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	<title>protein mislocalisation &#8211; BIOENGINEER.ORG</title>
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		<title>How a Leukaemia Mutation Hijacks Cell Division: New Clues from the Chromosome Periphery</title>
		<link>https://bioengineer.org/how-a-leukaemia-mutation-hijacks-cell-division-new-clues-from-the-chromosome-periphery/</link>
		
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		<pubDate>Mon, 12 Oct 2026 19:15:36 +0000</pubDate>
				<category><![CDATA[Health]]></category>
		<category><![CDATA[acute myeloid leukaemia]]></category>
		<category><![CDATA[cancer mutations]]></category>
		<category><![CDATA[cell division]]></category>
		<category><![CDATA[de-compartmentalisation]]></category>
		<category><![CDATA[Ki-67]]></category>
		<category><![CDATA[mitosis]]></category>
		<category><![CDATA[mitotic chromosome periphery]]></category>
		<category><![CDATA[NPM1c+]]></category>
		<category><![CDATA[nucleolus]]></category>
		<category><![CDATA[nucleophosmin]]></category>
		<category><![CDATA[prognosis]]></category>
		<category><![CDATA[protein mislocalisation]]></category>
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					<description><![CDATA[A new Nature Communications study reveals how the common AML mutation NPM1c+ exploits failures in mitotic chromosome periphery binding and nuclear de-compartmentalisation to stay locked out of the nucleolus, and shows that Ki-67 expression interacts with mutation status to shape patient survival.]]></description>
		
		
		
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