The transcription factor p53 protects neurons from transformation and DNA damage through the induction of cell-cycle arrest, DNA repair and apoptosis in a range of in vitro and in vivo conditions...
- Asymmetry-defective oligodendrocyte progenitors are glioma precursorsSista Sugiarto
Department of Neurological Surgery, University of California San Francisco, USA
Cancer Cell 20:328-40. 2011..Regulators of asymmetric cell division are misexpressed in low-grade oligodendrogliomas. Our results identify loss of asymmetric division associated with the neoplastic transformation of OPC...
- Multiple stress signals activate mutant p53 in vivoYoung Ah Suh
Department of Genetics, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA
Cancer Res 71:7168-75. 2011..the upstream signals that regulate wild-type p53 are known; however, limited information for the regulation of mutant p53 exists...
- WAF1, a potential mediator of p53 tumor suppressionW S El-Deiry
Oncology Center, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231
Cell 75:817-25. 1993..hybridization approach, we identified a gene, named WAF1, whose induction was associated with wild-type but not mutant p53 gene expression in a human brain tumor cell line. The WAF1 gene was localized to chromosome 6p21...
- No requirement for V(D)J recombination in p53-deficient thymic lymphomaM J Liao
Department of Biochemistry and Biophysics, University of North Carolina at Chapel Hill Medical School, Chapel Hill, North Carolina 27599, USA
Mol Cell Biol 18:3495-501. 1998The p53 tumor suppressor is activated in response to a variety of cellular stress signals, although specific in vivo signals that trigger tumor suppression are unknown...
- Tumorigenesis in mice carrying a truncating Brca1 mutationT Ludwig
Department of Anatomy and Cell Biology, Columbia University, New York, New York 10032, USA
Genes Dev 15:1188-93. 2001..The mammary tumors showed striking variability in histopathological patterns suggesting stochastic engagement of tumorigenic pathways in their progression, to which the Brca1(tr/tr) mutation was apparently a late participant...
- Reversal of senescence in mouse fibroblasts through lentiviral suppression of p53Annette M G Dirac
Division of Molecular Carcinogenesis, and Center for Biomedical Genetics, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands
J Biol Chem 278:11731-4. 2003..In mouse embryo fibroblasts (MEFs), induction of senescence requires the presence of p19(ARF) and p53, as genetic ablation of either of these genes allows escape from senescence and leads to immortalization...
- Combinations of genetic mutations in the adult neural stem cell compartment determine brain tumour phenotypesThomas S Jacques
Neural Development Unit, UCL Institute of Child Health and Department of Histopathology, Great Ormond Street Hospital, London, UK
EMBO J 29:222-35. 2010..We deleted Rb/p53, Rb/p53/PTEN or PTEN/p53 in adult subventricular stem cells; in ectopically neurografted stem cells; in mature ..
- p53-dependent senescence delays Emu-myc-induced B-cell lymphomagenesisS M Post
Department of Genetics, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA
Oncogene 29:1260-9. 2010The effect of p53-dependent cell-cycle arrest and senescence on Emu-myc-induced B-cell lymphoma development remains controversial...
- Calorie restriction delays spontaneous tumorigenesis in p53-knockout transgenic miceS D Hursting
Laboratory of Nutritional and Molecular Regulation, National Cancer Institute Frederick Cancer Research and Development Center, MD 21702
Proc Natl Acad Sci U S A 91:7036-40. 1994Transgenic mice with both alleles of the p53 tumor suppressor gene (frequently mutated in human tumors) knocked out by gene targeting provide a potentially useful tumorigenesis model because these mice rapidly develop spontaneous tumors...
- p53 protein stability in tumour cells is not determined by mutation but is dependent on Mdm2 bindingC A Midgley
Department of Biochemistry, University of Dundee, UK
Oncogene 15:1179-89. 1997..b>Mutant p53 proteins are however frequently detected at constitutively high levels in many tumours and tumour cell lines, ..
- A senescence program controlled by p53 and p16INK4a contributes to the outcome of cancer therapyClemens A Schmitt
Cold Spring Harbor Laboratory, 1 Bungtown Road, New York 11724, USA
Cell 109:335-46. 2002b>p53 and INK4a/ARF mutations promote tumorigenesis and drug resistance, in part, by disabling apoptosis. We show that primary murine lymphomas also respond to chemotherapy by engaging a senescence program controlled by p53 and p16(INK4a)...
- Nutrient availability regulates SIRT1 through a forkhead-dependent pathwayShino Nemoto
Cardiovascular Branch, National Heart, Lung, and Blood Institute NHLBI, Bethesda, MD 20892, USA
Science 306:2105-8. 2004..Stimulation of SIRT1 transcription by Foxo3a was mediated through two p53 binding sites present in the SIRT1 promoter, and a nutrient-sensitive physical interaction was observed between ..
- BH3-only proteins Puma and Bim are rate-limiting for gamma-radiation- and glucocorticoid-induced apoptosis of lymphoid cells in vivoMiriam Erlacher
Division of Experimental Pathophysiology and Immunology, Biocenter, Innsbruck Medical University, A 6020 Innsbruck, Austria
Blood 106:4131-8. 2005Numerous p53 target genes have been implicated in DNA damage-induced apoptosis signaling, but proapoptotic Bcl-2 (B-cell leukemia 2) family members of the BH3 (Bcl-2 homolog region [BH] 3)-only subgroup appear to play the critical ..
- 53BP1 cooperates with p53 and functions as a haploinsufficient tumor suppressor in miceIrene M Ward
Division of Oncology Research, Mayo Clinic and Foundation, Rochester, Minnesota 55905, USA
Mol Cell Biol 25:10079-86. 2005b>p53 binding protein 1 (53BP1) is a putative DNA damage sensor that accumulates at sites of double-strand breaks (DSBs) in a manner dependent on histone H2AX...
- Formation of dynamic gamma-H2AX domains along broken DNA strands is distinctly regulated by ATM and MDC1 and dependent upon H2AX densities in chromatinVelibor Savic
Cell and Molecular Biology Graduate Program, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
Mol Cell 34:298-310. 2009..Our data suggest that H2AX fuels a gamma-H2AX self-reinforcing mechanism that retains MDC1 and activated ATM in chromatin near DSBs and promotes continued local phosphorylation of H2AX...
- Tissue regenerative delays and synthetic lethality in adult mice after combined deletion of Atr and Trp53Yaroslava Ruzankina
Abramson Family Cancer Research Institute, Department of Cancer Biology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
Nat Genet 41:1144-9. 2009b>Trp53 loss of function has previously been shown to rescue tissue maintenance and developmental defects resulting from DNA damage or DNA-repair gene mutations...
- Non-stem cell origin for oligodendrogliomaAnders I Persson
Department of Neurology, University of California, San Francisco, 94158, USA
Cancer Cell 18:669-82. 2010..Our results suggest that oligodendroglioma cells show hallmarks of OPCs, and that a progenitor rather than a NSC origin underlies improved prognosis in patients with this tumor...
- The requirement of p53 for maintaining chromosomal stability during tetraploidizationChui Chui Ho
Division of Life Science, Hong Kong University of Science and Technology, Clear Water Bay, Hong Kong
Oncotarget 1:583-95. 2010..Due to the unequal segregation of chromosomes during multipolar mitosis, the majority of cells were eliminated by p53-dependent mechanisms after tetraploidization...
- Deletion of p37Ing1 in mice reveals a p53-independent role for Ing1 in the suppression of cell proliferation, apoptosis, and tumorigenesisAndrew H Coles
Department of Cell Biology, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA
Cancer Res 67:2054-61. 2007..of the inhibitor of growth family, encodes p37(Ing1), a plant homeodomain (PHD) protein that interacts with the p53 tumor suppressor protein and seems to be a critical cofactor in p53-mediated regulation of cell growth and ..
- ARF functions as a melanoma tumor suppressor by inducing p53-independent senescenceLinan Ha
Laboratory of Cancer Biology and Genetics, National Cancer Institute, Bethesda, MD 20892 4264, USA
Proc Natl Acad Sci U S A 104:10968-73. 2007Inactivation of the p53 pathway represents the most common molecular defect of human cancer...
- Loss of p53 causes mitochondrial DNA depletion and altered mitochondrial reactive oxygen species homeostasisMaria A Lebedeva
Department of Pathology, Yale University School of Medicine, New Haven, CT 06520 8023, USA
Biochim Biophys Acta 1787:328-34. 2009In addition to its central role in cellular stress signaling, the tumor suppressor p53 modulates mitochondrial respiration through its nuclear transcription factor activity and localizes to mitochondria, where it enhances apoptosis and ..
- Expression of mutant p53 proteins implicates a lineage relationship between neural stem cells and malignant astrocytic glioma in a murine modelYuan Wang
Department of Internal Medicine, Division of Molecular Medicine and Genetics, University of Michigan Medical School, Ann Arbor, MI 48109, USA
Cancer Cell 15:514-26. 2009..Our data show that accumulation of a detectable level of mutant p53 proteins occurs first in neural stem cells in the subventricular zone (SVZ) and that subsequent expansion of ..
- Overexpression of Mdm2 in mice reveals a p53-independent role for Mdm2 in tumorigenesisS N Jones
Department of Cell Biology, University of Massachusetts Medical School, Worcester, MA 01655, USA
Proc Natl Acad Sci U S A 95:15608-12. 1998..Because Mdm2 protein forms a complex with the p53 tumor suppressor protein and down-regulates p53 function, the oncogenic potential of Mdm2 is presumed to be p53-..
- Akt activation synergizes with Trp53 loss in oral epithelium to produce a novel mouse model for head and neck squamous cell carcinomaMarta Moral
Division of Biomedicine, Molecular Oncology Unit, CIEMAT, Madrid, Spain
Cancer Res 69:1099-108. 2009..Here we show that mice displaying constitutive Akt activity (myrAkt) in combination with Trp53 loss in stratified epithelia develop oral cavity tumors that phenocopy human HNSCC...
- p53 regulates mitochondrial respirationSatoaki Matoba
Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
Science 312:1650-3. 2006..Here, we show that p53, one of the most frequently mutated genes in cancers, modulates the balance between the utilization of respiratory ..
- Synergy of p53 and Rb deficiency in a conditional mouse model for metastatic prostate cancerZongxiang Zhou
Department of Biomedical Sciences, Cornell University, Ithaca, NY 14853 6401, USA
Cancer Res 66:7889-98. 2006Pathways mediated by p53 and Rb are frequently altered in aggressive human cancers, including prostate carcinoma...
- In vitro growth characteristics of embryo fibroblasts isolated from p53-deficient miceM Harvey
Division of Molecular Virology, Baylor College of Medicine, Houston, Texas 77030
Oncogene 8:2457-67. 1993Fibroblast cultures were derived from mouse embryos containing either one (p53+/-) or two (p53-/-) inactivated p53 alleles and compared to normal embryo fibroblasts for a number of growth parameters...
- INK4a/ARF mutations accelerate lymphomagenesis and promote chemoresistance by disabling p53C A Schmitt
Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA
Genes Dev 13:2670-7. 1999The INK4a/ARF locus encodes upstream regulators of the retinoblastoma and p53 tumor suppressor gene products...
- Negative control of p53 by Sir2alpha promotes cell survival under stressJ Luo
Institute of Cancer Genetics and Department of Pathology, College of Physicians and Surgeons, Columbia University, 1150 St Nicholas Avenue, New York, NY 10032, USA
Cell 107:137-48. 2001..Here, we show that mammalian Sir2alpha physically interacts with p53 and attenuates p53-mediated functions...
- The C-terminal lysines fine-tune P53 stress responses in a mouse model but are not required for stability control or transactivationKurt A Krummel
The Salk Institute for Biological Studies, Gene Expression Laboratory, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA
Proc Natl Acad Sci U S A 102:10188-93. 2005b>P53 is an unstable transcription factor that is mutated in a majority of human cancers...
- Chromatin-bound p53 anchors activated Smads and the mSin3A corepressor to confer transforming-growth-factor-beta-mediated transcription repressionDeepti Srinivas Wilkinson
Department of Biochemistry and Molecular Biology, Unit 1000, University of Texas M D Anderson Cancer Center, 1515 Holcombe Blvd, Houston, TX 77030, USA
Mol Cell Biol 28:1988-98. 2008In hepatic cells, Smad and SnoN proteins converge with p53 to repress transcription of AFP, an oncodevelopmental tumor marker aberrantly reactivated in hepatoma cells...
- p53-targeted LSD1 functions in repression of chromatin structure and transcription in vivoWen Wei Tsai
Dept of Biochemistry and Molecular Biology, University of Texas M D Anderson Cancer Center, 1515 Holcombe Blvd, Box 1000, Houston, TX 77030, USA
Mol Cell Biol 28:5139-46. 2008Despite years of study focused on the tumor suppressor p53, little is understood about its functions in normal, differentiated cells...
- p53 regulates the self-renewal and differentiation of neural precursorsA Armesilla-Diaz
Department of Cellular and Molecular Physiopathology, Consejo Superior de Investigaciones Cientificas, Ramiro de Maeztu, 9, 28040 Madrid, Spain
Neuroscience 158:1378-89. 2009..In the present work we report that the absence of tumor suppressor protein p53 increases the number of neurosphere-forming cells and the proliferation of stem cells derived from 13...
- Phosphorylation of p53 by IkappaB kinase 2 promotes its degradation by beta-TrCPYifeng Xia
Laboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA
Proc Natl Acad Sci U S A 106:2629-34. 2009Functional inactivation of p53 and constitutive activation of the NF-kappaB pathway has been associated with several human cancers...
- Loss of p53 enhances catalytic activity of IKKbeta through O-linked beta-N-acetyl glucosamine modificationKeiko Kawauchi
Department of Molecular Oncology, Institute of Gerontology, Nippon Medical School, Kawasaki, Kanagawa 211 8533, Japan
Proc Natl Acad Sci U S A 106:3431-6. 2009The IkappaB kinase (IKK)-NF-kappaB pathway plays a critical role in oncogenesis. Recently, we have shown that p53 regulates glucose metabolism through the IKK-NF-kappaB pathway and that, in the absence of p53, the positive feedback loop ..
- p53 Attenuates lipopolysaccharide-induced NF-kappaB activation and acute lung injuryGang Liu
Department of Medicine, University of Alabama at Birmingham, AL 35294, USA
J Immunol 182:5063-71. 2009The transcriptional factor p53 has primarily been characterized for its central role in the regulation of oncogenesis...
- An ARF-independent c-MYC-activated tumor suppression pathway mediated by ribosomal protein-Mdm2 InteractionEverardo Macias
Department of Radiation Oncology, School of Medicine, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599 7512, USA
Cancer Cell 18:231-43. 2010In vitro studies have shown that inhibition of ribosomal biogenesis can activate p53 through ribosomal protein (RP)-mediated suppression of Mdm2 E3 ligase activity...
- mdm2 Is critical for inhibition of p53 during lymphopoiesis and the response to ionizing irradiationSusan M Mendrysa
Department of Oncology, School of Medicine Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, Wisconsin 53706, USA
Mol Cell Biol 23:462-72. 2003The function of the p53 tumor suppressor protein must be highly regulated because p53 can cause cell death and prevent tumorigenesis...
- Telomere dysfunction suppresses spontaneous tumorigenesis in vivo by initiating p53-dependent cellular senescenceWilfredo Cosme-Blanco
Department of Cancer Genetics, The MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA
EMBO Rep 8:497-503. 2007Dysfunctional telomeres induce p53-dependent cellular senescence and apoptosis, but it is not known which function is more important for tumour suppression in vivo...
- Rescue of embryonic lethality in Mdm2-deficient mice by absence of p53S N Jones
Department of Molecular and Human Genetics, Howard Hughes Medical Institute, Baylor College of Medicine, Houston, Texas 77030, USA
Nature 378:206-8. 1995..The Mdm2 oncoprotein forms a complex with the p53 tumour-suppressor protein and inhibits p53-mediated transregulation of gene expression...
- Genetic background alters the spectrum of tumors that develop in p53-deficient miceM Harvey
Division of Molecular Virology, Baylor College of Medicine, Houston, Texas 77030
FASEB J 7:938-43. 1993Using gene targeting in embryonic stem cells, we have generated mice with one or two null p53 germ line alleles...
- Complementary effects of platelet-derived growth factor autocrine stimulation and p53 or Ink4a-Arf deletion in a mouse glioma modelGöran Hesselager
Department of Genetics and Pathology, Rudbeck Laboratory, University Hospital, SE 75185 Uppsala, Sweden
Cancer Res 63:4305-9. 2003INK4a-ARF and p53 inactivation are common but rarely concurrent findings in glioblastoma multiforme...
- Modeling the therapeutic efficacy of p53 restoration in tumorsCarla P Martins
Cancer Research Institute and Department of Cellular and Molecular Pharmacology, Comprehensive Cancer Center, University of California, San Francisco, San Francisco, CA 94143, USA
Cell 127:1323-34. 2006Although restoration of p53 function is an attractive tumor-specific therapeutic strategy, it remains unclear whether p53 loss is required only for transition through early bottlenecks in tumorigenesis or also for maintenance of ..
- The p53-Mdm2 network in progenitor cell expansion during mouse postnatal developmentG Liu
Department of Cancer Genetics, University of Texas M D Anderson Cancer Center, Houston, TX 77030, USA
J Pathol 213:360-8. 2007Mdm2, an E3 ubiquitin ligase, negatively regulates the tumour suppressor p53. Loss of Mdm2 in mice results in p53-dependent apoptosis and embryonic lethality...
- Prevention of the neurocristopathy Treacher Collins syndrome through inhibition of p53 functionNatalie C Jones
Stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, Missouri 64110, USA
Nat Med 14:125-33. 2008..Haploinsufficiency of Tcof1 perturbs mature ribosome biogenesis, resulting in stabilization of p53 and the cyclin G1-mediated cell-cycle arrest that underpins the specificity of neuroepithelial apoptosis and neural ..
- Caspases and p53 modulate FOXO3A/Id1 signaling during mouse neural stem cell differentiationMarcia M Aranha
iMed UL, University of Lisbon, Portugal
J Cell Biochem 107:748-58. 2009..p-Akt, p-FOXO3A, and Id1 were significantly reduced throughout differentiation. Caspase-3 processing, p53 phosphorylation, and p53 transcriptional activation increased at 3 days of differentiation, with no evidence of ..
- Manganese superoxide dismutase versus p53: the mitochondrial centerAaron K Holley
Graduate Center for Toxicology, University of Kentucky, Lexington, Kentucky 40536, USA
Ann N Y Acad Sci 1201:72-8. 2010..b>p53 is an important tumor suppressing protein that regulates many cellular activities, such as cell cycle regulation, ..
- Tumor suppressor gene expression during normal and pathologic myocardial growthK K Kim
Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis 46202 4800
J Biol Chem 269:22607-13. 1994Previous studies have identified several host proteins (p53, p107, and p193), which form prominent complexes with SV40 T antigen in transformed cardiomyocytes...
- Conditional mouse osteosarcoma, dependent on p53 loss and potentiated by loss of Rb, mimics the human diseaseCarl R Walkley
Department of Pediatric Oncology, Dana Farber Cancer Institute, Division of Hematology Oncology, Boston, MA 02115, USA
Genes Dev 22:1662-76. 2008..Analysis of familial cancer syndromes and sporadic cases has strongly implicated both p53 and pRb in its pathogenesis; however, the relative contribution of these mutations to the initiation of ..
- Alternatively spliced p53 RNA in transformed and normal cells of different tissue typesK A Han
Program of Biochemistry, Grace Cancer Drug Center, Roswell Park Cancer Institute, Buffalo, NY 14263
Nucleic Acids Res 20:1979-81. 1992The alternatively spliced RNA species of tumor suppressor gene p53, containing an additional 96 bases derived from intron 10, is present at approximately 25 to 30% the level of regularly spliced p53 RNA in both normal epidermal and ..
- Temporally distinct patterns of p53-dependent and p53-independent apoptosis during mouse lens developmentH Pan
Department of Anatomy, University of Wisconsin Medical School, Madison 53706, USA
Genes Dev 9:2157-69. 1995..The tumor suppressor protein p53 is known to mediate apoptosis induced by the DNA tumor virus oncoproteins, adenovirus E1A (AdE1A) and SV40 T ..
- Transcription Factor P53 in Terminal Nephron DifferentZubaida Saifudeen; Fiscal Year: 2004..The results of this work will provide information on what determines terminal renal differentiation. In addition, these data will advance our understanding of the role the tumor suppressor p53 in kidney development.
- A flexible somatic and sporadic mouse model for pancreatic ductal adenocarcinomaBrian Lewis; Fiscal Year: 2007..genetic lesions required for tumor formation, PyMT-encoding retroviruses will be delivered to mice in which the p53 or Ink4a/Arftumor suppressor gene loci, or both, are deleted within the pancreas...
- FUNCTION OF NOGGIN IN HAIR FOLLICLE GROWTH AND DISEASEVladimir Botchkarev; Fiscal Year: 2006....
- Molecular mediators of metastasis in hepatocellular carcinomaBrian C Lewis; Fiscal Year: 2010..recently generated a mouse model for HCC in which lung metastases occur in mice with liver-specific deletion of the p53 and Ink4a/Arftumor suppressor loci, but not in mice with liver-specific deletion of p53 alone...
- A ROLE FOR NOGGIN AND BMP2/4 IN HAIR GROWTH CONTROLVladimir Botchkarev; Fiscal Year: 2003..abstract_text> ..
- Characterization of Siva in Nervous System Development and ApoptosisLAURA ATTARDI; Fiscal Year: 2008..The p53 tumor suppressor is a regulator of cell death known to play a role both in proper neural tube closure and in ..
- MOLECULAR MECHANISMS OF CHEMOTHERAPY-INDUCED HAIR LOSSVladimir Botchkarev; Fiscal Year: 2005..Our general strategy is to focus on the p53 transcription factor, which mediates apoptosis and growth arrest induced by chemotherapy and is essential for ..
- Apoptotic Mediators in HIV Associated DementiaGwenn Garden; Fiscal Year: 2006..Experiments proposed here will examine how the pro-apoptotic transcription factor p53 promotes neuronal injury or dysfunction in tissue culture and in vivo models of HAD...
- The Role of Mdm2 in Lymphoma DevelopmentCHRISTINE EISCHEN; Fiscal Year: 2007unreadable] DESCRIPTION (provided by applicant): Mdm2, an oncoprotein that regulates the tumor suppressor p53, and Myc, an oncoprotein that paradoxically drives both cell cycle progression and apoptosis, are overexpressed in many human ..
- 2006 Cancer Model MechanismsWilliam Kaelin; Fiscal Year: 2006..unreadable] [unreadable] [unreadable] [unreadable]..
- Ubiquitin, Mitochondrial Stress and AD PathogenesisZhiqun Tan; Fiscal Year: 2006..Elucidation of the molecular basis of the adverse effects of UPS-mitochondria interactions may contribute to the development of novel pharmacological approaches to treat AD ..
- Imaging Kinase Activity In VivoWilliam Weiss; Fiscal Year: 2006..unreadable] [unreadable]..
- Precancerous Mammary Transcriptome in Mice after Estrog*Teresa Rose Hellekant; Fiscal Year: 2006..Knowing more about cancer molecules will bring more preventive agents quickly to clinical trials. ..
- Lung epithelial and vascular morphogenesisDavid Warburton; Fiscal Year: 2006..abstract_text> ..
- The role of Hypoxia Inducible Factor-1 alpha in strokeDavid Rempe; Fiscal Year: 2007..3, we will examine the cell type-specific expression of HIF-1 alpha targets as it relates to hypoxic severity and p53 function...
- Real-Time Imaging of Hypoxia based on VHL ActivityWilliam Kaelin; Fiscal Year: 2006..unreadable] [unreadable]..
- Olympus FV-1000 Confocal MicroscopeGwenn Garden; Fiscal Year: 2006..unreadable] [unreadable] [unreadable]..
- Novel Functions for Telomerase Enzyme Complex in VivoSteven Artandi; Fiscal Year: 2005..Through analysis of a conditional knockout mouse, we will determine the role of endogenous telomerase in cells in culture and in stern/progenitor compartments in vivo. ..
- The Role of Double Strand Breaks in CarcinogenesisCHRISTOPHER KEMP; Fiscal Year: 2006DESCRIPTION: (PROVIDED BY APPLICANT) The induction of p53 and apoptosis in response to ionizing radiation and other stressors in vivo varies greatly between normal tissues, between cell types within a tissue, and between tumor types...
- Bcl-2 family and redox control of genomic instabilityCHARLES KNUDSON; Fiscal Year: 2007..Understanding the pathways that control genomic instability may result in novel therapeutic strategies for the prevention or treatment of lymphoma and other diverse human malignancies. ..
- Third International Mdm2 WorkshopUte Moll; Fiscal Year: 2005..Scientific Description: The MDM2 protein is the principal negative regulator of the tumor suppressor protein p53. MDM2, a p53-specific E3 ubiquitin lipase, mediates p53 degradation via the 26S proteasome pathway, thus keeping ..
- Dendritic Cell-Specific Gene Targeting and ExpressionBoris Reizis; Fiscal Year: 2007..unreadable] [unreadable] [unreadable] [unreadable]..
- IGF-1 Signaling & ER crosstalk in mammary cancer in vivoRobin Fuchs Young; Fiscal Year: 2008..2) Evaluate the importance of IGF-1 mediated activation of ER signaling (crosstalk) in mammary tumorigenesis and in the development of tamoxifen/antiestrogen resistance in vivo. [unreadable] [unreadable]..
- ATM and DNA Damage in the Nervous SystemPETER MCKINNON; Fiscal Year: 2007..abstract_text> ..
- STEM CELLS AND AGINGStewart Sell; Fiscal Year: 2008..First, the number and homing capacity of bone marrow stem cells from wild type p53+/+ and premature ageing p53+/m C57BL/6J mice will be assayed in vitro and in vivo...
- Mutant mouse models of exocrine pancreatic cancerDAVID TUVESON; Fiscal Year: 2008..Information gained from this murine model should facilitate further understanding of human pancreatic cancer. ..
- A Luciferase Fusion Protein Library to Identify & Monitor Ubiquitylation TargetsWilliam Kaelin; Fiscal Year: 2008..Reisolation of HIF in aims 2 and 3 would constitute proof of concept with respect to the potential utility of this approach. ..
- AUTOCRINE/PARACRINE GROWTH FACTORS & LUNG MORPHOGENESISDavid Warburton; Fiscal Year: 2009..Aim 4: To determine the role of tyrosine phosphorylation in protein-protein interaction and supra-molecular assembly of mSPRY2 with SHP2 and FRS2. Aim 5: To determine the functional importance of Shp2 in lung morphogenesis in vivo. ..
- Inhibition of Fas-apoptosis in Gastric CancerJeanMarie Houghton; Fiscal Year: 2010..These studies will provide critical insight into novel preventive, and anti-cancer strategies aimed at restoring Fas sensitivity within tumor cells and provide a new direction for cancer treatment. ..
- Mechanisms of Lymphocyte Gene Regulation by E2A and Notch1BARBARA LYNNE KEE; Fiscal Year: 2010..abstract_text> ..
- Role of the Putative Tumor Suppressor PinX1 in the Etiology of Liver CancerXiao Zhen Zhou; Fiscal Year: 2010..These studies would establish new animal models for studying liver cancer and provide novel insight into the etiology and treatment of liver cancer. ..
- Regulation of Nanog in DNA damage response, development and tumorigenesisYang Xu; Fiscal Year: 2010..b>Tumor suppressor p53 is required for this process and suppresses the expression of Nanog by direct binding to its promoter...
- Histone Deacetylases and Kidney DevelopmentSamir S El Dahr; Fiscal Year: 2010..Thus, understanding the epigenetic regulation of kidney development may open new avenues to the treatment or prevention of kidney and urinary tract malformations and kidney failure. ..
- HEPTOCYTE PROLIFERATION AND AFLATOXIN METABOLISMStewart Sell; Fiscal Year: 2004..in regard to metabolism of aflatoxin (AFB1) and development of hepatocellular carcinoma (HCC) will be analyzed in p53 null and p53ser246 mutant transgenic, and HBV mice...
- AFB1 AND P53 CARCINOGENESIS IN HBSAG TRANSGENIC MICEStewart Sell; Fiscal Year: 2002..and aflatoxin (AFB1) exposure, and these tumors have a high frequency of mutations in the tumor suppressor gene p53 at codon 249 (p53ser249)...
- TRANSFORMING GROWTH FACTOR BETA IN OXIDANT LUNG INJURYMICHAEL O REILLY; Fiscal Year: 2002..These studies are significant because understanding how ROS injure and kill pulmonary epithelial cells is critically important for improving clinical therapies that rely on supplemental oxygen. ..
- CALGB LABORATORY STUDIES IN THE ELDERLYWilliam Cance; Fiscal Year: 2002..abstract_text> ..
- GENETIC AND HORMONAL MECHANISMS OF BREAST CANCERTeresa Rose Hellekant; Fiscal Year: 2002....
- CASPASE ENZYMES & APOPTOSIS IN HIV INDUCED NEURAL INJURYGwenn Garden; Fiscal Year: 2003..abstract_text> ..
- TRANSGENIC MOUSE MODELS OF PANCREATIC EXOCRINE FUNCTIONROBERT DE LISLE; Fiscal Year: 2003..That over expresses Muclin in the pancreatic acinar cell using the rat elastase promoter to direct cell specific expression. ..
- PATHOGENEISIS OF CYSTIC FIBROSIS IN THE GI SYSTEMROBERT DE LISLE; Fiscal Year: 2003..Pathology and Muclin expression will be compared in CF mice, and CF mice crossed with gastrin deficient mice (lack gastric acid secretion) to normalize intestinal Ph. ..
- CHRONIC HEPATITIS C: MOLECULAR & CELLULAR MARKERSGeoffrey Farrell; Fiscal Year: 2003..It will also allow the design of adjunctive treatments more appropriately targeted towards the key pathogenic processes that determine disease progression. ..
- Role of Fas/NF kB in H.pylori induced gastric carcinomaJeanMarie Houghton; Fiscal Year: 2003..Defining the regulation of these pathways will help define the complex relationship helicobacter shares with its host. ..
- Early Events in Colitis-Associated Colorectal CancerWen Chi Chang; Fiscal Year: 2003..In particular, mutation of the p53 gene appears to be an early event in colitis-associated CRC as is evident from the presence of p53 mutations in the ..
- P53 AND MOUSE MAMMARY TUMORIGENESISDaniel Medina; Fiscal Year: 2004The p53 tumor suppressor gene is one of the most frequently mutated genes in human breast cancer and includes gain of function mutations as well as deletion mutations...
- IR-INDUCED APOPTOSIS IN THE DEVELOPING NERVOUS SYSTEMPETER MCKINNON; Fiscal Year: 2004..the analysis of these genes by selecting those that are regulated in wildtype mice, but not in mice such as Atm or p53-null, with defective IR-induced neural apoptosis...
- PinX1, a Putative Tumor Suppressor for Prostate CancerXiao Zhou; Fiscal Year: 2004..Furthermore, these pilot studies are novel and will serve as the first step in obtaining R01 support from NIH to start a new project on prostate cancer. ..
- p53-independent Role of MDM2, TGFb Resistance and CancerPeiqing Sun; Fiscal Year: 2006..Our results indicate that an oncogene, mdm2, is a likely cause of TGFbeta resistance through a p53-independent mechanism, most likely by interference with the Rb/3E2F functions...
- FUNCTIONAL STUDIES OF IMMUNOGLOBULIN KAPPA ENHANCERSYang Xu; Fiscal Year: 2004..We will again employ genetic approaches to further explore the functions of MiEkappa in somatic hypermutations of Igkappa in a physiological context. ..
- GENETICS OF A TRANSGENIC MOUSE MODEL FOR NEUROBLASTOMAWilliam Weiss; Fiscal Year: 2004..Given the poor outcome associated with childhood neuroblastoma, this work has the potential to increase our understanding of the pathogenesis of neuroblastoma, and may result in improved therapies for children with this disorder. ..
- Excess TGF beta in neonatal lung injury and repairDavid Warburton; Fiscal Year: 2004..abstract_text> ..
- APC PATHWAY--A TARGET FOR CHEMOPREVENTIVE INTERVENTIONWen Chi Chang; Fiscal Year: 2005..in nutritional biochemistry when combined with the proposed training in cancer prevention and molecular genetics will provide her with the unique ability to develop both natural and synthetic compounds as clinical chemopreventive agents ..
- TELOMERE DYSFUNCTION, GENOMIC INSTABILITY AND CANCERSteven Artandi; Fiscal Year: 2005..Continued proliferation leads to replicative senescence, a block to continued cell growth. Inactivation of RB and p53 can bypass senescence, allowing further cell division and telomere shortening that triggers crisis, a state of ..
- DIFFERENTIATION OF BLOOD STEM CELLS INTO LIVER CELLSStewart Sell; Fiscal Year: 2005..If this project is successful, it would overcome a major hurdle in the possible use of hepatic stem cells for treatment of liver failure or ex vivo gene therapy. ..
- Using Synthetic Lethality to Select Cancer Drug TargetsWilliam Kaelin; Fiscal Year: 2005..Moreover, they may establish a new paradigm for the selection of anticancer drug targets based on inactivating mutations of TSG. ..
- Regulation of cell growth and oncogenesis by BcI-2 & BaxCHARLES KNUDSON; Fiscal Year: 2005..Our molecular studies will provide insight into the cross talk that occurs between cell death and cell proliferative pathways. ..
- Restoration of beta-catenin signaling by perillyl alcoh*Wen Chi Chang; Fiscal Year: 2005..Results from the proposed research will determine the feasibility of developing POH as a chemopreventive agent for patients with colorectal cancer and provide the basis for future R01 funding. ..
- Modulation of a breast cancer pathway by pregnancyTeresa Rose Hellekant; Fiscal Year: 2005..This application has the following specific aims: Aim 1. Develop transgenic mice that permit manipulation of TGFa expression in mammary epithelium. Aim 2. Establish how prior pregnancy affects TGFa -induced mammary tumorigenesis. ..
- Melanoma in p16INK4a and p19ARF Deficient MiceNORMAN SHARPLESS; Fiscal Year: 2006..Previous work in the mouse, however, shows p19ARF, through its regulation of p53, to be a critical tumor suppressor gene in a wide range of tissues...
- PROGESTERONE RECEPTOR IN MYOMETRIUM AND LEIOMYOMARobin Fuchs Young; Fiscal Year: 2002....