Journal of Cancer Research and Treatment
ISSN (Print): 2374-1996 ISSN (Online): 2374-2003 Website: http://www.sciepub.com/journal/jcrt Editor-in-chief: Jean Rommelaere
Open Access
Journal Browser
Go
Journal of Cancer Research and Treatment. 2015, 3(2), 25-27
DOI: 10.12691/jcrt-3-2-2
Open AccessEditorial

Tumor Protein p53: Novel Aspects of an Old Tumor Marker

Ahmed M. Kabel1, 2,

1Department of Clinical Pharmacy, College of Pharmacy, Taif University, Taif, Saudi Arabia

2Department of Pharmacology, Faculty of Medicine, Tanta University, Tanta, Egypt

Pub. Date: July 24, 2015

Cite this paper:
Ahmed M. Kabel. Tumor Protein p53: Novel Aspects of an Old Tumor Marker. Journal of Cancer Research and Treatment. 2015; 3(2):25-27. doi: 10.12691/jcrt-3-2-2

Abstract

P53 gene is a tumor suppressor gene that stops the formation of tumors. If a person inherits only one functional copy of the p53 gene from his parents, he will be predisposed to cancer and usually develop several tumors in various tissues in early adulthood. However, mutations in p53 are found in most tumor types, and so contribute to a number of molecular events leading to tumor formation. There are numerous informations that exist on all aspects of p53 normal function and mutant expression in human cancers, reflecting its key role in the pathogenesis of human cancers.

Keywords:
p53 tumor marker

Creative CommonsThis work is licensed under a Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

References:

[1]  Surget S, Khoury MP, Bourdon JC (2013). Uncovering the role of p53 splice variants in human malignancy: a clinical perspective. OncoTargets and Therapy; 7: 57-68.
 
[2]  Jiang L, Kon N, Li T, Wang SJ, Su T, Hibshoosh H, Baer R, Gu W (2015). Ferroptosis as a p53-mediated activity during tumour suppression. Nature; 520 (7545):57-62.
 
[3]  Bourdon JC, Fernandes K, Murray-Zmijewski F, Liu G, Diot A, Xirodimas DP et al. (2005). p53 isoforms can regulate p53 transcriptional activity. Genes & Development; 19 (18): 2122-37.
 
[4]  Abdel-Rahman MN, Kabel AM (2012). Comparative study between the effect of methotrexate and valproic acid on solid Ehrlich tumour. J Egypt Natl Canc Inst; 24(4):161-7.
 
[5]  Larsen S, Yokochi T, Isogai E, Nakamura Y, Ozaki T, Nakagawara A (2010). LMO3 interacts with p53 and inhibits its transcriptional activity. Biochem Biophys Res Commun; 392 (3): 252-7.
 
[6]  Harms KL, Chen X (2005). The C Terminus of p53 Family Proteins Is a Cell Fate Determinant. Mol Cell Biol; 25 (5): 2014-30.
 
[7]  Bell S, Klein C, Müller L, Hansen S, Buchner J (2002). p53 contains large unstructured regions in its native state. J Mol Biol; 322 (5): 917-27.
 
[8]  Khoury MP, Bourdon J-C (2011). p53 Isoforms: An Intracellular Microprocessor?. Genes Cancer; 2(4): 453-465.
 
[9]  Zhu J, Zhang S, Jiang J, Chen X (2000). Definition of the p53 functional domains necessary for inducing apoptosis. The Journal of Biological Chemistry; 275 (51): 39927-34.
 
[10]  Bourdon JC (2007). p53 and its isoforms in cancer. Br J Cancer; 97(3):277-82.
 
[11]  Hasty P, Christy BA (2013). p53 as an intervention target for cancer and aging. Pathobiology of Aging & Age Related Diseases; 3:10.3402/pba.v3i0.22702.
 
[12]  Mraz M, Malinova K, Kotaskova J, Pavlova S, Tichy B, Malcikova J et al. (2009). "MiR-34a, miR-29c and miR-17-5p are downregulated in CLL patients with TP53 abnormalities". Leukemia, U.K.; 23 (6): 1159-63.
 
[13]  Cui R, Widlund HR, Feige E, Lin JY, Wilensky DL, Igras VE et al. (2007). Central role of p53 in the suntan response and pathologic hyperpigmentation. Cell; 128 (5): 853-64.
 
[14]  Han ES, Muller FL, Pérez VI, Qi W, Liang H, Xi L et al. (2008). The in vivo Gene Expression Signature of Oxidative Stress. Physiol Genomics; 34 (1): 112-26.
 
[15]  Loughery J, Cox M, Smith LM, Meek DW (2014). Critical role for p53-serine 15 phosphorylation in stimulating transactivation at p53-responsive promoters. Nucl Acids Res; 2014.
 
[16]  Vakhrusheva O, Smolka C, Gajawada P, Kostin S, Boettger T, Kubin T et al. (2008). Sirt7 increases stress resistance of cardiomyocytes and prevents apoptosis and inflammatory cardiomyopathy in mice. Circ Res; 102 (6): 703-10.
 
[17]  Monique G. C. T. van Oijen MGCT, Slootweg PJ (2000). Gain-of-Function Mutations in the Tumor Suppressor Gene p53. Clin Cancer Res; 6:2138.
 
[18]  Herce HD, Deng W, Helma J, Leonhardt H, Cardoso MC (2013). Visualization and targeted disruption of protein interactions in living cells. Nat Commun; 4: 2660.
 
[19]  White EA, Walther J, Javanbakht H, Howley PM (2014). Genus Beta Human Papillomavirus E6 Proteins Vary in Their Effects on the Transactivation of p53 Target Genes. J Virol; 88(15): 8201-12.
 
[20]  Angeletti PC, Zhang L, Wood C (2008). "The Viral Etiology of AIDS-Associated Malignancies". Adv Pharmacol; 56: 509-57.
 
[21]  Muller PAJ, Vousden KH (2014). Mutant p53 in Cancer: New Functions and Therapeutic Opportunities. Cancer Cell; 25(3):304-317.