Luis Francisco Zirnberger Batista

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-|[[Image:Luis.jpg|150px|left]]+[[Image:Luis.jpg|150px|left]]
Graduated with a major in Biology at the University of Sao Paulo. Currently developing my PhD project, I am interested on the role that DNA repair efficiency plays in the resistance that human glioma cells present towards chemotherapeutical agents that are currently being used in clinical trials. Graduated with a major in Biology at the University of Sao Paulo. Currently developing my PhD project, I am interested on the role that DNA repair efficiency plays in the resistance that human glioma cells present towards chemotherapeutical agents that are currently being used in clinical trials.
-== Resumo do Projeto ==+== Project description==
-Nova abordagens genéticas e bioquímicas vêem permitindo um enorme progresso no entendimento da biologia tumoral nesta ultima década. Um dos fatos mais importantes deste tipo de pesquisa foi o reconhecimento de que a resistência à morte celular, em especial à apoptose, é um aspecto de extrema importância tanto em tumorigênese, quanto na resistência que tumores apresentam à quimioterapia. +New genetic and biochemical approaches acomplished during the last decade generated a huge progress in our understanding of tumor biology. Among them is the finding that the resistance that tumor cells present to therapy is offtenly related to an intrinsic resistance against cell death triggering, and more precisely, against apoptosis signalling.
- A maior parte de quimioterápicos disponíveis atualmente têm como principal alvo a molécula de DNA, gerando uma ampla variedade de lesões nessa molécula. Neste sentido, um dos grandes desafios atuais é o de descrever o mecanismo de morte celular provocado por estes agentes, na tentativa de aumentar a eficácia do tratamento. Apesar das vias moleculares de apoptose terem sido estudadas em grande detalhe em diversos tipos celulares, o mecanismo de sinalização para esse processo é ainda em grande parte desconhecido. Existem dois motivos principais para isso: 1) agentes específicos de danos ao DNA geralmente induzem diversos tipos de lesão, o que dificulta o entendimento de qual lesão na dupla-hélice é realmente a responsável pela sinalização para apoptose e 2) eles também podem provocar alterações não-genéticas, que também podem ativar respostas de stress e portanto culminar em morte celular.+ Several of the most utilized agents in chemotherapy clinical trials have as its main target the DNA molecule, inducing a wide variety of lesions in the double-helix. Therefore, one of the biggest problems we face is to describe the cell death mechanism induced by these agents, which would allow us to increase the efficency of treatment in human patients. In this sense, although the molecular pathways of apoptosis are already described in great detail, the triggering of this process the signaling to a specific pathway is still largely unknown. Two main reasons are accounted for that: 1) a specific chemotherapeutical agent usually induces several unrelated lesions in the DNA, which makes it hard to verify which one of these lesions is in fact triggering death and 2) they might also induce non-genetic alterations that could directly influence on death signaling as it is the case of tyrosine kinase inhibitors.
-Este projeto visa estudar como diferentes agentes quimioterápicos atualmente em uso em testes clínicos induzem morte celular em células de glioblastoma multiforme. Em particular estamos interessados no papel de p53 neste processo, e prinicipalmente na regulacao de vias de reparo de DNA ativados por estes agentes.+Our project aims to understand how different agents that are currently being used for glioma therapy induce cell death in human glioblastoma cells with different p53 status. More precisely, we are interested in the role that different DNA repair pathways play in the resistance that these cells present to therapy. The DNA repair pathways that we are currently investigating are Mismatch Repair, MGMT repair, Nucleotide Excision Repair and Homologous Recombination Repair.
-==Publicações==+==Publications==
 +'''Batista LF''', Roos WP, Christmann M, Menck CF and Kaina B. (2007). Cancer Research, 67, 11886-11895. <br>
Roos WP, '''Batista LF''', Naumann SC, Wick W, Weller M, Menck CF and Kaina B. (2007). Oncogene, 26, 186-97. <br> Roos WP, '''Batista LF''', Naumann SC, Wick W, Weller M, Menck CF and Kaina B. (2007). Oncogene, 26, 186-97. <br>
'''Batista LF''', Chigancas V, Brumatti G, Amarante-Mendes GP and Menck CF. (2006). Apoptosis, 11, 1139-48. <br> '''Batista LF''', Chigancas V, Brumatti G, Amarante-Mendes GP and Menck CF. (2006). Apoptosis, 11, 1139-48. <br>
Chigancas V, '''Batista LF''', Brumatti G, Amarante-Mendes GP, Yasui A and Menck CF. (2002). Cell Death Differ, 9, 1099-107. Chigancas V, '''Batista LF''', Brumatti G, Amarante-Mendes GP, Yasui A and Menck CF. (2002). Cell Death Differ, 9, 1099-107.

Current revision

Graduated with a major in Biology at the University of Sao Paulo. Currently developing my PhD project, I am interested on the role that DNA repair efficiency plays in the resistance that human glioma cells present towards chemotherapeutical agents that are currently being used in clinical trials.

Project description

New genetic and biochemical approaches acomplished during the last decade generated a huge progress in our understanding of tumor biology. Among them is the finding that the resistance that tumor cells present to therapy is offtenly related to an intrinsic resistance against cell death triggering, and more precisely, against apoptosis signalling. Several of the most utilized agents in chemotherapy clinical trials have as its main target the DNA molecule, inducing a wide variety of lesions in the double-helix. Therefore, one of the biggest problems we face is to describe the cell death mechanism induced by these agents, which would allow us to increase the efficency of treatment in human patients. In this sense, although the molecular pathways of apoptosis are already described in great detail, the triggering of this process the signaling to a specific pathway is still largely unknown. Two main reasons are accounted for that: 1) a specific chemotherapeutical agent usually induces several unrelated lesions in the DNA, which makes it hard to verify which one of these lesions is in fact triggering death and 2) they might also induce non-genetic alterations that could directly influence on death signaling as it is the case of tyrosine kinase inhibitors. Our project aims to understand how different agents that are currently being used for glioma therapy induce cell death in human glioblastoma cells with different p53 status. More precisely, we are interested in the role that different DNA repair pathways play in the resistance that these cells present to therapy. The DNA repair pathways that we are currently investigating are Mismatch Repair, MGMT repair, Nucleotide Excision Repair and Homologous Recombination Repair.

Publications

Batista LF, Roos WP, Christmann M, Menck CF and Kaina B. (2007). Cancer Research, 67, 11886-11895.
Roos WP, Batista LF, Naumann SC, Wick W, Weller M, Menck CF and Kaina B. (2007). Oncogene, 26, 186-97.
Batista LF, Chigancas V, Brumatti G, Amarante-Mendes GP and Menck CF. (2006). Apoptosis, 11, 1139-48.
Chigancas V, Batista LF, Brumatti G, Amarante-Mendes GP, Yasui A and Menck CF. (2002). Cell Death Differ, 9, 1099-107.

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