3. Bibliografía


3.     Bibliografía

Ashcroft M, Voudsen KH. Regulation of p53 stability. Oncogene 1999; 18(53): 7637-43.

Belka C, Budach W. Anti-apoptotic BCL-2 proteins: structure, function and relevance for radiation biology. Int J Radiat Biol 2002; 78(8): 643-58.

Brustugun OT, Fladmark KE, Doskeland SO, Orrenius S, Zhivotovsky B.Apoptosis induced by microinjection of cytochrome c is caspase-dependent and is inhibited by Bcl-2.Cell Death Differ. 1998 Aug; 5(8): 660-8. Erratum in: Cell Death Differ 1999 Mar; 6(3): 301.

Cuddihy AR, Bristol RG. The p53 protein family and radiation sensitivity: Yes or no? Cancer Metastasis Rev 2004; 23(3-4): 237-57.

Fink SL and Cookson BT. Apoptosis, pyroptosis, and necrosis: Mechanistic description of dead and dying eukaryotic cells. Infect immun 2005; 73(4): 1907-16.

Hockenbery DM, Zutter M, Hickey W, Nahm M, Korsmeyer S. Bcl-2 protein is topographically restricted in tissues characterized by apoptotic cell death. Proc Natl Acad Sci USA 1991; 88 (16): 6961-5.

Jacobson MD, Weil M, Raff MC. Programmed cell death in animal development. Cell1997; 88 (3): 347-54.

Kerr JF, Searle J. A suggested explanation for the paradoxically slow growth rate of basal-cell

carcinomas that contain numerous mitotic figures. J Pathol 1972; 107(1):41-4.

Korsmeyer SJ, Shutter JR, Veis DJ, Merry DE, Oltvai ZN. Bcl-2/bax: a rheostat that regulates an anti-oxidant pathway and cell death. Sem Canc Biol 1993; 4(6): 327-32.

Levine AJ, Momand J, Finlay CA. The p53 tumor suppresor gene. Nature 1991; 351(6326): 453-6.

Lockshin RA, Zakeri Z. Programmed cell death and apoptosis: origins of the theory.Nat Rev Mol Cell Biol 2001; 2(7): 545-50.

Lloret M, Pérez S, Santana C, Lera J, Rey A, Falcón O, Lara P.C. Proliferación (IM, Ki67), apoptosis (IA) y genes reguladores (P53, BAX y BCL-2) en carcinoma de cérvix: relación con factores pronósticos clásicos, control local y supervivencia. Carcinoma infiltrante de Cérvix: de los aspectos clínicos a la investigación aplicada. Editorial Bristol-Myers, S.A 2001; D.L: M-15738.Capítulo 3:53-69.

Majno G,Joris I.Apoptosis, Oncosis, and Necrosis. An overview of cell death. A J P 1995; 146:3-15.

Marzo I, Brenner C, Zamzami N, Jurgensmeier JM, Susin SA, Vieira HL, Prevost MC, Xie Z, Matsuyama S, Reed JC, Kroemer G. Bax and adenine nucleotide translocator cooperative in the mitochondrial control of apoptosis. Science 1998; 281(5385): 2027-31.

Elisa Bordón Rodríguez et al.

May P and May E: Twenty years of p53 research. Structural and functional aspects of the p53 protein. Oncogene 1999;18(53):7621-36.

Mikulski SM. Pathogenesis of cancer in view of mutually opposing apoptotic and anti-apoptotic growth signals (Review). Int J Oncol 1994; 4:1257-63.

Morris SM: a role for p53 in the frequency and mechanism of mutations. Mutat Res 2002; 511(1): 45-62.

Narita M, Shimizu S, Ito T, Chittenden T, Lutz RJ, Matsuda H, Tsujimoto Y.Bax interacts with the permeability transition pore to induce permeability transition and cytochrome c release in isolated mitochondria. Proceedings of the National Academy of Sciences, USA 1998; 95(25): 14681-6.

Petros AM, Gunasekera A, Xu N, Olejniczak ET, Fesik SW. Defining the p53 DNA-binding domain/Bcl-x (L)-binding interface using NMR.FEBS Lett 2004; 559(1-3): 171-4.

Pezzella F, Gatter K. What is the value of bcl-2 protein detection for histopathologist? Histopathology 1995; 26(1): 89-93.

Raff MC. Social control on cell survival and cell death. Nature1992; 356(6368): 397-400.

Sigal A, Rotter V. Oncogenic mutations of the p53 tumor suppressor: the demons of the guardian of the genome. Cancer Res 2000; 60(24): 6788-93.

Susin SA, Lorenzo HK, Zamzami N, Marzo I, Snow BE, Brothers GM, Mangion J, Jacotot E, Constantini P, Loeffler M, Larochette N, Goodlett DR, Aebersold R, Siderovski DP, Penninger JM, Kroemer G. Molecular Characterization of mitochondrial apoptosis-inducing factor. Nature 1999; 397(6718): 441-6.

Vaux DL, Cory S, Adams JM. Bcl-2 gene promotes haemopoitic cell survival and cooperates with c-myc to inmortalize pre-B cells. Nature 1988; 335:440-2.