3 edition of p53-independent growth arrest of human astrocytomas by p14arf found in the catalog.
p53-independent growth arrest of human astrocytomas by p14arf
Craig Leslie Stewart
Thesis (M.Sc.) -- University of Toronto, 2000.
|Series||Canadian theses = -- Thèses canadiennes|
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signal transduction in cancer There are a number of challenges and unanswered questions. The immediate anti-tumor effects of biologic therapies targeting growth factor pathways may be difficult to ascertain given their cytostatic activity (Owa, Yoshino, Yoshimatsu, & Nagasu, ; Rewcastle et al., ; Thompson et al., ). Hirose Y., Berger M.S., Pieper R.O. Abrogation of the Chk1-mediated G(2) checkpoint pathway potentiates temozolomide-induced toxicity in a pindependent manner in human glioblastoma cells. Cancer Res. – PubMed Google ScholarCited by:
Bladder Cancer – From Basic Science to Robotic Surgery, Edited by Abdullah Erdem Canda p. cm. ISBN free online editions of InTech Books and Journals can be found at www. This growth arrest is similar to telomere-based replicative senescence in most, but not all, regards. For example, in both types of growth arrest cells cannot divide even if stimulated by mitogens, cells remain metabolically active, and cells show characteristic changes in morphology.
Health Publica Icon Health Publications - Glioblastoma - A Medical Dictionary Bibliography and Annotated Research Guide to Internet References (). in vivo tracking spio labelled mesenchymal stem cell tropism toin vivo tracking nanoparticle-labelled stem cell tropism to brain malignant glioma after systematical injection by a clinical t mr jianhong zhu (china) p53 independent abrogation of g1 arrest in murine brain tumor-derived stem like cells after ionizing radiation cynthia wetmore.
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Abstract pIndependent Growth Arrest of Human Astrocytomas by ~14~~ Master of Science, Craig Stewart, Department of Laboratory Medicine and Pathobiology, University of Toronto The role of the two distinct tumour suppressor proteins expressed frorn the CDKIV2A locus, ~16'"~~~ and pllAE, has been intensely studied due, in part, to their frequent inacti-Author: Craig Leslie Stewart.
The p19 ARF tumor suppressor antagonizes Mdm2 to induce pdependent cell cycle arrest. Individual TKO (triple knock out) mice nullizygous for ARF, p53, and Mdm2 develop multiple tumors at a frequency greater than those observed in animals lacking both p53 and Mdm2 or p53 alone, demonstrating that p19 ARF can act independently of the Mdm2-p53 axis in tumor by: Abstract.
The p19 ARF tumor suppressor antagonizes Mdm2 to induce pdependent cell cycle arrest. Individual TKO (triple knock out) mice nullizygous for ARF, p53, and Mdm2 develop multiple tumors at a frequency greater than those observed in animals lacking both p53and Mdm2 or p53 alone, demonstrating that p19 ARF can act independently of the Mdm2-p53 axis in tumor by: ARF (p14 ARF in human and p19 Arf in mouse) is functionally coupled to p53 through its inhibition of Mdm2-mediated p53 degradation, and overexpression of p19 Arf leads to pdependent growth arrest and cellular senescence in vitro and in vivo in some tissues (3,5,6).
Wip1 Over-Expression Correlated With TP53/p14(ARF) Pathway Disruption in Human Astrocytomas Article in Journal of Surgical Oncology (6) November with. dependent growth arrest (Weber et al.
To deter-mine whether the same protein interaction domain of ARF was required to arrest proliferation of MEFs lacking Mdm2, we introduced ARF 1–14 into TKO cells by ret-roviral gene transfer. In the experiment shown, the level p53 p53 ARF and ARF/pARF/p53/. Whatever the exact mechanisms involved, growth arrest by p19Arf depends to a great extent on pdependent transcription, which up-regulates many antiproliferative pDependent and -Independent Functions of the Arf Tumor Suppressor C.J.
SHERR,*† D. BERTWISTLE,* †W. DEN BESTEN, M.-L. KUO,* †M. SUGIMOTO,* K. TAGO,*†. p14ARF activates a Tipdependent and pindependent ATM/ATR/CHK pathway in response to genotoxic stress.
Mol Cell B Crossref, Medline, Google Scholar; Eymin B, Leduc C, Coll JL, Brambilla E, Gazzeri S (). p14ARF induces G2 arrest and apoptosis independently of p53 leading to regression of tumours established in nude mice. TP53 is a pivotal gene that often mutates in diffuse gliomas and especially in astrocytomas (Sarkar et al., ).
TP53 encodes p53, a transcription factor that regulates the cell cycle to. The protein products of the targeted genes are the effectors of p53, inducing either cell growth arrest or apoptosis depending upon the cellular context in which they are expressed, In the absence of stress or damage, p53 levels and activity are kept in check by Mdm2, coded for by the proto-oncogene MDM, Mdm2 binds p53 tightly Author: Bryson W.
Katona, John P. Lynch. Selivanova, G. et al. Restoration of the growth suppression function of mutant p53 by a synthetic peptide derived from the p53 C-terminal domain.
Nat. Med. 3, – ().Cited by: human cancers, controls multiple signaling pathways by regulating the genes involved in cell cycle arrest, apoptosis, DNA repair, cellular senescence and inhibition of angiogenesis (1).
Stabilization of p53 protein occurs in response to various stress stimuli including DNA damage, viral infection or. Furthermore, overexpression of molecules that induce the transcription of S-phase genes, such as E2-F (mentioned earlier) or B-myb , may enable tumor cells to overcome pmediated growth arrest, p21 is also induced during pdependent apoptosis, but not during apoptosis that occurs by pindependent mechanisms .Author: W.
Andrew Yeudall, Katharine H. Wrighton. The gliomas are a group of tumors that arise in the central nervous system (CNS) and share features of some degree of glial differentiation. During development, the neuroectoderm surrounding the Cited by: 5. Gliomas are the most frequent primary tumors of central nervous system and represent a heterogeneous group of tumors that originates from the glial cells.
TP53, PTEN, and CDKN2A are important tumor suppressor genes that encode proteins involved in sustaining cellular homeostasis by different signaling pathways. Though genetic alterations in these genes play a significant role in tumorigenesis Cited by: 1.
Long non-coding RNAs (lncRNAs) are functional RNAs longer than nucleotides in length. LncRNAs are as diverse as mRNAs and they normally share the same biosynthetic machinery based on RNA polymerase II, splicing and polyadenylation. However, lncRNAs have low coding potential. Compared to mRNAs, lncRNAs are preferentially nuclear, more tissue specific and expressed at lower by: Yet, in a later study, sirtinol-induced growth arrest and increased p53 levels were observed using concentrations above 50 µM (Ota et al.
Salermide, a sirtinol derivative, inhibits the protein deacetylase activities of purified SirT1 and SirT2 and causes apoptosis in cultured human cancer cell lines (Lara et al. p53 is one of the most studied tumor suppressors in the cancer research field. Of note, over 50% of human tumors carry loss of function mutations, and thus p53 has been considered to be a classical Knudson-type tumor suppressor.
From the functional point of view, p53 is a nuclear transcription factor to transactivate a variety of its target genes implicated in the induction of cell cycle Cited by: In response to stress, cells can activate a myriad of signalling pathways to bring about a specific cellular outcome, including cell cycle arrest, DNA repair, senescence and apoptosis.
This response is pivotal for tumour suppression as all of these outcomes result in restriction of the growth and/or elimination of damaged and pre-malignant cells.
Figure 1. TP53 gene: Structure, chromosome localization and protein domains distribution. TP53 is mapped on human chromosome site 17p It is a long gene, w base pair comprising 11 exons that codify a protein with amino acids long, in which the transactivation, proline-rich, DNA binding and the oligomerization domains are : Igor Andrade Pessôa, Fabio P.
Estumano da Silva, Nilson PraiaAnselmo, Edivaldo Herculano C. de Olive. Research Report - Max Delbrück Center for Molecular Max Delbrück Center for Molecular Medicine Berlin-Buch (MDC) Research Report Research Report MAX DELBRÜCK CENTER FOR MOLECULAR MEDICINE BERLIN-BUCH MEMBER OF THE HELMHOLTZ ASSOCIATION Research Report Editor-in-Chief (covers the period ) Pamela Cohen Max Delbrück Center for .For example, astrocytomas (World Health Organization grades II–IV) in children/ young adults may demonstrate loss of heterozygosity for chr 17p and/or mutations in p53 (–); astrocytomas in older adults often have mutations in amplification of the epidermal growth factor receptor, and no mutations in p53 (,).Berlin-Buch - Imaging Netzwerk Berlin Title_RZ_ Uhr Seite 1 Max Delbrück Center for Molecular Medicine Berlin-Buch (MDC) Max Delbrück Center for Molecular Medicine Research Report MDC Berlin-Buch Research Report MDC Berlin-Buch Max Delbrück Center for Molecular Medicine MDC_RR_RZ_intro_cardio Uhr Seite I Research Report Covers the .