Activation of tumor suppressor p53 gene expression by magnetic thymine-imprinted chitosan nanoparticles

2016 ◽  
Vol 52 (10) ◽  
pp. 2137-2140 ◽  
Author(s):  
Mei-Hwa Lee ◽  
James L. Thomas ◽  
Jian-Zhou Chen ◽  
Jeng-Shiung Jan ◽  
Hung-Yin Lin
Keyword(s):  
Gene Expression ◽  
Magnetic Nanoparticles ◽  
Tumor Suppressor ◽  
Hepg2 Cells ◽  
Chitosan Nanoparticles ◽  
P53 Gene ◽  
Tumor Suppressor P53

Chitosan nanoparticles imprinted with thymine (and containing magnetic nanoparticles for ease in separations) were found to have dramatic effects on the expression of p53 in HepG2 cells.

Loss of the Tumor Suppressor p53 Gene at the Liver Cirrhosis Stage in Japanese Patients with Hepatocellular Carcinoma

Oncology ◽  
1997 ◽  
Vol 54 (4) ◽  
pp. 304-310 ◽  
Author(s):  
Yosuke Kishimoto ◽  
Goshi Shiota ◽  
Yoshinori Kamisaki ◽  
Kouichirou Wada ◽  
Kentaro Nakamoto ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Cirrhosis ◽  
Tumor Suppressor ◽  
P53 Gene ◽  
Japanese Patients ◽  
Tumor Suppressor P53

scholarly journals Tumor suppressor p53 regulates heparanase gene expression

Oncogene ◽  
2006 ◽  
Vol 25 (28) ◽  
pp. 3939-3947 ◽  
Author(s):  
L Baraz ◽  
Y Haupt ◽  
M Elkin ◽  
T Peretz ◽  
I Vlodavsky
Keyword(s):  
Gene Expression ◽  
Tumor Suppressor ◽  
Tumor Suppressor P53

Tumor suppressor p53 gene codon 72 polymorphism and imatinib cytogenetic response in chronic myeloid leukemia

2019 ◽  
Vol 32 (4) ◽  
pp. 1485
Author(s):  
YasminA. H Sadek Younis ◽  
KhaledAbd Almoamen Khalifa ◽  
EnasS Essa ◽  
WafaaM Shehata Radwan ◽  
EnasA Elkholy
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Tumor Suppressor ◽  
Myeloid Leukemia ◽  
P53 Gene ◽  
Cytogenetic Response ◽  
Tumor Suppressor P53 ◽  
Codon 72 ◽  
Codon 72 Polymorphism

The Tumor Suppressor p53 Down-Regulates Glucose Transporters GLUT1 and GLUT4 Gene Expression

2004 ◽  
Vol 64 (7) ◽  
pp. 2627-2633 ◽  
Author(s):  
Fabiana Schwartzenberg-Bar-Yoseph ◽  
Michal Armoni ◽  
Eddy Karnieli
Keyword(s):  
Gene Expression ◽  
Tumor Suppressor ◽  
Glucose Transporters ◽  
Tumor Suppressor P53 ◽  
Glut4 Gene Expression

T.47. Human Tumor Suppressor p53 Modulates HIV-1 Vif and Tat Functions: Implications in HIV-1 Gene Expression and Replication

2009 ◽  
Vol 131 ◽  
pp. S63-S64
Author(s):  
Vikas Sood ◽  
Rajesh Ranjan ◽  
V. Ramachandran ◽  
Akhil Banerjea
Keyword(s):  
Gene Expression ◽  
Tumor Suppressor ◽  
Human Tumor ◽  
Tumor Suppressor P53 ◽  
Hiv 1

Gelsolin negatively regulates the activity of tumor suppressor p53 through their physical interaction in hepatocarcinoma HepG2 cells

2011 ◽  
Vol 412 (1) ◽  
pp. 44-49 ◽  
Author(s):  
Joo-Hee An ◽  
Jung-Woong Kim ◽  
Sang-Min Jang ◽  
Chul-Hong Kim ◽  
Eun-Jin Kang ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Hepg2 Cells ◽  
Physical Interaction ◽  
Tumor Suppressor P53

scholarly journals Isochromosome der(17)(q10)t(15;17) in acute promyelocytic leukemia resulting in an additional copy of the RARA-PML and loss of one p53 gene: Report of two cases and literature review

2019 ◽  
Vol 76 (9) ◽  
pp. 960-967
Author(s):  
Vesna Djordjevic ◽  
Marija Dencic-Fekete ◽  
Jelica Jovanovic ◽  
Marijana Virijevic ◽  
Nada Kraguljac-Kurtovic ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Acute Promyelocytic Leukemia ◽  
P53 Gene ◽  
Promyelocytic Leukemia ◽  
Chromosome 17 ◽  
Gene Copy ◽  
Fish Analysis ◽  
Derivative Chromosome ◽  
Tumor Suppressor P53 ◽  
Poor Prognostic Factor

Introduction. The isochromosome of the long arm of derivative chromosome 17, that originates from the translocation t(15;17) [ider(17)(q10)t(15;17), or ider(17q)] in acute promyelocytic leukemia (APL), is a rare chromosome aberration associated with a poor prognosis. Case report. We report the clinical and laboratory data associated with ider(17q) for two APL patients. Cytogenetic analysis of bone marrow cells in both cases showed a mosaic karyotype with the ider(17q); reverse transcription polymerase chain reaction (RT-PCR) was positive for the long (L) isoform of the retionic acid receptor alpha (PML-RARA) fusion transcript in each patient. Fluorescence in situ hybridization (FISH) analysis with the DNA probes for the PML gene on 15q24.1, and the RARA gene on 17q21.2, confirmed the extra copy of the RARA-PML fusion gene or ider(17q). Additionally, the FISH analysis with a DNA probe for the p53 gene on 17p13.1 confirmed loss of one copy of the universal tumor suppressor p53 in both patients. Conclusion. Both reported APL patients with ider(17q) had predominance of the clone with ider(17q) compared to those with t(15;17) and/or the normal karyotype, indicating that duplication of der(17) may provide a growth advantage allowing the relevant clone to become dominant. Moreover, as an important oncogenic event and poor prognostic factor in leukemia, loss of one gene copy of the tumor suppressor p53, may also contribute to this growth advantage. Although the clinical and prognostic significance for the patients with an ider(17q) remains unclear, cytogenetic and molecular-genetic analysis should be combined to reveal more details about this complex and rare chromosomal abnormality.

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