Dec 21, 2015 - Mutations in the TP53 gene occur in almost every type of cancer, ... 10% (hematopoietic malignancies) and 96% (high grade ovarian serous carcinoma) (1). .... p53-null background of non-small lung carcinoma H1299 cells ...
In the present study, we have investigated the mechanisms by which the restoration of wild-type (wt) p53 functions in p53 mutant cells increases their ...
miR-34a microRNA.2 p53 can also localize to mitochondria and ... Submitted: 05/08/09; Accepted: 06/29/09 ... Cancer and Development Laboratory-Equipe labellisée 'La Ligue,' CNRS UMR 5238; Université ..... Oncogene 2007; 26:2157-65.
ASTE1. (5'-ATGGGTATCCGAGGACTAATGAG-3' and. 5'-GTCCCGCAACTTCAAATCAGT-3'); for mouse version: MMP2. (5'-. CAAGTTCCCCGGCGATGTC-3'.
damaging agent, abrogated the restraint apoptosis mediated by mutant p53. ...... ial Chair in Cancer Research at the Weizmann Institute. Patrick D Sutphin (PDS) ...
Runzhao Li, Patrick D Sutphin, Dov Schwartz, Devorah Matas, Nava Almog,. Roland Wolkowicz, Naomi Goldfinger, Huiping Pei, Miron Prokocimer and Varda ...
May 23, 2018 - Harris, S.L.; Levine, A.J. The p53 pathway: Positive and negative feedback loops. ... Gottlieb, T.M.; Oren, M. p53 and apoptosis. Semin. Cancer ...
Sep 18, 2006 - whether Mut PML could affect p53âdependent transcription in haematopoietic cells. To this end, we infected HL60 cells with Mut. PML or vector ...
Dec 13, 2013 - Results: Ectopic expression of Id4 in DU145 cells resulted in ... Gain of Id4 resulted in increased acetylation of mutant p53 whereas loss of Id4 ...
Jul 8, 2013 - 1Department of Cell Biology, Harvard Medical School, Boston, ... Cancer Institute, Miller School of Medicine, University of Miami, Florida 33136, USA; ... chaperone-mediated autophagy in a lysosome-dependent fashion.
is a precursor hairpin miRNA (pre-miRNA), which is exported to the cytoplasm by ... Snail1 pathway, the miR-200 family consisting of 5 miRNAs. (miR-200aâc ..... for miR-605, miR-192, miR-194 and miR-215 and p53.85,86 These. miRNAs are ...
Apr 22, 2010 - of c-Myc and Klf4 in reprogramming is less clear. Several ... Iris Kamer,1 Osnat Ezra,1 Alina Molchadsky,1 Naomi Goldfinger,1. Ori Brenner,2 ...
Jun 1, 2012 - Liu K, Ling S, Lin WC (2011) TopBP1 mediates mutant p53 gain of function through NF-Y and p63/p73. Mol Cell Biol 31: 4464â4481. 18.
Chester Beatty Laboratories, 237 Fulham Road, London SW3 6JB; 2CRC Laboratories, Department of Pathology, University of. Edinburgh Medical School ...
Keywords: apoptosis; mutant p53; etoposide; chemo- resistance. Introduction. The p53 tumor suppressor gene is the most frequent target for genetic alterations ...
their endogenous p53 loci as a model for the human Li-Fraumeni syndrome. The mutant p53R172H knock-in mice spontaneously develop tumors with high ...
Feb 5, 2015 - E2F4 to transcriptionally downregulate RAD17 and BRCA1 ... recruitment of mutp53/E2F4 complex onto specific regions of BRCA1 and RAD17.
Dec 27, 2013 - ... by National Institutes of Health Grant CA 121137 and CA 076069. ...... Petitjean A, Achatz MI, Borresen-Dale AL, Hainaut P, Olivier M (2007).
Mar 8, 1994 - Wen-Biao Liu, Jerry W.Shay' and. Albert B.Deisseroth2 ...... Mercer,W.E., Shields,M.T., Amin,M., Sauve,G.J., Appella,E.,. Romano,J.W. and ...
Abstrad. HL6O cells, which lack the p.5.3 gene due to a deletion, were used as an in vitro model system to study the effed of wild-type p53 gene expression on.
Dec 14, 2009 - Messi D'Oro 156, 00158 Rome, Italy and the §National Council of Research, Istituto di Neurobiologia e Medicina Molecolare,. 00133 Rome ...
Sep 2, 2016 - Dihydrocapsaicin (DHC), a saturated structural analog of capsaicin, induces autophagy in human cancer cells in a catalase regulated manner.
Jun 7, 2018 - Basso, A.D.; Solit, D.B.; Chiosis, G.; Giri, B.; Tsichlis, P.; Rosen, N. Akt forms ... Evan, G.I. Temporal dissection of p53 function in vitro and in vivo.
tected in examples of both primary and metastatic disease and did not appear to be associated .... family (43) with Li-Fraumeni syndrome (44). The detection of.
Abstract. We have previously shown that p53 mutations are associated with cisplatin resistance in ovarian carcinoma. IGROV-1/Pt 1 cells. The relationship ...
Vol. 10, 473– 478, July 1999
Cell Growth & Differentiation
Emergence of p53 Mutant Cisplatin-resistant Ovarian Carcinoma Cells following Drug Exposure: Spontaneously Mutant Selection1 Sabina C. Righetti, Paola Perego, Elisabetta Corna, Marco A. Pierotti, and Franco Zunino2 Istituto Nazionale per lo Studio e la Cura dei Tumori, 20133 Milan, Italy
Abstract We have previously shown that p53 mutations are associated with cisplatin resistance in ovarian carcinoma IGROV-1/Pt 1 cells. The relationship between p53 status and the development of resistance has not been completely elucidated; in particular, the biological mechanisms behind the acquired drug-resistant p53mutant phenotype were not clearly explained. Thus, in this study, we investigated whether the p53 mutations found in IGROV-1/Pt 1 cells (270 and 282 codons) resulted from selection, under the selective pressure of the cytotoxic treatment, of a spontaneously mutant cell population preexistent in the cisplatin-sensitive parental cell line (IGROV-1) or were induced by drug (genotoxic) treatment. For this purpose, an allele-specific PCR approach was used. Primers carrying the desired mutations (T3 A codon 270, C3 T codon 282) in the 3* terminus, and the corresponding wild-type primers were used to amplify genomic DNA from the original IGROV-1 cell line used to select the mutant IGROV-1/Pt 1. To increase sensitivity, we hybridized blots of the PCRs with the radiolabeled PCR fragment from IGROV-1/Pt 1. Amplification was obtained for IGROV-1 DNA with the mutated allele-specific primers, indicating the preexistence of a mutated population in the IGROV-1 cell line. Titration experiments suggested that the frequency of the mutated alleles was
