Aim of this study is to present the latest researches in the field of molecular medicine, in terms of treatments in malignant hemopathies, emerged from the P53 gene deletion in human lymphoma genome. Method: In recent years proved that the best techniques in the investigation of malignant lymphocytes are the Flow Cytometry, Elisa, ICT and Fluorescence in Situ Hybridization (FISH). This method is used as an alternative to chromosomal banding, a conventional application in molecular medicine. Discussion: 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 2, Issue 6) |
| DOI | 10.11648/j.ajlm.20170206.12 |
| Page(s) | 119-125 |
| 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), 2017. Published by Science Publishing Group |
P-53 Gene, Apoptosis, Fluorescence in Situ Hybridization, Phosphatase-Tensin Homolog, Tumor Necrosis Factor Receptor, Antigen Presenting Cells
| [1] | Zaidi N, Swinnen JV, Smans K. ATP-citrate lyase: a key player in cancer metabolism Cancer Res 2012 (11): 3709-14. |
| [2] | Craig N, Mark S. P. Sansom. Defining the Membrane-Associated State of the PTEN Tumor Suppressor Protein. Biophys J 2013; 5; 104 (3): 613–21. |
| [3] | Patrick S., Craig B. Thompson. Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate Cancer Cell 2012; 21: 297-308. |
| [4] | Busse M, Vaupel P. Accumulation of purine catabolites in solid tumors exposed to therapeutic hyperthermia. Experientia 1996; 52: 469–73. |
| [5] | Tomowiak C, Kennel A, Gary-Gouy, Hadife N. High Membrane Cholesterol in CLL B-Cells and Differential Expression of Cholesterol Synthesis Genes in IG GENE Unmutated vs Mutated Cells. British Journal of Medicine & Medical Research 2012; 2 (3): 313-26. |
| [6] | Antonioli L, Blandizzi C, Pacher P, Haskó G. Immunity, inflammation and cancer: a leading role for adenosine. Nature Reviews Cancer 2013; 13: 842–57. |
| [7] | Naor D 1, Nedvetzki S, Golan I, Melnik L, Faitelson Y. CD44 in cancer. Crit Rev Clin Lab Sci. 2012; 39 (6): 527-79. |
| [8] | Li H, Jogl G. Structural and biochemical studies of TIGAR (TP53-induced glycolysis and apoptosis regulator). J Biol Chem 2009 284: 1748–54. |
| [9] | Niki TH, Ishida N. Role of p53 in the entrainment of mammalian circadian behavior rhythms. Genes Cells 2014; 9 (5): 441–48. |
| [10] | 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. |
| [11] | Ledford H. A host of detailed cell atlases could revolutionize understanding of cancer and other diseases. Nature magazine, e-Book, accessed in January 2017. |
| [12] | Kutsch N, Schwamb J. Over-expression of TOSO in CLL is triggered by B-cell receptor signaling and associated with progressive disease. Blood 2008; 112: 4213-19. |
| [13] | Lunt YS, Heiden VGM. Aerobic Glycolysis: Meeting the Metabolic Requirements of Cell Proliferation. Annual Review of Cell and Developmental Biology 2011; 27: 441-64. |
| [14] | Chung S, Hu W, Park C. The role of microRNAs in hematopoietic stem cell and leukemic stem cell function. Therapeutic Advances in Hematology 2011; 5 (2): 317-34. |
| [15] | Shapiro IG. Cyclin-Dependent Kinase Pathways As Targets for Cancer Treatment, JCO 2006; 24 (11): 1770-83. |
| [16] | Gerriets AV, Rathmell C. J. 2012. Metabolic pathways in T cell fate and Function. Trends in Immunology 2012; 33 (4): 168-73. |
| [17] | Michalek RD. Cutting edge: distinct glycolytic and lipid oxidative metabolic programs are essential for effector and regulatory CD4+ T cell subsets. J. Immunol 2011; 1869: 3299–03. |
| [18] | Shi LZ, Wang R, Huang G, Vogel Pl. HIF1 alpha-dependent glycolytic pathway orchestrates a metabolic checkpoint for the differentiation of TH17 and Treg cells. J. Exp. Med 2011; 208: 1367–76. |
| [19] | Beavis AP, Stagg J, Darcy KP Smyth J. M. CD73: a potent suppressor of anti-tumor immune responses. Trends in Immunology 2012; 1: 1471-78. |
| [20] | Sharm P, Allison PJ. Immune Checkpoint Targeting in Cancer Therapy: Toward Combination Strategies with Curative Potential. Cell. 2011; 16 (2): 205–214. |
| [21] | Frauwirth K. A, Riley J. L, Harris M. H, Parry R. V, Rathmell J. C. The CD28 signaling pathway regulates glucose metabolism. Immunity 2002; 16: 769–77. |
| [22] | Wang R., Dillon C. P, Shi L. Z, Milasta S. The transcription factor Myc controls metabolic reprogramming upon T lymphocyte activation. Immunity 2011; 35: 871–82. |
| [23] | Semenza G. L. Regulation of oxygen homeostasis by hypoxia inducible factor 1. Physiology Bethesda 2009; 24: 97–106. |
| [24] | HYPERLINK "https://en.wikipedia.org/wiki/Gene_therapyHuman Cloning and Genetic Modification. Association of Reproductive Health Officials 2013; accessed in January 2016. |
APA Style
Aurelian Udriştoiu. (2017). New Principles of Treatments in Malignant Hematological Diseases, as Acute and Chronic Lymphocytic Leukemia or Multiple Myeloma. American Journal of Laboratory Medicine, 2(6), 119-125. https://doi.org/10.11648/j.ajlm.20170206.12
ACS Style
Aurelian Udriştoiu. New Principles of Treatments in Malignant Hematological Diseases, as Acute and Chronic Lymphocytic Leukemia or Multiple Myeloma. Am. J. Lab. Med. 2017, 2(6), 119-125. doi: 10.11648/j.ajlm.20170206.12
AMA Style
Aurelian Udriştoiu. New Principles of Treatments in Malignant Hematological Diseases, as Acute and Chronic Lymphocytic Leukemia or Multiple Myeloma. Am J Lab Med. 2017;2(6):119-125. doi: 10.11648/j.ajlm.20170206.12
Share This Article
Twitter
Linked In
Facebook
Copy
Download@article{10.11648/j.ajlm.20170206.12,
author = {Aurelian Udriştoiu},
title = {New Principles of Treatments in Malignant Hematological Diseases, as Acute and Chronic Lymphocytic Leukemia or Multiple Myeloma},
journal = {American Journal of Laboratory Medicine},
volume = {2},
number = {6},
pages = {119-125},
doi = {10.11648/j.ajlm.20170206.12},
url = {https://doi.org/10.11648/j.ajlm.20170206.12},
eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajlm.20170206.12},
abstract = {Aim of this study is to present the latest researches in the field of molecular medicine, in terms of treatments in malignant hemopathies, emerged from the P53 gene deletion in human lymphoma genome. Method: In recent years proved that the best techniques in the investigation of malignant lymphocytes are the Flow Cytometry, Elisa, ICT and Fluorescence in Situ Hybridization (FISH). This method is used as an alternative to chromosomal banding, a conventional application in molecular medicine. Discussion: 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 = {2017}
}
TY - JOUR T1 - New Principles of Treatments in Malignant Hematological Diseases, as Acute and Chronic Lymphocytic Leukemia or Multiple Myeloma AU - Aurelian Udriştoiu Y1 - 2017/10/30 PY - 2017 N1 - https://doi.org/10.11648/j.ajlm.20170206.12 DO - 10.11648/j.ajlm.20170206.12 T2 - American Journal of Laboratory Medicine JF - American Journal of Laboratory Medicine JO - American Journal of Laboratory Medicine SP - 119 EP - 125 PB - Science Publishing Group SN - 2575-386X UR - https://doi.org/10.11648/j.ajlm.20170206.12 AB - Aim of this study is to present the latest researches in the field of molecular medicine, in terms of treatments in malignant hemopathies, emerged from the P53 gene deletion in human lymphoma genome. Method: In recent years proved that the best techniques in the investigation of malignant lymphocytes are the Flow Cytometry, Elisa, ICT and Fluorescence in Situ Hybridization (FISH). This method is used as an alternative to chromosomal banding, a conventional application in molecular medicine. Discussion: 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 - 2 IS - 6 ER -
Information
Email: