{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Shaurova T"],"funding":["NIDCR NIH HHS","NCI NIH HHS","National Institutes of Health","NIH HHS"],"pagination":["E675"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7140110"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(3)"],"pubmed_abstract":["EGFR tyrosine kinase inhibitors (EGFR TKIs) are the standard of care treatment for patients with <i>EGFR</i>-mutant lung adenocarcinoma (LUAD). Although initially effective, EGFR TKIs are not curative. Disease inevitably relapses due to acquired drug resistance. We hypothesized that vitamin D metabolites could be used with EGFR TKIs to prevent therapeutic failure. To test this idea, we investigated the link between serum 25-hydroxyvitamin D3 (25(OH)D3) and progression-free survival (PFS) in patients with <i>EGFR</i>-mutant LUAD that received EGFR TKIs (erlotinib n = 20 and afatinib n = 1). Patients who were 25(OH)D3-sufficient experienced significantly longer benefit from EGFR TKI therapy (mean 14.5 months) than those with 25(OH)D3 insufficiency (mean 10.6 months, <i>p</i> = 0.026). In con"],"journal":["Cancers"],"pubmed_title":["Vitamin D3 Metabolites Demonstrate Prognostic Value in <i>EGFR</i>-Mutant Lung Adenocarcinoma and Can be Deployed to Oppose Acquired Therapeutic Resistance."],"pmcid":["PMC7140110"],"funding_grant_id":["P30CA016056","R01 CA207757","R03 CA249411","R01 CA234162","R01 DE024595","DE024595"],"pubmed_authors":["Johnson CS","Hutson A","Hershberger PA","Battaglia S","Seshadri M","Shaurova T","Zhang Y","Goodrich DW","Lovly CM","Dy GK","Zhang L"],"additional_accession":[]},"is_claimable":false,"name":"Vitamin D3 Metabolites Demonstrate Prognostic Value in <i>EGFR</i>-Mutant Lung Adenocarcinoma and Can be Deployed to Oppose Acquired Therapeutic Resistance.","description":"EGFR tyrosine kinase inhibitors (EGFR TKIs) are the standard of care treatment for patients with <i>EGFR</i>-mutant lung adenocarcinoma (LUAD). Although initially effective, EGFR TKIs are not curative. Disease inevitably relapses due to acquired drug resistance. We hypothesized that vitamin D metabolites could be used with EGFR TKIs to prevent therapeutic failure. To test this idea, we investigated the link between serum 25-hydroxyvitamin D3 (25(OH)D3) and progression-free survival (PFS) in patients with <i>EGFR</i>-mutant LUAD that received EGFR TKIs (erlotinib n = 20 and afatinib n = 1). Patients who were 25(OH)D3-sufficient experienced significantly longer benefit from EGFR TKI therapy (mean 14.5 months) than those with 25(OH)D3 insufficiency (mean 10.6 months, <i>p</i> = 0.026). In con","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Mar","modification":"2026-04-07T17:50:10.696Z","creation":"2026-04-07T16:14:44.136Z"},"accession":"S-EPMC7140110","cross_references":{"pubmed":["32183160"],"doi":["10.3390/cancers12030675"]}}