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		<title>Why EGFR Drugs Fail in Glioblastoma: A STAT3 Escape Route Takes Center Stage</title>
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		<pubDate>Fri, 09 Oct 2026 13:44:09 +0000</pubDate>
				<category><![CDATA[Cancer]]></category>
		<category><![CDATA[adaptive resistance]]></category>
		<category><![CDATA[brain tumor]]></category>
		<category><![CDATA[drug resistance]]></category>
		<category><![CDATA[EGFR]]></category>
		<category><![CDATA[Glioblastoma]]></category>
		<category><![CDATA[glioma stem cells]]></category>
		<category><![CDATA[immunosuppression]]></category>
		<category><![CDATA[JAK/STAT pathway]]></category>
		<category><![CDATA[STAT3]]></category>
		<category><![CDATA[targeted therapy]]></category>
		<category><![CDATA[temozolomide]]></category>
		<category><![CDATA[tumor microenvironment]]></category>
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					<description><![CDATA[A new review argues that glioblastoma evades EGFR-targeted therapies through compensatory STAT3 activation, positioning the EGFR–STAT3 axis as an adaptive resistance hub that must be attacked with combination strategies.]]></description>
		
		
		
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