<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Biyik-Sit R</submitter><funding>NIGMS NIH HHS</funding><pagination>9</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11542166</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>29(1)</volume><pubmed_abstract>The majority of malignant tumors exhibit an altered metabolic phenotype that ultimately provides the required energy and molecular precursors necessary for unregulated cell division. Within this, phosphoserine aminotransferase 1 (PSAT1) is involved in &lt;i>de novo&lt;/i> serine biosynthesis and its activity promotes various biochemical processes, including one-carbon metabolism. It also directly generates α-ketoglutarate (α-KG), a Kreb cycle intermediate and epigenetic-regulating metabolite. Prior studies examining PSAT1 depletion have identified individual affected downstream pathways, such as GSK3β and E2F, in several cancer types, including non-small-cell lung cancer (NSCLC). However, global gene expression examination in response to PSAT1 loss, particularly in EGFR mutant NSCLC, has not bee</pubmed_abstract><journal>Oncology letters</journal><pubmed_title>Bioinformatics analysis of PSAT1 loss identifies downstream pathways regulated in EGFR mutant NSCLC and a selective gene signature for predicting the risk of relapse.</pubmed_title><pmcid>PMC11542166</pmcid><funding_grant_id>P20 GM103436</funding_grant_id><funding_grant_id>P30 GM106396</funding_grant_id><pubmed_authors>Biyik-Sit R</pubmed_authors><pubmed_authors>Waigel S</pubmed_authors><pubmed_authors>Andreeva K</pubmed_authors><pubmed_authors>Rouchka E</pubmed_authors><pubmed_authors>Clem BF</pubmed_authors></additional><is_claimable>false</is_claimable><name>Bioinformatics analysis of PSAT1 loss identifies downstream pathways regulated in EGFR mutant NSCLC and a selective gene signature for predicting the risk of relapse.</name><description>The majority of malignant tumors exhibit an altered metabolic phenotype that ultimately provides the required energy and molecular precursors necessary for unregulated cell division. Within this, phosphoserine aminotransferase 1 (PSAT1) is involved in &lt;i>de novo&lt;/i> serine biosynthesis and its activity promotes various biochemical processes, including one-carbon metabolism. It also directly generates α-ketoglutarate (α-KG), a Kreb cycle intermediate and epigenetic-regulating metabolite. Prior studies examining PSAT1 depletion have identified individual affected downstream pathways, such as GSK3β and E2F, in several cancer types, including non-small-cell lung cancer (NSCLC). However, global gene expression examination in response to PSAT1 loss, particularly in EGFR mutant NSCLC, has not bee</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Jan</publication><modification>2026-06-01T20:38:51.378Z</modification><creation>2025-04-04T11:42:05.507Z</creation></dates><accession>S-EPMC11542166</accession><cross_references><pubmed>39512505</pubmed><doi>10.3892/ol.2024.14755</doi></cross_references></HashMap>