<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Deng H</submitter><funding>National Natural Science Foundation of China</funding><pagination>56-66</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10846321</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>1(1)</volume><pubmed_abstract>Small cell lung cancer (SCLC) is a highly aggressive tumor type for which limited therapeutic progress has been made. Platinum-based chemotherapy with or without thoracic radiotherapy remains the backbone of treatment, but most patients with SCLC acquire therapeutic resistance. Given the need for more effective therapies, better elucidation of the molecular pathogenesis of SCLC is imperative. The phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway is frequently activated in SCLC and strongly associated with resistance to ionizing radiation in many solid tumors. This pathway is an important regulator of cancer cell glucose metabolism, and its activation probably effects radioresistance by influencing bioenergetic processes in SCLC. Glucose me</pubmed_abstract><journal>Cancer pathogenesis and therapy</journal><pubmed_title>PI3K/AKT/mTOR pathway, hypoxia, and glucose metabolism: Potential targets to overcome radioresistance in small cell lung cancer.</pubmed_title><pmcid>PMC10846321</pmcid><funding_grant_id>81672972</funding_grant_id><pubmed_authors>Hang Q</pubmed_authors><pubmed_authors>Chen M</pubmed_authors><pubmed_authors>Li P</pubmed_authors><pubmed_authors>Chen Y</pubmed_authors><pubmed_authors>Jin Y</pubmed_authors><pubmed_authors>Deng H</pubmed_authors><pubmed_authors>Zhang P</pubmed_authors></additional><is_claimable>false</is_claimable><name>PI3K/AKT/mTOR pathway, hypoxia, and glucose metabolism: Potential targets to overcome radioresistance in small cell lung cancer.</name><description>Small cell lung cancer (SCLC) is a highly aggressive tumor type for which limited therapeutic progress has been made. Platinum-based chemotherapy with or without thoracic radiotherapy remains the backbone of treatment, but most patients with SCLC acquire therapeutic resistance. Given the need for more effective therapies, better elucidation of the molecular pathogenesis of SCLC is imperative. The phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway is frequently activated in SCLC and strongly associated with resistance to ionizing radiation in many solid tumors. This pathway is an important regulator of cancer cell glucose metabolism, and its activation probably effects radioresistance by influencing bioenergetic processes in SCLC. Glucose me</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jan</publication><modification>2025-04-04T10:38:57.533Z</modification><creation>2025-04-04T10:38:57.533Z</creation></dates><accession>S-EPMC10846321</accession><cross_references><pubmed>38328610</pubmed><doi>10.1016/j.cpt.2022.09.001</doi></cross_references></HashMap>