Lucía Pasarín López, BSc thesis. F. Javier Aguado Domínguez. PhD thesis. Marce Abal Sanisidro, MSc thesis. Cristina de la Parte Rodríguez, MSc thesis. Diana Guallar Artal, Postdoc (Campus Vida's International Postdoctoral Fellow). Paula Alonso Batán, Research Assistant (CiMUS Initiation-To-Research Contract) Since his PhD thesis, working on DNA repair mechanisms of ASFV (large DNA virus), he has been very interested in DNA replication and repair mechanisms and how these mechanisms evolved. Modesto Redrejo Rodríguez (PI) He is very interested in the use of multidisciplinary approaches, using biochemistry, structural biology, genetics and Underlying mechanisms of cell cycle-dependent DNA repair will be addressed using cell biological techniques, including live cell imaging. The PhD position will be for 4 years, and should result in a PhD thesis at the University of Groningen
PhD student position in cancer biology
Goellner, Eva Demonstrating functional crosstalk between DNA base excision repair and cellular bioenergetics: A strategy for the treatment of chemotherapy resistant glioblastoma, dna phd repair thesis. Dna phd repair thesis Dissertation, University of Pittsburgh. DNA damaging agents are commonly used in the clinic dna phd repair thesis the treatment of cancer.
In particular, the DNA alkylating agent, temozolomide, is the primary chemotherapeutic option for the treatment of glioblastoma, a particularly aggressive form of brain cancer. Temozolomide produces three main DNA lesions: O6-methylguanine, N7-methylguanine and N3-methyladenine. Most of the clinical toxicity is a result of the O6-methylguanine lesion, which activates the mismatch repair pathway and results in apoptosis.
The N7 methylguanine and N3-methyladenine lesions are effectively repaired by the base excision repair pathway BER and hence the toxicity of these lesions is minimal. Resistance to O6-methylguanine mediated cell death is prevalent, particularly in recurrent glioblastomas, at which point treatment options are limited. We have previously shown that targeting of the BER pathway through genetic means or small molecules resulting in BER failure can produce tumor cell death independent of the O6-methylguanine lesion.
This dissertation addresses the critical questions of the mechanisms by which BER failure results in tumor cell death and investigates new combinational therapy options to enhance tumor cell death by BER failure. Cell death after BER failure results from accumulation of repair intermediates and hyperactivation of PARP1. In particular, nuclear PARP activation results in a severe block to glycolysis and a defect in mitochondrial respiratory capacity.
These metabolic defects result in subcellular ATP loss from the mitochondria as well as from the nuclear and cytosolic compartments. This suggests that targeting both BER and cellular energetic pathways would enhance N7-methylguanine and N3-methyladenine mediated toxicity, dna phd repair thesis. This site is hosted by the University Library System of the University of Pittsburgh as part of its D-Scribe Digital Publishing Program.
The ULS Office of Scholarly Communication and Publishing fosters and supports new modes of publishing and information-sharing among researchers. The University of Pittsburgh and D-Scholarship Pitt support Open Access to research. RSS 1. RSS 2. My Account Login. Dna phd repair thesis Main Page Getting Started Submitting Your ETD Repository Policies About FAQ Help. Demonstrating functional crosstalk between DNA base excision repair and cellular bioenergetics: A strategy for the treatment of chemotherapy resistant glioblastoma.
Unpublished Preview. Title Member Email Address Pitt Username ORCID Committee Chair Romero, Guillermo ggr pitt. edu GGR Thesis Advisor Sobol, Robert rws9 pitt, dna phd repair thesis.
edu RWS9 Committee Member Van Houten, Bennett bev15 pitt. edu BEV15 Committee Member Bakkenist, Christopher bakkenistcj upmc. edu CJB38 Committee Member Yu, Jian yuj2 upmc. edu JIY3. Demonstrating functional crosstalk between DNA base excision repair and cellular bioenergetics: A strategy for the treatment of chemotherapy resistant glioblastoma Goellner, Eva Dna phd repair thesis functional crosstalk between DNA base excision repair and cellular bioenergetics: A strategy for the treatment of chemotherapy resistant glioblastoma.
PDF Primary Text Download 6MB Preview. Select format Citation - Text Citation - HTML Endnote BibTex Dublin Core OpenURL MARC ISO METS MODS EP3 XML Reference Manager Refer. Creators Email Pitt Username ORCID Goellner, Eva. Title Member Email Address Pitt Username ORCID Committee Chair. Glioblastoma, DNA damage, Base excision repair, Bioenergetics, Cancer, Temozolomide.
Zhicheng Ji PhD thesis defense
, time: 57:31Top 50 Genetics Research Topics for Written Projects
Genome-wide analysis of DNA damage and repair _____ Vom Fachbereich Biologie der Technischen Universität Darmstadt zur Erlangung des akademischen Grades eines Doctor rerum naturalium genehmigte Dissertation von blogger.com Bioinf. Wei Yu aus JiangXi, China Berichterstatter (1. Referent): Prof. Dr. M. Cristina Cardoso Mitberichterstatter (2 Lucía Pasarín López, BSc thesis. F. Javier Aguado Domínguez. PhD thesis. Marce Abal Sanisidro, MSc thesis. Cristina de la Parte Rodríguez, MSc thesis. Diana Guallar Artal, Postdoc (Campus Vida's International Postdoctoral Fellow). Paula Alonso Batán, Research Assistant (CiMUS Initiation-To-Research Contract) Underlying mechanisms of cell cycle-dependent DNA repair will be addressed using cell biological techniques, including live cell imaging. The PhD position will be for 4 years, and should result in a PhD thesis at the University of Groningen
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