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F, Mascaux C, Meert AP, Vallot F, Lafitte JJ, and Sculier JP. Role of p53 as a prognostic factor for survival in ling cancer: a systematic review of the literature with a meta-analysis. Eur Resp J. 2001;18(4):705-19. doi:10.1183/09031936.01.00062201 PMID:11716177 Sidransky D and Hollstein M. Clinical application of the p53 gene. Annu Rev Med. 1996;47:285-301. doi:10.1146/annurev.med.47.1.285 PMID:8712782 Chiba I, Takahashi T, Nau MM, D, Amico D, Curiel DT, Mitsudomi T, Butchhagen DL, Carbone D. Mutations in the p53 gene are frequent in primary, resected non

). Transferring receptors in human tissues: Their distribution and possible clinical relevance, Journal of Clinical Pathology 36 (5): 539-545. Geva-Zatorsky, N., Rosenfeld, N., Itzkovitz, S., Milo, R., Sigal, A., Dekel, E., Yarnitzky, T., Liron, Y., Polak, P., Lahav, G. and Alon, U. (2006). Oscillations and variability in the p53 system, Molecular Systems Biology 2 : 2006.0033. Giono, L. and Manfredi, J. (2007). Mdm2 is required for inhibition of cdk2 activity by p21, thereby contributing to p53-dependent cell cycle arrest, Molecular Cell Biology 27 (11): 4166

: 4285-91. 10.1200/JCO.2002.02.068 4. Lowe SW, Bodis S, McClatchey A, Remington L, Ruley HE, Fisher DE, et al. p53 status and the efficacy of cancer therapy in vivo. Science. 1994; 266:807-10. 5. O’Connor PM, Jackman J, Bae I, Myers TG, Fan S, Mutoh M, et al. Characterization of the p53 tumor suppressor pathway in cell lines of the National Cancer Institute anticancer drug screen and correlations with the growth-inhibitory potency of 123 anticancer agents. Cancer Res. 1997; 57:4285-300. 6. Gregorc V, Ludovini V, Pistola L, Darwish S, Floriani I, Bellezza G, et al

, Fang M, Tao S, Green CL, Khavari PA. CDK4 coexpression with Ras generates malignant human epidermal tumorigenesis. Nat Med. 2002;8(10):1105-1114 12. Tomas D: Apoptosis, UV-radiation, precancerosis and skin tumors.. Acta Med Croatica. 2009;63 Suppl 2:53-8. 13. Isobe M, Emanuel BS, Givol D, Oren M, Croce CM. Localization of gene for human p53 tumour antigen to band 17p13. Nature 1986; 320:84–5. 14. Petitjean A, Achatz MI, Borresen-Dale AL, Hainaut P, Olivier M. TP53 mutations in human cancers: functional selection and impact on cancer prognosis and outcomes. Oncogene

Srivastava, Analysis of the immunoexpression of Ki-67 and Bcl-2 in the pericoronal tissues of impacted teeth, dentigeous cysts and gingiva using software image analysis, Dent Res J (Isfahan), 2013; 10:31-37. 6. Ozveren A, Tuskan C, Yaltirik M, Et all. Expresion or the tumor suppresor gene p53 in odontogenic cyst. Turk J Med Sci, 2003; 33:243-247. 7. Maryam Seyedmajidi, Shima Nafarzadeh, Sepideh Siadati, Shahryar Shafaee, Ali Bijani, Nazanin Kehmiri, p53 and PCNA expressin in Keratocystic odontogenic tumors compared with Selected Odontogenic Cysts, IJMCM, 2013, Vol 2, No 4

multiple myeloma: A study including 107 cases treated with high-dose melphalan-based chemotherapy and autologous stem cell transplant. Leukemia Lymphoma , 47 (1), 43–47. Chang, H., Yeung, J., Qi, C., Xu, W. (2007). Aberrant nuclear p53 protein expression detected by immunohistochemistry is associated with hemizygous P53 deletion and poor survival for multiple myeloma. Brit. J. Haematol. , 138 (3), 324–329. Chen, M. H., Qi, C. X., Saha, M. N., Chang, H. (2012). p53 nuclear expression correlates with hemizygous TP53 deletion and predicts an adverse out-come for

Genet. 1995; 11:101-5. 10.1016/S0168-9525(00)89010-1 5. Hall PA, Meek D, Lane DP. p53-integrating the complexity. J Pathol. 1996; 180:1-5. 10.1002/(SICI)1096-9896(199609)180:1<1::AID-PATH712>3.0.CO;2-U 6. Miyashita T, Krajewski S, Krajewska M, Wang HG, Lin HK, Liebermann DA, et al. Tumor suppressor p53 is a regulator of bcl-2 and bax gene expression in vitro and in vivo. Oncogene. 1994; 9:1799-805. 7. Serrano M, Hannon GJ, Beach D. A new regulatory motif in cell cycle control causing specific inhibition of cyclin D/CDK4. Nature. 1993; 366:704-7. 8. Mork J, Lie AK

with a slower progressive form of the disease and a better prognosis [ 8 ]. The P53 gene protects the integrity of the genome. The p53 gene is functionally ineffective in all cancers and has a role in preventing tumorigenesis [ 9 ]. The P53 pathway responds to stresses in cell division and replication. Stress signals are also transmitted to the p53 protein [ 10 ]. In response to the P53 activation, P53-mediated down-stream events consist of cell cycle arrest and apoptosis. DNA damage can activate p53 with the inclusion of DNA double-strand break and DNA repair

References 1. Tavassoli FA. Pathology of the Breast, 2nd ed. Stamford, Connecticut; Appleton & Lange; 1999. 2. Moinfar F. ed. Essentials of Diagnostic Breast Pathology, Berlin: Heidelberg: Springer; 2007. 3 Soerjomataram I, Louwman MW, Ribot JG, Roukema JA, Coebergh JW. An overview of prognostic factors for long-term survivors of breast cancer. Breast Cancer Res Treat. 2008; 107: 309-330. 4. Borresen-Dale AL. TP53 and breast cancer. Hum Mutat. 2003; 21: 292-300. 5. Lacroix M, Toillon RA, Leclercq G. p53 and breast cancer, an update. Endocr Relat Cancer. 2006; 13

Telomerase Activity and MDS/EVI Gene Fusion in Myelodysplastic Syndrome. Correlation to the Immunohistochemical Expression of Ki-67, Bcl-2 and p53 in Bone Marrow Biopsy Samples

Background. Myelodysplastic syndrome (MDS) as a complex disorder comprised of 7 entities may arise as a primary disorder, or in a setting of an underlying disease, or as therapy related (secondary MDS). Some cases show MDS/EVI1 gene fusion, and some studies have pinpointed the association between the high-risk MDS and increased telomerase activity.

Aim. To determine the frequency of MDS/EVI1 gene fusion in cases of primary MDS, and to evaluate the possibility for detection of increased telomerase activity in peripheral blood samples from patients with MDS.

Material and methods. We isolated DNA from 35 bone marrow biopsies, and measured the blood telomerase activity (RTA) in 21 of the patients. We performed immunostainigs for Ki-67, Bcl-2 and p53 on the biopsy samples in order to test the correlations to the RTA and MDS/EVI1 presence. MDS/EVI1 fusion was detected with touch-down-direct PCR, and RTA was measured using the "TeloTAGGG-PCR-ELISA-plus kit".

Results. We found MDS/EVI1 fusion in 17.39% of high-risk MDS cases (overall 11.43%). RTA was highly variable in the analyzed group, with 1,8 fold increase of the mean RTA compared to the controls. It was due to the significant RTA increase in high-risk MDS cases, compared to the low-risk cases (p<0.01).

Conclusion. RTA showed correlation to the immunohistochemical expression of Ki-67, and MDS/EVI1 fusion was correlated to the Bcl-2 expression.