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	<id>https://transhumanist.ru/index.php?action=history&amp;feed=atom&amp;title=DIP2A</id>
	<title>DIP2A - История изменений</title>
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	<updated>2026-04-10T21:33:12Z</updated>
	<subtitle>История изменений этой страницы в вики</subtitle>
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		<id>https://transhumanist.ru/index.php?title=DIP2A&amp;diff=6378&amp;oldid=prev</id>
		<title>OdysseusBot: Новая страница: «Disco-interacting protein 2 homolog A (EC 6.2.1.1) (DIP2 homolog A) [C21orf106] [DIP2] [KIAA0184]  ==Publications==  {{medline-entry |title=Blocking the FSTL1...»</title>
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		<updated>2021-05-12T15:27:24Z</updated>

		<summary type="html">&lt;p&gt;Новая страница: «Disco-interacting protein 2 homolog A (EC 6.2.1.1) (DIP2 homolog A) [C21orf106] [DIP2] [KIAA0184]  ==Publications==  {{medline-entry |title=Blocking the &lt;a href=&quot;/FSTL1&quot; title=&quot;FSTL1&quot;&gt;FSTL1&lt;/a&gt;...»&lt;/p&gt;
&lt;p&gt;&lt;b&gt;Новая страница&lt;/b&gt;&lt;/p&gt;&lt;div&gt;Disco-interacting protein 2 homolog A (EC 6.2.1.1) (DIP2 homolog A) [C21orf106] [DIP2] [KIAA0184]&lt;br /&gt;
&lt;br /&gt;
==Publications==&lt;br /&gt;
&lt;br /&gt;
{{medline-entry&lt;br /&gt;
|title=Blocking the [[FSTL1]]-[[DIP2A]] Axis Improves Anti-tumor Immunity.&lt;br /&gt;
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30110636&lt;br /&gt;
|abstract=Immune dysfunction is a strong factor in the resistance of cancer to treatment. Blocking immune checkpoint pathways is a promising approach to improve anti-tumor immunity, but the clinical efficacies are still limited. We previously identified follistatin-like 1 ([[FSTL1]]) as a determinant of immune dysfunction mediated by mesenchymal stromal/stem cells (MSCs) and immunoregulatory cells. Here, we demonstrate that blocking [[FSTL1]] but not immune checkpoint pathways significantly suppresses cancer progression and metastasis in several mouse tumor models with increased MSCs. Expression of [[DIP2A]] (the receptor of [[FSTL1]]) in tumor cells is critical for [[FSTL1]]-induced immunoresistance. [[FSTL1]]/[[DIP2A]] co-positivity in tumor tissues correlates with poor prognosis in NSCLC patients. Thus, breaking the [[FSTL1]]-[[DIP2A]] axis may be a useful strategy for successfully inducing anti-tumor immunity.&lt;br /&gt;
|mesh-terms=* Animals&lt;br /&gt;
* Carcinoma, Non-Small-Cell Lung&lt;br /&gt;
* Carrier Proteins&lt;br /&gt;
* Case-Control Studies&lt;br /&gt;
* Cell Line, Tumor&lt;br /&gt;
* Cell Movement&lt;br /&gt;
* Cell Proliferation&lt;br /&gt;
* Disease Progression&lt;br /&gt;
* Female&lt;br /&gt;
* Follistatin-Related Proteins&lt;br /&gt;
* Gene Expression Regulation, Neoplastic&lt;br /&gt;
* Humans&lt;br /&gt;
* Immunity, Innate&lt;br /&gt;
* Lung Neoplasms&lt;br /&gt;
* Male&lt;br /&gt;
* Mesenchymal Stem Cells&lt;br /&gt;
* Mice&lt;br /&gt;
* Mice, Inbred BALB C&lt;br /&gt;
* Mice, Inbred C57BL&lt;br /&gt;
* Nuclear Proteins&lt;br /&gt;
* Prognosis&lt;br /&gt;
* RNA, Small Interfering&lt;br /&gt;
* Signal Transduction&lt;br /&gt;
* Survival Analysis&lt;br /&gt;
* Tumor Burden&lt;br /&gt;
* Xenograft Model Antitumor Assays&lt;br /&gt;
|keywords=* FSTL1&lt;br /&gt;
* aging&lt;br /&gt;
* antibody&lt;br /&gt;
* cancer metastasis&lt;br /&gt;
* immune checkpoint&lt;br /&gt;
* immune exhaustion&lt;br /&gt;
* immunosuppression&lt;br /&gt;
* lung cancer&lt;br /&gt;
* mesenchymal stromal/stem cells&lt;br /&gt;
|full-text-url=https://sci-hub.do/10.1016/j.celrep.2018.07.043&lt;br /&gt;
}}&lt;/div&gt;</summary>
		<author><name>OdysseusBot</name></author>
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