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p53/Surviving Ratio as a Parameter for Chemotherapy Induction Response in Children with Acute Myeloid Leukemia

Journal of Tropical Life Science : International Journal of Theoretical, Experimental, and Applied Life Sciences · Vol. 6 No. 3 (2016) · hlm. 142–150

DOI
10.11594/jtls.06.03.02
ISSN
2527-4376, 2087-5517
Terbit
2016-11-01
Penerbit
Journal of Tropical Life Science
Bahasa
eng

Abstrak

Acute myeloid leukemia (AML) is a malignancy that is often found in children. Many studies into the failure of apoptosis function, or programmed cell death, is one of the most important regulatory mechanisms of cellular hemostasis which is closely linked to the development of cancer, are important. Also, regulation of the apoptotic (p53) and anti-apoptotic (surviving) proteins influence treatment outcome. One role of p53 is to monitor cellular stress necessary to induce apoptosis. Surviving (BIRC5) is a group of proteins in the apoptosis inhibitor which works by inhibiting caspase-3. The role of surviving is considered very important in oncogenesis proliferation and cell growth regulation. Chemotherapy in childhood AML can inhibit cell growth and induce slowing as well as stopping the cell cycle. Thus, the aim of this study was to compare p53 and surviving before and after receiving induction chemotherapy in children with AML and also to determine the p53/surviving ratio. Peripheral blood mononuclear cells were collected from AML children before treatment and three months after starting their induction therapy. p53 and surviving were measured by flowcytometry using monoclonal antibodies. Data were analyzed by t-test for comparison between groups and Spearman’s test to find out the correlation between variables with a significant value of p < 0.05. A total of 8 children were evaluated. The intensity of p53 expression was not significantly increased after induction phase chemotherapy (p = 0.224), but surviving expression and the ratio of p53/surviving were significantly increased in the treatment group compared with the levels prior to chemotherapy (p = 0.002, p = 0.034), and there was a strong negative correlation between p53 and surviving after chemotherapy (r = −0.63, p = 0.049).

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  • University of Brawijaya
  • Universitas Jember
  • RSUD Prof. Dr. Saiful Anwar Malang
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Rekan penulisOrganisasiArtikel bersama
Renny SuwarniatyUniversity of Brawijaya2
Muhammad Ali ShodikinUniversitas Jember1
Sumarno Reto PrawiroUniversity of Brawijaya1
Hamid Hunaif Dhofi AlluzaUniversity of Brawijaya1
Ema Dianita MayasariUniversity of Brawijaya1
Mohammad Saifur RahmanAfiliasi tidak diketahui1
Loeki Enggar FitriUniversity of Brawijaya1
Rachmania PutriUniversity of Brawijaya1
Tatit NursetaRSUD Prof. Dr. Saiful Anwar Malang1
Riny NatalinaUniversity of Brawijaya1
Wisnu BarliantoAfiliasi tidak diketahui1
Desy WulandariUniversity of Brawijaya1
Tita Luthfia SariUniversity of Brawijaya1

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Sumber metadata: OAI-PMH (metadata jurnal) http://jtrolis.ub.ac.id/index.php/jtrolis/oai, pertama di-harvest 9 Nov 2026, terakhir terlihat 9 Nov 2026.
Metadata asli (oai_dc)
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	<dc:title xml:lang="en">p53/Surviving Ratio as a Parameter for Chemotherapy Induction Response in Children with Acute Myeloid Leukemia</dc:title>
	<dc:creator xml:lang="en">Lenggana, Rinaldi</dc:creator>
	<dc:creator xml:lang="en">Nugroho, Susanto</dc:creator>
	<dc:creator xml:lang="en">Winarsih, Sri</dc:creator>
	<dc:subject xml:lang="en">p53</dc:subject>
	<dc:subject xml:lang="en">surviving</dc:subject>
	<dc:subject xml:lang="en">acute myeloid leukemia</dc:subject>
	<dc:description xml:lang="en">Acute myeloid leukemia (AML) is a malignancy that is often found in children. Many studies into the failure of apoptosis function, or programmed cell death, is one of the most important regulatory mechanisms of cellular hemostasis which is closely linked to the development of cancer, are important. Also, regulation of the apoptotic (p53) and anti-apoptotic (surviving) proteins influence treatment outcome. One role of p53 is to monitor cellular stress necessary to induce apoptosis. Surviving (BIRC5) is a group of proteins in the apoptosis inhibitor which works by inhibiting caspase-3. The role of surviving is considered very important in oncogenesis proliferation and cell growth regulation. Chemotherapy in childhood AML can inhibit cell growth and induce slowing as well as stopping the cell cycle. Thus, the aim of this study was to compare p53 and surviving before and after receiving induction chemotherapy in children with AML and also to determine the p53/surviving ratio. Peripheral blood mononuclear cells were collected from AML children before treatment and three months after starting their induction therapy. p53 and surviving were measured by flowcytometry using monoclonal antibodies. Data were analyzed by t-test for comparison between groups and Spearman’s test to find out the correlation between variables with a significant value of p &amp;lt; 0.05. A total of 8 children were evaluated. The intensity of p53 expression was not significantly increased after induction phase chemotherapy (p = 0.224), but surviving expression and the ratio of p53/surviving were significantly increased in the treatment group compared with the levels prior to chemotherapy (p = 0.002, p = 0.034), and there was a strong negative correlation between p53 and surviving after chemotherapy (r = −0.63, p = 0.049).</dc:description>
	<dc:publisher xml:lang="en">Journal of Tropical Life Science</dc:publisher>
	<dc:date>2016-11-01</dc:date>
	<dc:type>info:eu-repo/semantics/article</dc:type>
	<dc:type>info:eu-repo/semantics/publishedVersion</dc:type>
	<dc:format>application/pdf</dc:format>
	<dc:identifier>https://jtrolis.ub.ac.id/index.php/jtrolis/article/view/432</dc:identifier>
	<dc:identifier>10.11594/jtls.06.03.02</dc:identifier>
	<dc:source xml:lang="en">Journal of Tropical Life Science; Vol. 6 No. 3 (2016); 142 -150</dc:source>
	<dc:source>2527-4376</dc:source>
	<dc:source>2087-5517</dc:source>
	<dc:language>eng</dc:language>
	<dc:relation>https://jtrolis.ub.ac.id/index.php/jtrolis/article/view/432/pdf</dc:relation>
	<dc:rights xml:lang="en">Copyright (c) 2016 Journal of Tropical Life Science</dc:rights>
</oai_dc:dc>