<?xml version="1.0" encoding="utf-8"?>
<journal>
<title>Iranian Biomedical Journal</title>
<title_fa>مجله بیومدیکال ایران</title_fa>
<short_title>IBJ</short_title>
<subject>Basic Sciences</subject>
<web_url>http://ibj.pasteur.ac.ir</web_url>
<journal_hbi_system_id>1</journal_hbi_system_id>
<journal_hbi_system_user>admin</journal_hbi_system_user>
<journal_id_issn>1028-852X</journal_id_issn>
<journal_id_issn_online>2008-823X</journal_id_issn_online>
<journal_id_pii>-</journal_id_pii>
<journal_id_doi>10.61882/ibj</journal_id_doi>
<journal_id_iranmedex></journal_id_iranmedex>
<journal_id_magiran></journal_id_magiran>
<journal_id_sid>-</journal_id_sid>
<journal_id_nlai>8888</journal_id_nlai>
<journal_id_science>-</journal_id_science>
<language>en</language>
<pubdate>
	<type>jalali</type>
	<year>1404</year>
	<month>2</month>
	<day>1</day>
</pubdate>
<pubdate>
	<type>gregorian</type>
	<year>2025</year>
	<month>5</month>
	<day>1</day>
</pubdate>
<volume>29</volume>
<number>3</number>
<publish_type>online</publish_type>
<publish_edition>1</publish_edition>
<article_type>fulltext</article_type>
<articleset>
	<article>


	<language>en</language>
	<article_id_doi></article_id_doi>
	<title_fa></title_fa>
	<title>Multifaceted Cooperation Between WNT and PI3K Signaling Axis through the Long Noncoding RNA SNHG16 and TCF7 in de novo Acute Lymphoblastic Leukemia Patients</title>
	<subject_fa>Cancer Biology</subject_fa>
	<subject>Cancer Biology</subject>
	<content_type_fa>مقاله کامل</content_type_fa>
	<content_type>Full Length/Original Article</content_type>
	<abstract_fa></abstract_fa>
	<abstract>&lt;div&gt;&lt;span style=&quot;font-family:Times New Roman;&quot;&gt;&lt;span style=&quot;font-size:11pt&quot;&gt;&lt;span style=&quot;line-height:normal&quot;&gt;&lt;b&gt;&lt;span style=&quot;font-size:10.5pt&quot;&gt;Background: &lt;/span&gt;&lt;/b&gt;&lt;span style=&quot;font-size:10.5pt&quot;&gt;Acute lymphoblastic leukemia (ALL) is the most prevalent form of acute leukemia in children, arising from the known and unknown factors. This complexity has limited advancements in patient recovery. Recently, &lt;/span&gt;&lt;span lang=&quot;EN-GB&quot; style=&quot;font-size:9.0pt&quot;&gt;long noncoding RNAs lncRNA (&lt;/span&gt;&lt;span style=&quot;font-size:10.5pt&quot;&gt;lncRNA) molecules have emerged as significant but not fully understood players in leukemia research. Studies have indicated that &lt;i&gt;c-Myc&lt;/i&gt; can stimulate and enhance gene expression through multiple pathways, particularly by activating the PI3K and WNT pathways. The present study investigated the expression levels of lncRNAs involved in the upstream regulation of the PI3K/WNT pathways in patients diagnosed with ALL. &lt;/span&gt;&lt;/span&gt;&lt;/span&gt;&lt;br&gt;
&lt;span style=&quot;font-size:11pt&quot;&gt;&lt;span style=&quot;line-height:normal&quot;&gt;&lt;b&gt;&lt;span style=&quot;font-size:10.5pt&quot;&gt;Methods: &lt;/span&gt;&lt;/b&gt;&lt;span style=&quot;font-size:10.5pt&quot;&gt;&lt;span style=&quot;color:#1f1f1f&quot;&gt;This case-control cross-sectional study was conducted using RNA from blood samples. The study examined 36 patients with ALL and 36 healthy controls. The expression levels of &lt;i&gt;SNHG16&lt;/i&gt; and &lt;i&gt;TCF7&lt;/i&gt; lncRNAs and their target genes were determined using qRT-PCR.&lt;/span&gt;&lt;/span&gt;&lt;/span&gt;&lt;/span&gt;&lt;/span&gt;&lt;/div&gt;

&lt;div style=&quot;text-align: justify;&quot;&gt;&lt;span style=&quot;font-family:Times New Roman;&quot;&gt;&lt;span style=&quot;font-size:11pt&quot;&gt;&lt;span style=&quot;line-height:normal&quot;&gt;&lt;b&gt;&lt;span style=&quot;font-size:10.5pt&quot;&gt;Results: &lt;/span&gt;&lt;/b&gt;&lt;/span&gt;&lt;/span&gt;&lt;span style=&quot;font-size:10.5pt&quot;&gt;&lt;span style=&quot;line-height:115%&quot;&gt;The expression of &lt;i&gt;Akt&lt;/i&gt;, &lt;i&gt;&amp;beta;-catenin &lt;/i&gt;and&lt;i&gt; c-Myc &lt;/i&gt;genes in the patient group showed a significant increase compared to the control group&amp;nbsp;(&lt;i&gt;p&lt;/i&gt; &lt; 0.05).&lt;b&gt; &lt;/b&gt;The expression levels of &lt;i&gt;SNHG16&lt;/i&gt; and &lt;i&gt;TCF7&lt;/i&gt; were significantly elevated in ALL patients compared to the control group (&lt;i&gt;p&lt;/i&gt; &lt; 0.05). Furthermore, a significant positive correlation was observed between the expression levels of these two lncRNAs in the patient group (&lt;i&gt;p&lt;/i&gt; &lt; 0.05). &lt;/span&gt;&lt;/span&gt;&lt;span style=&quot;font-size:11pt&quot;&gt;&lt;span style=&quot;line-height:normal&quot;&gt;&lt;span style=&quot;font-size:10.5pt&quot;&gt; &lt;/span&gt;&lt;/span&gt;&lt;/span&gt;&lt;/span&gt;&lt;/div&gt;

&lt;div&gt;&lt;span style=&quot;font-family:Times New Roman;&quot;&gt;&lt;b&gt;&lt;span style=&quot;font-size:10.5pt&quot;&gt;&lt;span style=&quot;line-height:115%&quot;&gt;Conclusion: &lt;/span&gt;&lt;/span&gt;&lt;/b&gt;&lt;span style=&quot;font-size:10.5pt&quot;&gt;&lt;span style=&quot;line-height:115%&quot;&gt;Our findings demonstrate that &lt;i&gt;SNHG16&lt;/i&gt; and &lt;i&gt;TCF7&lt;/i&gt; lncRNA may act as crucial regulators of the &lt;i&gt;Akt&lt;/i&gt; and &lt;i&gt;&amp;beta;-catenin &lt;/i&gt;in ALL, which in turn influence &lt;i&gt;c-Myc&lt;/i&gt; expression levels in affected individuals. Further research is needed to better understand the molecular mechanisms underlying ALL, potentially leading to improved treatment and monitoring strategies for patients. &lt;/span&gt;&lt;/span&gt;&lt;/span&gt;&lt;/div&gt;</abstract>
	<keyword_fa></keyword_fa>
	<keyword>SNHG16 lncRNA, TCF7, Wnt signaling pathway</keyword>
	<start_page>104</start_page>
	<end_page>113</end_page>
	<web_url>http://ibj.pasteur.ac.ir/browse.php?a_code=A-10-6206-1&amp;slc_lang=en&amp;sid=1</web_url>


<author_list>
	<author>
	<first_name>Mohadeseh</first_name>
	<middle_name></middle_name>
	<last_name>Khani</last_name>
	<suffix></suffix>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email>mohadesekhani1997.mk@gmail.com</email>
	<code></code>
	<orcid>0009-0002-9385-4349</orcid>
	<coreauthor>No</coreauthor>
	<affiliation>Arak University of Medical Sciences, Arak, Iran</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Atbin</first_name>
	<middle_name></middle_name>
	<last_name>Latifi</last_name>
	<suffix></suffix>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email>latifiatbin@gmail.com</email>
	<code></code>
	<orcid>0000-0003-2115-9910</orcid>
	<coreauthor>No</coreauthor>
	<affiliation>Department of Internal Medicine, School of Medical Sciences, Arak University of Medical Sciences, Arak, Iran</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Mohammad</first_name>
	<middle_name></middle_name>
	<last_name>Sayyadi</last_name>
	<suffix></suffix>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email>m.sayyadi88@gmail.com</email>
	<code></code>
	<orcid>0000-0003-2927-9669</orcid>
	<coreauthor>Yes
</coreauthor>
	<affiliation>Department of Medical Laboratory Sciences, School of Allied Medical Sciences, Arak University of Medical Sciences, Arak, Iran</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


</author_list>


	</article>
</articleset>
</journal>
