PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 26695721-12 2016 The associations of maternal 25(OH)D levels with childhood eGFR were partly explained by childhood vitamin D status. Vitamin D 99-108 epidermal growth factor receptor Homo sapiens 59-63 26654942-1 2016 Epidemiologic studies implicate vitamin D status as a factor that influences growth of EGFR mutant lung cancers. Vitamin D 32-41 epidermal growth factor receptor Homo sapiens 87-91 26654942-6 2016 To study anti-proliferative activity and signaling, EGFR mutant lung cancer cells were treated with the circulating metabolite of vitamin D, 25-hydroxyvitamin D3 (25D3). Vitamin D 130-139 epidermal growth factor receptor Homo sapiens 52-56 26654942-13 2016 These results identify EGFR mutant lung cancer as a vitamin D-responsive disease and diet-derived 25D3 as a direct VDR agonist and therapeutic agent. Vitamin D 52-61 epidermal growth factor receptor Homo sapiens 23-27 26450935-7 2015 In Cox regression analyses, we assessed associations of vitamin D with developing increased albuminuria or reduced eGFR and potential interaction with sodium intake. Vitamin D 56-65 epidermal growth factor receptor Homo sapiens 115-119 26100522-3 2015 In the present study, we examined the impact of 1,25(OH)2D3, the active metabolite of the nutritional supplement vitamin D on the chemopreventive efficacy of the EGFR inhibitor, erlotinib, against HNSCC. Vitamin D 113-122 epidermal growth factor receptor Homo sapiens 162-166 25294851-1 2015 BACKGROUND: In secondary hyperparathyroidism (SHPT), enhanced parathyroid levels of transforming growth factor-alpha (TGFalpha) increase EGF receptor (EGFR) activation causing parathyroid hyperplasia, high parathyroid hormone (PTH) and also reductions in vitamin D receptor (VDR) that limit vitamin D suppression of SHPT. Vitamin D 255-264 epidermal growth factor receptor Homo sapiens 137-149 25294851-1 2015 BACKGROUND: In secondary hyperparathyroidism (SHPT), enhanced parathyroid levels of transforming growth factor-alpha (TGFalpha) increase EGF receptor (EGFR) activation causing parathyroid hyperplasia, high parathyroid hormone (PTH) and also reductions in vitamin D receptor (VDR) that limit vitamin D suppression of SHPT. Vitamin D 255-264 epidermal growth factor receptor Homo sapiens 151-155 25522365-7 2014 Use cases presented herein cover 1) the comprehensive identification of chemical matter for a dopamine receptor drug discovery program 2) the identification of compounds active against all targets in the Epidermal growth factor receptor (ErbB) signaling pathway that have a relevance to disease and 3) the evaluation of established targets in the Vitamin D metabolism pathway to aid novel Vitamin D analogue design. Vitamin D 347-356 epidermal growth factor receptor Homo sapiens 238-242 25522365-7 2014 Use cases presented herein cover 1) the comprehensive identification of chemical matter for a dopamine receptor drug discovery program 2) the identification of compounds active against all targets in the Epidermal growth factor receptor (ErbB) signaling pathway that have a relevance to disease and 3) the evaluation of established targets in the Vitamin D metabolism pathway to aid novel Vitamin D analogue design. Vitamin D 389-398 epidermal growth factor receptor Homo sapiens 238-242 24703961-17 2014 CONCLUSIONS: Lower eGFR is associated strongly with reduced vitamin D catabolism, as measured by circulating 24,25(OH)2D3 concentration. Vitamin D 60-69 epidermal growth factor receptor Homo sapiens 19-23 24641586-18 2014 The mechanism of vitamin D resistance remains unknown and is associated with progressive loss of eGFR. Vitamin D 17-26 epidermal growth factor receptor Homo sapiens 97-101 24217116-2 2013 We previously reported that non-small cell lung cancer (NSCLC) cells which harbor epidermal growth factor receptor (EGFR) mutations display elevated VDR expression (VDRhigh) and are vitamin D-sensitive. Vitamin D 182-191 epidermal growth factor receptor Homo sapiens 82-114 24217116-2 2013 We previously reported that non-small cell lung cancer (NSCLC) cells which harbor epidermal growth factor receptor (EGFR) mutations display elevated VDR expression (VDRhigh) and are vitamin D-sensitive. Vitamin D 182-191 epidermal growth factor receptor Homo sapiens 116-120 23974111-1 2013 By means of an unbiased, automated fluorescence microscopy-based screen, we identified the epidermal growth factor receptor (EGFR) inhibitors erlotinib and gefitinib as potent enhancers of the differentiation of HL-60 acute myeloid leukemia (AML) cells exposed to suboptimal concentrations of vitamin A (all-trans retinoic acid, ATRA) or vitamin D (1alpha,25-hydroxycholecalciferol, VD). Vitamin D 338-347 epidermal growth factor receptor Homo sapiens 91-123 23974111-1 2013 By means of an unbiased, automated fluorescence microscopy-based screen, we identified the epidermal growth factor receptor (EGFR) inhibitors erlotinib and gefitinib as potent enhancers of the differentiation of HL-60 acute myeloid leukemia (AML) cells exposed to suboptimal concentrations of vitamin A (all-trans retinoic acid, ATRA) or vitamin D (1alpha,25-hydroxycholecalciferol, VD). Vitamin D 338-347 epidermal growth factor receptor Homo sapiens 125-129 23364486-9 2013 Among the participants with a normal eGFR, the LAPACQ score, vitamin D supplementation, season, log PTH value and eGFR were correlated with log 25-OH-vitamin D levels. Vitamin D 150-159 epidermal growth factor receptor Homo sapiens 114-118 21458521-4 2011 A novel vitamin D response element was identified in intron 1 of the EGFR genome, a known hotspot for its transcriptional regulation. Vitamin D 8-17 epidermal growth factor receptor Homo sapiens 69-73 21458521-7 2011 Over expression of an active EGFR in vitamin D sensitive ovarian cancer cells caused resistance to 1,25(OH)(2)D(3)-induced growth suppression and diminished the hormonal regulation of cyclin D1, cyclin E, Skp2 and p27, a group of cell cycle regulators that mediate 1,25(OH)(2)D(3)-induced cell cycle arrest at G1-S checkpoint. Vitamin D 37-46 epidermal growth factor receptor Homo sapiens 29-33 22468040-8 2011 Serum EGF-R levels correlated positively with hsCRP and NE, and were highest among CVD patients (n = 70) as well as negatively with vitamin D and HDL-C. EGF-R/HER-1/erbB-1 levels are increased in HTN and more in CHF patients. Vitamin D 132-141 epidermal growth factor receptor Homo sapiens 6-11 22468040-8 2011 Serum EGF-R levels correlated positively with hsCRP and NE, and were highest among CVD patients (n = 70) as well as negatively with vitamin D and HDL-C. EGF-R/HER-1/erbB-1 levels are increased in HTN and more in CHF patients. Vitamin D 132-141 epidermal growth factor receptor Homo sapiens 153-171 22468040-9 2011 This study confirms a strong association between catecholamines as well as EGF-R/HER-1/erbB-1 levels with PTH and low vitamin D levels, being related to hyperlipidemia and inflammation (hsCRP and fibrinogen) in CVD. Vitamin D 118-127 epidermal growth factor receptor Homo sapiens 75-93 20672448-9 2010 Tenofovir use was not associated with serum creatinine or eGFR overall but interacted with vitamin D status (P = 0.05 and P = 0.08, respectively), being linked to somewhat higher creatinine and lower eGFR among patients without VDD but higher eGFR in VDD patients. Vitamin D 91-100 epidermal growth factor receptor Homo sapiens 200-204 20672448-9 2010 Tenofovir use was not associated with serum creatinine or eGFR overall but interacted with vitamin D status (P = 0.05 and P = 0.08, respectively), being linked to somewhat higher creatinine and lower eGFR among patients without VDD but higher eGFR in VDD patients. Vitamin D 91-100 epidermal growth factor receptor Homo sapiens 200-204 16087726-2 2005 In the present report, functional mapping of the EGFR promoter in BT549 cells has revealed a sequence of DNA between nucleotide positions -536 and -478 that resembles a consensus vitamin D response element (VDRE) and confers a vitamin D response upon both the homologous and a minimal heterologous promoter. Vitamin D 179-188 epidermal growth factor receptor Homo sapiens 49-53 16087726-2 2005 In the present report, functional mapping of the EGFR promoter in BT549 cells has revealed a sequence of DNA between nucleotide positions -536 and -478 that resembles a consensus vitamin D response element (VDRE) and confers a vitamin D response upon both the homologous and a minimal heterologous promoter. Vitamin D 227-236 epidermal growth factor receptor Homo sapiens 49-53 15218361-0 2004 Growth and EGFR regulation in breast cancer cells by vitamin D and retinoid compounds. Vitamin D 53-62 epidermal growth factor receptor Homo sapiens 11-15 15218361-6 2004 Transfection of an EGFR promoter containing reporter plasmid demonstrated vitamin D induced changes in reporter gene activity that paralleled the changes observed in EGFR mRNA and protein. Vitamin D 74-83 epidermal growth factor receptor Homo sapiens 19-23 15218361-6 2004 Transfection of an EGFR promoter containing reporter plasmid demonstrated vitamin D induced changes in reporter gene activity that paralleled the changes observed in EGFR mRNA and protein. Vitamin D 74-83 epidermal growth factor receptor Homo sapiens 166-170 15218361-7 2004 Electrophoretic mobility shift assays using a putative vitamin D response element within this region of the EGFR promoter demonstrated specific VDR binding. Vitamin D 55-64 epidermal growth factor receptor Homo sapiens 108-112 15218361-8 2004 These results indicate that the vitamin D effect on EGFR expression in breast cancer cells has a transcriptional component likely mediated through a vitamin D responsive promoter sequence. Vitamin D 32-41 epidermal growth factor receptor Homo sapiens 52-56 15218361-8 2004 These results indicate that the vitamin D effect on EGFR expression in breast cancer cells has a transcriptional component likely mediated through a vitamin D responsive promoter sequence. Vitamin D 149-158 epidermal growth factor receptor Homo sapiens 52-56 15218361-9 2004 They also suggest that growth inhibition and EGFR down-regulation by vitamin D and retinoids may be related events in some breast cancer cells, but not in all. Vitamin D 69-78 epidermal growth factor receptor Homo sapiens 45-49 15225829-5 2004 At early stages of renal failure, vitamin D therapy efficiently counteracts uremia- and high phosphorus-induced hyperplasia by inhibiting the increases in parathyroid-TGFalpha/EGFR co-expression. Vitamin D 34-43 epidermal growth factor receptor Homo sapiens 176-180 15225829-6 2004 In established hyperparathyroidism, characterized by highly enhanced-TGFalpha/EGFR co-expression, vitamin D therapy arrests growth by suppressing EGFR-growth signals from the plasma membrane and nuclear EGFR actions as a transactivator of the cyclin D1 gene, an important contributor to parathyroid hyperplasia in humans. Vitamin D 98-107 epidermal growth factor receptor Homo sapiens 78-82 15225829-6 2004 In established hyperparathyroidism, characterized by highly enhanced-TGFalpha/EGFR co-expression, vitamin D therapy arrests growth by suppressing EGFR-growth signals from the plasma membrane and nuclear EGFR actions as a transactivator of the cyclin D1 gene, an important contributor to parathyroid hyperplasia in humans. Vitamin D 98-107 epidermal growth factor receptor Homo sapiens 146-150 15225829-6 2004 In established hyperparathyroidism, characterized by highly enhanced-TGFalpha/EGFR co-expression, vitamin D therapy arrests growth by suppressing EGFR-growth signals from the plasma membrane and nuclear EGFR actions as a transactivator of the cyclin D1 gene, an important contributor to parathyroid hyperplasia in humans. Vitamin D 98-107 epidermal growth factor receptor Homo sapiens 146-150 1677274-3 1991 Furthermore, the data embracing the hypothesis that the growth actions of hormone receptors that are homologous to the v-erbA oncogene (estrogens, progesterone, thyroid hormones, retinoic acid, and vitamin D) are mediated, in part, by modulating EGF-R and/or c-erbB-2 protooncogene transcription are reviewed. Vitamin D 198-207 epidermal growth factor receptor Homo sapiens 246-251 34362787-8 2021 Mean difference in eGFR from baseline was -1.0 ml/min per 1.73 m2 (95% CI, -1.3 to -0.7) in the vitamin D group and -0.1 ml/min per 1.73 m2 (95% CI, -0.4 to 0.2) in the placebo group; between-group difference was -1.0 ml/min per 1.73 m2 (95% CI, -1.4 to -0.6). Vitamin D 96-105 epidermal growth factor receptor Homo sapiens 19-23 33420892-12 2021 CONCLUSIONS: The prevalence of vitamin D deficiency was higher in patients with eGFR 30 - < 60 mL/min/1.73 m2 than those with eGFR >= 60 mL/min/1.73 m2. Vitamin D 31-40 epidermal growth factor receptor Homo sapiens 80-84 33420892-12 2021 CONCLUSIONS: The prevalence of vitamin D deficiency was higher in patients with eGFR 30 - < 60 mL/min/1.73 m2 than those with eGFR >= 60 mL/min/1.73 m2. Vitamin D 31-40 epidermal growth factor receptor Homo sapiens 126-130 32416695-8 2021 Participants with adequate vitamin D were older in age, more obese and having lower eGFR (pvalues<0.05). Vitamin D 27-36 epidermal growth factor receptor Homo sapiens 84-88 32610842-4 2020 Aims and Objectives: This cross-sectional study is designed "To assess Vitamin D status in CKD patients and to correlate Vitamin D status with eGFR. Vitamin D 121-130 epidermal growth factor receptor Homo sapiens 143-147 32610842-17 2020 The positive correlation was found between eGFR and vitamin D level and that was statistically significant. Vitamin D 52-61 epidermal growth factor receptor Homo sapiens 43-47 32610842-20 2020 eGFR was strongly associated with serum vitamin-D level. Vitamin D 40-49 epidermal growth factor receptor Homo sapiens 0-4 32183160-4 2020 We hypothesized that vitamin D metabolites could be used with EGFR TKIs to prevent therapeutic failure. Vitamin D 21-30 epidermal growth factor receptor Homo sapiens 62-66 32183160-11 2020 We conclude that vitamin D sufficiency portends increased PFS among EGFR-mutant LUAD patients that receive EGFR TKIs, and that vitamin D signaling maintains drug efficacy in this specific patient subset by opposing EMT. Vitamin D 17-26 epidermal growth factor receptor Homo sapiens 68-72 32183160-11 2020 We conclude that vitamin D sufficiency portends increased PFS among EGFR-mutant LUAD patients that receive EGFR TKIs, and that vitamin D signaling maintains drug efficacy in this specific patient subset by opposing EMT. Vitamin D 17-26 epidermal growth factor receptor Homo sapiens 107-111 31326626-0 2019 Differential response of lung cancer cell lines to vitamin D derivatives depending on EGFR, KRAS, p53 mutation status and VDR polymorphism. Vitamin D 51-60 epidermal growth factor receptor Homo sapiens 86-90 31326626-5 2019 The goal of our study was to establish if cells differing in EGFR, KRAS, p53 mutation status and VDR polymorphism were sensitive to antiproliferative activity of selected vitamin D derivatives (VDDs). Vitamin D 171-180 epidermal growth factor receptor Homo sapiens 61-65 30097651-10 2019 After adjustment for lipid markers, age, and gender, vitamin D deficiency was associated with increased odds of CRP, eGFR, gammaGT, FPG, HbA1c, and the surrogate for CVD. Vitamin D 53-62 epidermal growth factor receptor Homo sapiens 117-121 30097651-11 2019 CONCLUSIONS: In this exploratory analysis, the first of its kind in the MENA region, vitamin D deficiency was associated with abnormal lipid markers, non-lipid markers of CVD, male gender, lower eGFR, and a surrogate variable for CVD. Vitamin D 85-94 epidermal growth factor receptor Homo sapiens 195-199 31001917-0 2019 Evaluation of vitamin D biosynthesis and pathway target genes reveals UGT2A1/2 and EGFR polymorphisms associated with epithelial ovarian cancer in African American Women. Vitamin D 14-23 epidermal growth factor receptor Homo sapiens 83-87 29902012-0 2018 Tumor-Targeted Nanoparticles Deliver a Vitamin D-Based Drug Payload for the Treatment of EGFR Tyrosine Kinase Inhibitor-Resistant Lung Cancer. Vitamin D 39-48 epidermal growth factor receptor Homo sapiens 89-93 29902012-12 2018 Our results demonstrated that the delivery of vitamin D-based drug payloads via tumor-targeted EGFR-LP has promise as a new therapy for EFGR TKI resistant lung cancer. Vitamin D 46-55 epidermal growth factor receptor Homo sapiens 95-99 30600944-10 2018 The significant best-fitting predictors of vitamin D deficiency were living in rural area (OR=4.030, P < 0.021) and eGFR < 60 (OR=5.412, P < 0.034). Vitamin D 43-52 epidermal growth factor receptor Homo sapiens 119-123 30600944-12 2018 Low eGFR < 60, Alb/creat ratio more than 30 mg/24h and HbA1c > 9 could be considered as predictive factors of vitamin D deficiency in these patients. Vitamin D 116-125 epidermal growth factor receptor Homo sapiens 4-8