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<rss version="2.0"><channel><title>Dr. Abdelmuhsen Abusneina: Blog</title><link>https://molcellbiol.com/blog.html</link><description>Daily research briefs and articles in molecular biology, molecular therapeutics and cancer metabolism.</description><language>en</language><item><title>Programmable Cas13b Silences Cancer-Driving Fusion Transcripts, Including Drug-Resistant BCR::ABL1, in Cell Models</title><link>https://molcellbiol.com/briefs/2026-10-20-cas13b-fusion-transcripts.html</link><guid isPermaLink="true">https://molcellbiol.com/briefs/2026-10-20-cas13b-fusion-transcripts.html</guid><pubDate>Tue, 20 Oct 2026 06:00:00 +0200</pubDate><description>By guiding Cas13b to the breakpoint where two genes join, researchers silenced nine oncogenic fusions in cell lines, according to a Science Advances paper.</description><category>Molecular therapeutics</category><category>CRISPR</category><category>RNA therapeutics</category><category>Gene fusions</category><category>Drug resistance</category><category>Chronic myeloid leukemia</category></item><item><title>Nobel Prize in Physiology or Medicine 2026 Honors the Light-Gated Channels Behind Optogenetics</title><link>https://molcellbiol.com/briefs/2026-10-20-nobel-medicine-optogenetics.html</link><guid isPermaLink="true">https://molcellbiol.com/briefs/2026-10-20-nobel-medicine-optogenetics.html</guid><pubDate>Tue, 20 Oct 2026 06:00:00 +0200</pubDate><description>Karl Deisseroth, Peter Hegemann and Georg Nagel share the prize for discoveries that let researchers switch nerve cells on and off with light, according to the Nobel Assembly.</description><category>Nobel Prize</category><category>Optogenetics</category><category>Neuroscience</category><category>Ion channels</category><category>Molecular therapeutics</category></item><item><title>Why a Glutaminolysis Signature Falls With PTEN Loss: Passenger Co-Deletion, Not Metabolic Regulation</title><link>https://molcellbiol.com/posts/pten-glutaminolysis-codeletion.html</link><guid isPermaLink="true">https://molcellbiol.com/posts/pten-glutaminolysis-codeletion.html</guid><pubDate>Mon, 19 Oct 2026 06:00:00 +0200</pubDate><description>Across 14 tumor types, a five-gene glutaminolysis signature fell, rather than rose, as PTEN copy number fell. Thirty-seven neighboring genes with no role in glutaminolysis tracked PTEN just as closely, which points to co-deletion on chromosome 10q, not a metabolic program.</description><category>PTEN</category><category>Glutaminolysis</category><category>TCGA</category><category>Bioinformatics</category><category>Biomarkers</category><category>Cancer metabolism</category></item><item><title>Ammonium Ions Improve Survival of Glutamine-Starved Hybridoma Cells Without Blocking Core Apoptosis Events</title><link>https://molcellbiol.com/posts/ammonium-glutamine-starved-cells.html</link><guid isPermaLink="true">https://molcellbiol.com/posts/ammonium-glutamine-starved-cells.html</guid><pubDate>Mon, 19 Oct 2026 06:00:00 +0200</pubDate><description>Ammonium salts raised the viability of glutamine-starved mouse hybridoma cells from 30% to as much as 72%. They did not block caspase-3 activation or cytochrome c release, but they reduced nuclear condensation and fragmentation.</description><category>Glutamine</category><category>Ammonium</category><category>Glutaminolysis</category><category>Apoptosis</category><category>Hybridoma cells</category></item><item><title>MCL-1 and Apoptosis: What Obatoclax Teaches Us About Cancer Cell Death</title><link>https://molcellbiol.com/posts/mcl1-obatoclax-apoptosis.html</link><guid isPermaLink="true">https://molcellbiol.com/posts/mcl1-obatoclax-apoptosis.html</guid><pubDate>Mon, 19 Oct 2026 06:00:00 +0200</pubDate><description>In a mouse hybridoma cell line, glutamine starvation lowered levels of the survival protein MCL-1, and obatoclax, a drug that targets MCL-1, made starved cells more sensitive to apoptosis.</description><category>Apoptosis</category><category>Cell death</category><category>BCL-2 family</category><category>Obatoclax</category><category>Glutamine</category><category>Hybridoma cells</category></item><item><title>Glutamine Plus Chemotherapy for Advanced Pancreatic Cancer: A Small Phase 1 Trial Finds the Combination Feasible</title><link>https://molcellbiol.com/posts/glutamine-pancreatic-phase1.html</link><guid isPermaLink="true">https://molcellbiol.com/posts/glutamine-pancreatic-phase1.html</guid><pubDate>Mon, 19 Oct 2026 06:00:00 +0200</pubDate><description>In 16 people with advanced pancreatic cancer, taking oral glutamine alongside standard chemotherapy was feasible at the highest planned dose. The trial was not designed to show benefit.</description><category>Glutamine</category><category>Pancreatic cancer</category><category>Clinical trials</category><category>Chemotherapy</category><category>Cancer metabolism</category></item><item><title>Glutamine Addiction: Why Some Cancer Cells Depend on a Nonessential Amino Acid</title><link>https://molcellbiol.com/posts/glutamine-addiction.html</link><guid isPermaLink="true">https://molcellbiol.com/posts/glutamine-addiction.html</guid><pubDate>Mon, 19 Oct 2026 06:00:00 +0200</pubDate><description></description><category>Glutamine</category><category>Glutaminolysis</category><category>Cancer metabolism</category><category>MYC</category><category>Mitochondria</category></item><item><title>A New Class of Mitochondria-Targeted Compounds Induces Ferroptosis and Suppresses Tumors in Cancer Models</title><link>https://molcellbiol.com/briefs/2026-10-19-mito-ferroptosis-tetraoxanes.html</link><guid isPermaLink="true">https://molcellbiol.com/briefs/2026-10-19-mito-ferroptosis-tetraoxanes.html</guid><pubDate>Mon, 19 Oct 2026 06:00:00 +0200</pubDate><description>The compounds induce iron-dependent cell death without targeting GPX4 or FSP1, the proteins conventional strategies target, according to a Cell paper.</description><category>Ferroptosis</category><category>Mitochondria</category><category>Lipid peroxidation</category><category>Cancer metabolism</category><category>Immunotherapy</category><category>Cell death</category></item></channel></rss>
