Role of P53 Gene in Oncogenesis from Chronic Lymphocytic Leukemia

Aurelian Udristioiu

doi:doi:10.11648/j.ajlm.20160102.13

| Peer-Reviewed

Role of P53 Gene in Oncogenesis from Chronic Lymphocytic Leukemia

Aurelian Udristioiu

Published in American Journal of Laboratory Medicine (Volume 1, Issue 2)

Received: 27 August 2016 Accepted: 5 September 2016 Published: 24 September 2016

Views: Downloads:

Download PDF

Share This Article

Twitter
Linked In
Facebook

Abstract

Objective of this study is to present the latest researches in the field of molecular medicine, in terms of Chronic Lymphocytic Leukemia (CLL), emerged from the P53 gene deletion in human lymphoma genome. Method In recent years proved that the best technique in the investigation of malignant lymphocytes is the Fluorescence in situ hybridization (FISH). This method is used as an alternative to chromosomal banding, a conventional application in molecular medicine. Previous Results: In the literature it was registered, in previous years, on an international study, conducted on 109 cases of CLL, 79 cases (72.5%) who had more genetic abnormalities; the remaining 30 cases (27.5%) had normal results, using the technique Florescence in situ Hybridization, (FISH). The majority of patients, 67% (53.79) had a single anomaly and the remaining 33% had two or three genetic abnormalities. The band 14q32 /17p translocations in LLC genome, which appeared similar to some common, had demonstrated abnormalities involving IGH gene, located on chromosome14q32. Discussions: Identification of P53 gene mutations in regions of 17 chromosome of hematological neoplasm is important because these mutations have an impact on the clinical course of patients and requires an attitude adjustment therapeutic adequate. Restoring function to p53 can induce lymphoma, apoptosis. Recent, endogenous somatic gene therapy research is a basic of trial clinical and therapeutic trial. The DNA, is used to treat a disease arising as a result of mutations in chromosomal regions. In the past few years, this method has been included in the treatment of CLL, acute lymphocytic leukemia, [ALL], or multiple myeloma [MM]. Conclusion: The frequencies of P53 gene mutations and deletion in CLL can be categorized as individual biomarkers in proteomic and genomic profile for this type of leukemia that can be implemented in targeted patient treatment of personalized medicine.

Published in	American Journal of Laboratory Medicine (Volume 1, Issue 2)
DOI	10.11648/j.ajlm.20160102.13
Page(s)	16-22
Creative Commons	This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.
Copyright	Copyright © The Author(s), 2016. Published by Science Publishing Group

Keywords

P-53 Gene, Lymphocytic Leukemia, Apoptosis, Fluorescence in Situ Hybridization

References

[1]	Zenz T, Mertens D, Küppers R, Döhner et al. From pathogenesis to treatment of chronic lymphocytic leukaemia. Nat Rev Cancer. 2010; 10 (1): 37-5.
[2]	Udristioiu A, Florescu C, Popescu MA, Cojocaru M. High Concentration of anaerobic ATP implicated in aborted apoptosis from CLL. Lab Med 2010; 41: 203-08.
[3]	Hallek M. Chronic lymphocytic leukemia: 2015 Update on diagnosis, risk stratification, and treatment. Cancer Cell. 2010; 17(1): 28-40.
[4]	Gonzalez DK, Buzin HC, Dongqin Gu et. al. Beyond Li Fraumeni Syndrome: Clinical Characteristics of Families With p53 Germline Mutations. JCO 2009; 29 (8): 1250-6.
[5]	Read AP, Strachan T. Human molecular genetics 2. New York: Wiley, ISBN 0-471-33061-2, Chapter 18: Cancer Genetics 2009.
[6]	Nelson BP, Gupta R, Dewald GW, Paternoster SF et al. Chronic Lymphocytic Leukemia, Panel FISH: Impact about diagnosis. Am J Clin Pathol. 2007; 128 (2): 323-32.
[7]	Zerdoumi Y, Kasper E, Soubigou F, Adriouch S. A new genotoxicity assay based on p53 target gene induction. Mutat Res Genet Toxicol Environ Mutagen.. 2015; 789-790: 28-35.
[8]	Wang F, Lv P, Liu X, Zhu M, et al. MicroRNA-214 enhances the invasion ability of breast cancer cells by targeting p53. Int J Mol. 2015; 35(5): 1395-402.
[9]	Klein U, Lia M, Crespo M, Siegel R et al. The DLEU2/miR-15a/16-1 cluster controls B cell proliferation and its deletion leads to chronic lymphocytic leukemia. Proc Natl Acad Sci. 2002; 99(24): 15524-9.
[10]	Zhu J, Zhang S, Jiang J, Chen X. Definition of the p53 functional domains necessary for inducing apoptosis. The Journal of Biological Chemistry. 2000; (51): 39927–34.
[11]	Oncogenetic Tests, FISH panel LLC. MedLife Genetica]. https:/www.medlife.ro/genetics/teste-disponibile/teste-de-oncogeneticaa, accesat in/03/2016.
[12]	Isobe M, Emanuel BS, Givol D, Oren M, Croce CM. Localization of gene for human p53 tumour antigen to band 17p13. Nature. 1986; 6057: 59.
[13]	Kern SE, Kinzler KW, Bruskin A, Jarosz D, et a. Identification of p53 as a sequence-specific DNA-binding protein. Science. 1999; 235: 1708–11.
[14]	Hollstein M, Sidransky D, Vogelstein B, Harris CC. P53 mutations in human cancers. Science. 1991; 253 (5015): 49–53.
[15]	. Caruso JA, Talaska G, Stambrook JP, Stringer RJ. Mutation Research/Genetic Toxicology and Environmental Mutagenesis. Elsevier, Vol. 521, Issues 1–2, Pages 1-234; 2002.
[16]	Sabapathy K. The Contrived Mutant p53 Oncogene – Beyond Loss of Functions. Front Onco. 2015; 5: 27-60.
[17]	Hermeking H. MicroRNAs in the p53 network: micromanagement of tumour suppression. Nat Rev Cancer. (2012) 12(9):613–26. doi:10.1038/nrc3318.
[18]	Hoffman Y, Pilpel Y, Oren M. microRNAs and Alu elements in the p53-Mdm2-Mdm4 regulatory network. J Mol Cell Biol. (2014) 6(3): 192–7. doi:10.1093/jmcb/mju020
[19]	Meek DW. Regulation of the p53 response and its relationship to cancer. Biochem J 2015; 469(3): 325-46.
[20]	Derbyshire DJ, Basu BP, Serpell LC, Joo WS, Date T, et al. Role of 53BP1 in the Regulation of DNA Double-Strand Break Repair Pathway Choice. Radiat Res. 2014; 181 (1): 1–8.
[21]	Khoury MP, Bourdon JC. P53 Isoforms: An Intracellular Microprocessor?. Genes Cancer. 2011; 2 (4):453-65. doi: 10.1177/1947601911408893.
[22]	Zhang J, Shen L, Sun LQ. The regulation of radiosensitivity by p53 and its acetylation. Cancer Lett. 2015; 363(2):108-18.
[23]	Gottlieb E, Vousden KH. P53 regulation of metabolic pathways. Cold Spring Harb Perspect Biol. 2010; (4):A. 001040.
[24]	Tsai RY, McKay RD. A nucleolar mechanism controlling cell proliferation in stem cells and cancer cells. Genes & Development. 2002; 16 (23): 2991–3003.
[25]	Sabapathy K. The Contrived Mutant p53 Oncogene – Beyond Loss of Functions. Sci Rep. 2015; 7: 9997.
[26]	Niki TH, Ishida N. Role of p53 in the entrainment of mammalian circadian behavior rhythms. Genes Cells. 2014; 9 (5): 441–48.
[27]	Udristioiu A. Bioenergetics of normal and malignant cells: Chpt. Interference between the energies in normal and malignant cells, pg 125-135. Editor Everest, Academica Brancusi, Targu Jiu, 2002.
[28]	Li H, Jogl G. Structural and biochemical studies of TIGAR (TP53-induced glycolysis and apoptosis regulator). J Biol Chem. (2009) 284:1748–54. doi:10.1074/jbc.M807821200.
[29]	Lahav G. Oscillations by the p53-Mdm2 Feedback Loop. Cellular Oscillatory Mechanisms, edited by Miguel Maroto and Nicholas A.M.Monk. ©2008 Landes Bioscience and Springer Science+Business Media.
[30]	Gene Therapy Clinical Trials Worldwide Database. The Journal of Gene Medicine. Retrieved 22 March 2015; accessed in January 2016.
[31]	Ledford H. Cell therapy fights leukemia. Nature; 2011. doi:10.1038/news.2011.472.
[32]	Rosenberg SA, Aebersold P, K Cornetta; et al. Gene transfer into humans with advanced melanoma immunotherapy of Patients, using tumor-infiltrating lymphocytes modified by retroviral gene transduction. N. Engl. J. Med 1990; 323: 570-8.
[33]	Andy C. Gene therapy cures leukaemia in eight days. The New Scientist. 2013
[34]	Hosman E, Shanks P, Darnovsky M. Biopolitical News. Biopolitical Times on December 22nd, 2015.
[35]	Secchiero P, Voltan R, Iasio GM, Melloni. The oncogene DEK promotes leukemic cell survival and is down regulated by both Nutlin-3 and chlorambucil in B-chronic lymphocytic leukemic cells. Clin Cancer Res. 2010; 16: 1824–33.
[36]	Speetjens F, Kuppen P, Welters M, Essahsah F. Induction of p53-specific immunity by a p53 synthetic long peptide vaccine in patients treated for metastatic colorectal cancer. Clin Cancer Res. 2009 15: 1086–95.
[37]	Shangary S, Qin D, Mc Eachern D, Liu M. Temporal activation of p53 by a specific MDM2 inhibitor is selectively toxic to tumors and leads to complete tumor growth inhibition. Proc. Natl Acad. Sci. 2008; 105: 3933–38.
[38]	Van der Burg SH, Cock K, Menon AG, Franken KL. Long lasting p53-specific T cell memory responses in the absence of anti-p53 antibodies in patients with respected primary colorectal cancer. Eur. J. Immunol. 2001; 31: 146–55.

Cite This Article

Plain Text BibTeX RIS

APA Style

Aurelian Udristioiu. (2016). Role of P53 Gene in Oncogenesis from Chronic Lymphocytic Leukemia. American Journal of Laboratory Medicine, 1(2), 16-22. https://doi.org/10.11648/j.ajlm.20160102.13

Copy | Download

ACS Style

Aurelian Udristioiu. Role of P53 Gene in Oncogenesis from Chronic Lymphocytic Leukemia. Am. J. Lab. Med. 2016, 1(2), 16-22. doi: 10.11648/j.ajlm.20160102.13

Copy | Download

AMA Style

Aurelian Udristioiu. Role of P53 Gene in Oncogenesis from Chronic Lymphocytic Leukemia. Am J Lab Med. 2016;1(2):16-22. doi: 10.11648/j.ajlm.20160102.13

Copy | Download

@article{10.11648/j.ajlm.20160102.13,
  author = {Aurelian Udristioiu},
  title = {Role of P53 Gene in Oncogenesis from Chronic Lymphocytic Leukemia},
  journal = {American Journal of Laboratory Medicine},
  volume = {1},
  number = {2},
  pages = {16-22},
  doi = {10.11648/j.ajlm.20160102.13},
  url = {https://doi.org/10.11648/j.ajlm.20160102.13},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajlm.20160102.13},
  abstract = {Objective of this study is to present the latest researches in the field of molecular medicine, in terms of Chronic Lymphocytic Leukemia (CLL), emerged from the P53 gene deletion in human lymphoma genome. Method In recent years proved that the best technique in the investigation of malignant lymphocytes is the Fluorescence in situ hybridization (FISH). This method is used as an alternative to chromosomal banding, a conventional application in molecular medicine. Previous Results: In the literature it was registered, in previous years, on an international study, conducted on 109 cases of CLL, 79 cases (72.5%) who had more genetic abnormalities; the remaining 30 cases (27.5%) had normal results, using the technique Florescence in situ Hybridization, (FISH). The majority of patients, 67% (53.79) had a single anomaly and the remaining 33% had two or three genetic abnormalities. The band 14q32 /17p translocations in LLC genome, which appeared similar to some common, had demonstrated abnormalities involving IGH gene, located on chromosome14q32. Discussions: Identification of P53 gene mutations in regions of 17 chromosome of hematological neoplasm is important because these mutations have an impact on the clinical course of patients and requires an attitude adjustment therapeutic adequate. Restoring function to p53 can induce lymphoma, apoptosis. Recent, endogenous somatic gene therapy research is a basic of trial clinical and therapeutic trial. The DNA, is used to treat a disease arising as a result of mutations in chromosomal regions. In the past few years, this method has been included in the treatment of CLL, acute lymphocytic leukemia, [ALL], or multiple myeloma [MM]. Conclusion: The frequencies of P53 gene mutations and deletion in CLL can be categorized as individual biomarkers in proteomic and genomic profile for this type of leukemia that can be implemented in targeted patient treatment of personalized medicine.},
 year = {2016}
}

Copy | Download

TY  - JOUR
T1  - Role of P53 Gene in Oncogenesis from Chronic Lymphocytic Leukemia
AU  - Aurelian Udristioiu
Y1  - 2016/09/24
PY  - 2016
N1  - https://doi.org/10.11648/j.ajlm.20160102.13
DO  - 10.11648/j.ajlm.20160102.13
T2  - American Journal of Laboratory Medicine
JF  - American Journal of Laboratory Medicine
JO  - American Journal of Laboratory Medicine
SP  - 16
EP  - 22
PB  - Science Publishing Group
SN  - 2575-386X
UR  - https://doi.org/10.11648/j.ajlm.20160102.13
AB  - Objective of this study is to present the latest researches in the field of molecular medicine, in terms of Chronic Lymphocytic Leukemia (CLL), emerged from the P53 gene deletion in human lymphoma genome. Method In recent years proved that the best technique in the investigation of malignant lymphocytes is the Fluorescence in situ hybridization (FISH). This method is used as an alternative to chromosomal banding, a conventional application in molecular medicine. Previous Results: In the literature it was registered, in previous years, on an international study, conducted on 109 cases of CLL, 79 cases (72.5%) who had more genetic abnormalities; the remaining 30 cases (27.5%) had normal results, using the technique Florescence in situ Hybridization, (FISH). The majority of patients, 67% (53.79) had a single anomaly and the remaining 33% had two or three genetic abnormalities. The band 14q32 /17p translocations in LLC genome, which appeared similar to some common, had demonstrated abnormalities involving IGH gene, located on chromosome14q32. Discussions: Identification of P53 gene mutations in regions of 17 chromosome of hematological neoplasm is important because these mutations have an impact on the clinical course of patients and requires an attitude adjustment therapeutic adequate. Restoring function to p53 can induce lymphoma, apoptosis. Recent, endogenous somatic gene therapy research is a basic of trial clinical and therapeutic trial. The DNA, is used to treat a disease arising as a result of mutations in chromosomal regions. In the past few years, this method has been included in the treatment of CLL, acute lymphocytic leukemia, [ALL], or multiple myeloma [MM]. Conclusion: The frequencies of P53 gene mutations and deletion in CLL can be categorized as individual biomarkers in proteomic and genomic profile for this type of leukemia that can be implemented in targeted patient treatment of personalized medicine.
VL  - 1
IS  - 2
ER  -

Copy | Download

Author Information

Aurelian Udristioiu

Molecular Biology, Faculty of Medicine, Titu Maiorescu University, Bucharest, Romania

Download PDF

Sections

Plain Text BibTeX RIS

APA Style

Aurelian Udristioiu. (2016). Role of P53 Gene in Oncogenesis from Chronic Lymphocytic Leukemia. American Journal of Laboratory Medicine, 1(2), 16-22. https://doi.org/10.11648/j.ajlm.20160102.13

Copy | Download

ACS Style

Aurelian Udristioiu. Role of P53 Gene in Oncogenesis from Chronic Lymphocytic Leukemia. Am. J. Lab. Med. 2016, 1(2), 16-22. doi: 10.11648/j.ajlm.20160102.13

Copy | Download

AMA Style

Aurelian Udristioiu. Role of P53 Gene in Oncogenesis from Chronic Lymphocytic Leukemia. Am J Lab Med. 2016;1(2):16-22. doi: 10.11648/j.ajlm.20160102.13

Copy | Download

@article{10.11648/j.ajlm.20160102.13,
  author = {Aurelian Udristioiu},
  title = {Role of P53 Gene in Oncogenesis from Chronic Lymphocytic Leukemia},
  journal = {American Journal of Laboratory Medicine},
  volume = {1},
  number = {2},
  pages = {16-22},
  doi = {10.11648/j.ajlm.20160102.13},
  url = {https://doi.org/10.11648/j.ajlm.20160102.13},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajlm.20160102.13},
  abstract = {Objective of this study is to present the latest researches in the field of molecular medicine, in terms of Chronic Lymphocytic Leukemia (CLL), emerged from the P53 gene deletion in human lymphoma genome. Method In recent years proved that the best technique in the investigation of malignant lymphocytes is the Fluorescence in situ hybridization (FISH). This method is used as an alternative to chromosomal banding, a conventional application in molecular medicine. Previous Results: In the literature it was registered, in previous years, on an international study, conducted on 109 cases of CLL, 79 cases (72.5%) who had more genetic abnormalities; the remaining 30 cases (27.5%) had normal results, using the technique Florescence in situ Hybridization, (FISH). The majority of patients, 67% (53.79) had a single anomaly and the remaining 33% had two or three genetic abnormalities. The band 14q32 /17p translocations in LLC genome, which appeared similar to some common, had demonstrated abnormalities involving IGH gene, located on chromosome14q32. Discussions: Identification of P53 gene mutations in regions of 17 chromosome of hematological neoplasm is important because these mutations have an impact on the clinical course of patients and requires an attitude adjustment therapeutic adequate. Restoring function to p53 can induce lymphoma, apoptosis. Recent, endogenous somatic gene therapy research is a basic of trial clinical and therapeutic trial. The DNA, is used to treat a disease arising as a result of mutations in chromosomal regions. In the past few years, this method has been included in the treatment of CLL, acute lymphocytic leukemia, [ALL], or multiple myeloma [MM]. Conclusion: The frequencies of P53 gene mutations and deletion in CLL can be categorized as individual biomarkers in proteomic and genomic profile for this type of leukemia that can be implemented in targeted patient treatment of personalized medicine.},
 year = {2016}
}

Copy | Download

TY  - JOUR
T1  - Role of P53 Gene in Oncogenesis from Chronic Lymphocytic Leukemia
AU  - Aurelian Udristioiu
Y1  - 2016/09/24
PY  - 2016
N1  - https://doi.org/10.11648/j.ajlm.20160102.13
DO  - 10.11648/j.ajlm.20160102.13
T2  - American Journal of Laboratory Medicine
JF  - American Journal of Laboratory Medicine
JO  - American Journal of Laboratory Medicine
SP  - 16
EP  - 22
PB  - Science Publishing Group
SN  - 2575-386X
UR  - https://doi.org/10.11648/j.ajlm.20160102.13
AB  - Objective of this study is to present the latest researches in the field of molecular medicine, in terms of Chronic Lymphocytic Leukemia (CLL), emerged from the P53 gene deletion in human lymphoma genome. Method In recent years proved that the best technique in the investigation of malignant lymphocytes is the Fluorescence in situ hybridization (FISH). This method is used as an alternative to chromosomal banding, a conventional application in molecular medicine. Previous Results: In the literature it was registered, in previous years, on an international study, conducted on 109 cases of CLL, 79 cases (72.5%) who had more genetic abnormalities; the remaining 30 cases (27.5%) had normal results, using the technique Florescence in situ Hybridization, (FISH). The majority of patients, 67% (53.79) had a single anomaly and the remaining 33% had two or three genetic abnormalities. The band 14q32 /17p translocations in LLC genome, which appeared similar to some common, had demonstrated abnormalities involving IGH gene, located on chromosome14q32. Discussions: Identification of P53 gene mutations in regions of 17 chromosome of hematological neoplasm is important because these mutations have an impact on the clinical course of patients and requires an attitude adjustment therapeutic adequate. Restoring function to p53 can induce lymphoma, apoptosis. Recent, endogenous somatic gene therapy research is a basic of trial clinical and therapeutic trial. The DNA, is used to treat a disease arising as a result of mutations in chromosomal regions. In the past few years, this method has been included in the treatment of CLL, acute lymphocytic leukemia, [ALL], or multiple myeloma [MM]. Conclusion: The frequencies of P53 gene mutations and deletion in CLL can be categorized as individual biomarkers in proteomic and genomic profile for this type of leukemia that can be implemented in targeted patient treatment of personalized medicine.
VL  - 1
IS  - 2
ER  -

Copy | Download