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	<title>cancer metabolism &#8211; BIOENGINEER.ORG</title>
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		<title>Ferroptosis in Cancer: Metabolism and Therapeutic Opportunities</title>
		<link>https://bioengineer.org/ferroptosis-in-cancer-metabolism-and-therapeutic-opportunities/</link>
		
		<dc:creator><![CDATA[Bioengineer]]></dc:creator>
		<pubDate>Fri, 23 Jan 2026 09:22:50 +0000</pubDate>
				<category><![CDATA[Cancer]]></category>
		<category><![CDATA[cancer metabolism]]></category>
		<category><![CDATA[Cancer Therapy** * **Ferroptosis:** Ana konu]]></category>
		<category><![CDATA[doğrudan etiketlenmeli. * **Cancer Metabolism:** İçerikte kanser hücrelerinin metabolik adaptasyonları ve ferroptozdaki]]></category>
		<category><![CDATA[Ferroptosis in Cancer]]></category>
		<category><![CDATA[Ferroptosis in Cancer: Metabolism and Therapeutic Opportunities başlıklı yazı için 5 uygun etiket: **Ferroptosis]]></category>
		<category><![CDATA[iron-dependent cell death]]></category>
		<category><![CDATA[Lipid peroxidation]]></category>
		<category><![CDATA[Therapeutic Opportunities]]></category>
		<category><![CDATA[therapeutic targets]]></category>
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					<description><![CDATA[Ferroptosis, a form of regulated cell death distinct from apoptosis and necrosis, has emerged at the forefront of cancer research, igniting a fervent interest among scientists and oncologists alike. This unique cell death pathway is characterized by the accumulation of iron-dependent lipid peroxides to lethal levels, leading to cellular demise. Recent studies delineate not only [&#8230;]]]></description>
		
		
		
		<post-id xmlns="com-wordpress:feed-additions:1">319719</post-id>	</item>
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		<title>LKB1 Loss Reveals Leptin’s Role in Cancer Therapy</title>
		<link>https://bioengineer.org/lkb1-loss-reveals-leptins-role-in-cancer-therapy/</link>
		
		<dc:creator><![CDATA[Bioengineer]]></dc:creator>
		<pubDate>Tue, 20 Jan 2026 05:51:38 +0000</pubDate>
				<category><![CDATA[Cancer]]></category>
		<category><![CDATA[cancer metabolism]]></category>
		<category><![CDATA[cancer metabolism** **Kısa Açıklama:** 1. **LKB1 loss:** Makalenin temel odağı]]></category>
		<category><![CDATA[leptin]]></category>
		<category><![CDATA[LKB1]]></category>
		<category><![CDATA[Makalenin içeriğine ve anahtar kavramlarına göre en uygun 5 etiket: **LKB1 loss]]></category>
		<category><![CDATA[mitochondrial uncouplers]]></category>
		<category><![CDATA[targeted cancer therapy]]></category>
		<category><![CDATA[tümör baskılayıcı LKB1/STK11 kaybının sonuçları.]]></category>
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					<description><![CDATA[In the ever-evolving landscape of cancer research, a groundbreaking study has emerged that elucidates a novel mechanism linking the loss of the tumor suppressor LKB1/STK11 to a specific sensitivity to mitochondrial uncouplers mediated by leptin. Conducted by a team of researchers led by Angelopoulou, Theocharous, and Valakos, this study not only offers significant insights into [&#8230;]]]></description>
		
		
		
		<post-id xmlns="com-wordpress:feed-additions:1">318752</post-id>	</item>
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		<title>AHCY–Adenosine Complex Boosts Fatty Acids, Cancer</title>
		<link>https://bioengineer.org/ahcy-adenosine-complex-boosts-fatty-acids-cancer/</link>
		
		<dc:creator><![CDATA[Bioengineer]]></dc:creator>
		<pubDate>Mon, 19 Jan 2026 05:44:38 +0000</pubDate>
				<category><![CDATA[Health]]></category>
		<category><![CDATA[AHCY-adenosine complex]]></category>
		<category><![CDATA[cancer metabolism]]></category>
		<category><![CDATA[epitranscriptomic regulation** **Açıklama:** 1. **AHCY-adenosine complex:** Araştırmanın merkezindeki yeni keşfedilen moleküler kompleks. Doğrudan kon]]></category>
		<category><![CDATA[fatty acid biosynthesis]]></category>
		<category><![CDATA[İşte bu içerik için en uygun 5 etiket (virgülle ayrılmış): **AHCY-adenosine complex]]></category>
		<category><![CDATA[mRNA methylation]]></category>
		<category><![CDATA[tumorigenesis]]></category>
		<guid isPermaLink="false">https://bioengineer.org/ahcy-adenosine-complex-boosts-fatty-acids-cancer/</guid>

					<description><![CDATA[In a groundbreaking study set to redefine our understanding of cancer metabolism and RNA modification, researchers have uncovered a novel molecular mechanism linking the AHCY–adenosine complex to the reprogramming of mRNA methylation, thereby enhancing fatty acid biosynthesis and accelerating tumorigenesis. This discovery not only elucidates a pivotal cellular pathway but also opens promising avenues for [&#8230;]]]></description>
		
		
		
		<post-id xmlns="com-wordpress:feed-additions:1">318159</post-id>	</item>
		<item>
		<title>Hexokinase Release Sparks Warburg Effect, Boosts ATP</title>
		<link>https://bioengineer.org/hexokinase-release-sparks-warburg-effect-boosts-atp/</link>
		
		<dc:creator><![CDATA[Bioengineer]]></dc:creator>
		<pubDate>Fri, 16 Jan 2026 16:19:36 +0000</pubDate>
				<category><![CDATA[Health]]></category>
		<category><![CDATA[cancer metabolism]]></category>
		<category><![CDATA[Compartmentalized ATP]]></category>
		<category><![CDATA[Hexokinase localization]]></category>
		<category><![CDATA[HK1-HK2 izoform dinamikleri]]></category>
		<category><![CDATA[Kanser metabolizma terapileri]]></category>
		<category><![CDATA[Kompartmantalize ATP sentezi]]></category>
		<category><![CDATA[Metabolic targeting]]></category>
		<category><![CDATA[Mitokondriyal hexokinaz lokalizasyonu]]></category>
		<category><![CDATA[Warburg Effect]]></category>
		<category><![CDATA[Warburg etkisi mekanizması]]></category>
		<guid isPermaLink="false">https://bioengineer.org/hexokinase-release-sparks-warburg-effect-boosts-atp/</guid>

					<description><![CDATA[In a groundbreaking study that challenges long-standing assumptions about cancer metabolism, researchers have uncovered a crucial link between the spatial dynamics of hexokinase enzymes and the metabolic phenomena that fuel tumor growth. Hexokinase (HK), the enzyme responsible for initiating glucose metabolism by converting glucose to glucose 6-phosphate, plays an unexpectedly complex role in cancer cell [&#8230;]]]></description>
		
		
		
		<post-id xmlns="com-wordpress:feed-additions:1">317496</post-id>	</item>
		<item>
		<title>Cancer Cells Exploit Alternative Pathways to Sustain Their Growth</title>
		<link>https://bioengineer.org/cancer-cells-exploit-alternative-pathways-to-sustain-their-growth/</link>
		
		<dc:creator><![CDATA[Bioengineer]]></dc:creator>
		<pubDate>Mon, 08 Sep 2025 17:28:09 +0000</pubDate>
				<category><![CDATA[Cancer]]></category>
		<category><![CDATA[acetyl-CoA synthesis]]></category>
		<category><![CDATA[cancer metabolism]]></category>
		<category><![CDATA[metabolic plasticity]]></category>
		<category><![CDATA[tumor proliferation]]></category>
		<category><![CDATA[β-hydroxybutyrate pathways]]></category>
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					<description><![CDATA[In the ever-evolving landscape of cancer metabolism, new insights often challenge long-standing paradigms about how malignant cells sustain their aggressive proliferation. Emerging research from Van Andel Institute (VAI), recently published in Nature Metabolism, reveals an alternative biochemical pathway cancer cells employ to fuel their growth. This revealing study unpacks the complexity of nutrient utilization in [&#8230;]]]></description>
		
		
		
		<post-id xmlns="com-wordpress:feed-additions:1">267588</post-id>	</item>
		<item>
		<title>Rice University-Led Team Explores Mitochondrial Targets for Innovative Leukemia Treatments</title>
		<link>https://bioengineer.org/rice-university-led-team-explores-mitochondrial-targets-for-innovative-leukemia-treatments/</link>
		
		<dc:creator><![CDATA[Bioengineer]]></dc:creator>
		<pubDate>Wed, 04 Jun 2025 21:38:40 +0000</pubDate>
				<category><![CDATA[Cancer]]></category>
		<category><![CDATA[acute myeloid leukemia treatment]]></category>
		<category><![CDATA[cancer metabolism]]></category>
		<category><![CDATA[mitochondrial targeting in cancer]]></category>
		<category><![CDATA[personalized oncology]]></category>
		<category><![CDATA[translational cancer research]]></category>
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					<description><![CDATA[Acute myeloid leukemia (AML) represents one of the most formidable challenges in contemporary oncology due to its aggressive nature and remarkable resistance to existing therapies. Traditional treatment modalities such as high-dose chemotherapy and allogeneic bone marrow transplantation have prolonged survival for some patients, yet the overall prognosis remains poor, primarily because of the high rate [&#8230;]]]></description>
		
		
		
		<post-id xmlns="com-wordpress:feed-additions:1">248381</post-id>	</item>
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