PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 34944900-5 2021 ERalpha-positive breast cancer cells that developed resistance showed greatly reduced ERalpha levels and responsiveness to fulvestrant and a 10-fold increased sensitivity to lapatinib, suggesting that targeting rewired processes in the resistant state may provide benefits and prolong anticancer effectiveness. Lapatinib 174-183 estrogen receptor 1 Homo sapiens 0-7 32988919-7 2020 CONCLUSION: Mutations in TP53 and PIK3CA hotspot at exon 9 may be potential negative predictors of ER+HER2+ BC treated with neoadjuvant letrozole and lapatinib, while MLL2 inactivating mutation might confer therapeutic benefit in these patients. Lapatinib 150-159 estrogen receptor 1 Homo sapiens 99-101 31477168-14 2019 CONCLUSION: In early-stage HER2-positive breast cancer, the neoadjuvant treatment with T-DM1, lapatinib, and nab-paclitaxel was more effective than the standard treatment, particularly in the ER-positive cohort. Lapatinib 94-103 estrogen receptor 1 Homo sapiens 28-30 32942617-0 2020 HSP90 Inhibitor, 17-DMAG, Alone and in Combination with Lapatinib Attenuates Acquired Lapatinib-Resistance in ER-positive, HER2-Overexpressing Breast Cancer Cell Line. Lapatinib 56-65 estrogen receptor 1 Homo sapiens 110-112 32942617-0 2020 HSP90 Inhibitor, 17-DMAG, Alone and in Combination with Lapatinib Attenuates Acquired Lapatinib-Resistance in ER-positive, HER2-Overexpressing Breast Cancer Cell Line. Lapatinib 86-95 estrogen receptor 1 Homo sapiens 110-112 32942617-9 2020 These results suggest that HSP90 inhibitors in patients with lapatinib-resistant Estrogen Receptor (ER) (+) HER2 (+) breast cancer are promising therapeutics for future clinical trials. Lapatinib 61-70 estrogen receptor 1 Homo sapiens 81-98 29069787-0 2017 Proteasome inhibitors prevent bi-directional HER2/estrogen-receptor cross-talk leading to cell death in endocrine and lapatinib-resistant HER2+/ER+ breast cancer cells. Lapatinib 118-127 estrogen receptor 1 Homo sapiens 50-67 29476008-7 2018 Reduced ESR1 expression in turn prevents ERalpha-mediated transcription of NOXA, mitigating apoptosis following treatment with the HER2i lapatinib. Lapatinib 137-146 estrogen receptor 1 Homo sapiens 8-12 27942916-0 2017 Synergistic disruption of ERalpha/HER2 crosstalk by endoxifen and lapatinib in breast cancer cells. Lapatinib 66-75 estrogen receptor 1 Homo sapiens 26-33 27942916-6 2017 Simultaneous antagonism of ERalpha and HER2 using endoxifen and lapatinib could overcome these problems. Lapatinib 64-73 estrogen receptor 1 Homo sapiens 27-34 27942916-10 2017 Synergistic activity was uncovered for lapatinib and endoxifen against BT474, TAM-R and MCF-7/HER2 models of ERalpha/HER2 crosstalk. Lapatinib 39-48 estrogen receptor 1 Homo sapiens 109-116 26557906-0 2015 Activated estrogen receptor-mitogen-activated protein kinases cross talk confer acquired resistance to lapatinib. Lapatinib 103-112 estrogen receptor 1 Homo sapiens 10-27 27491481-0 2016 Phase II trial of neoadjuvant letrozole and lapatinib in Asian postmenopausal women with estrogen receptor (ER) and human epidermal growth factor receptor 2 (HER2)-positive breast cancer [Neo-ALL-IN]: Highlighting the TILs, ER expressional change after neoadjuvant treatment, and FES-PET as potential significant biomarkers. Lapatinib 44-53 estrogen receptor 1 Homo sapiens 89-106 27491481-13 2016 CONCLUSIONS: When this chemo-free, combination neoadjuvant therapy with letrozole and lapatinib is given for Asian postmenopausal ER+HER2+ breast cancer, TILs, change of ER expression following neoadjuvant treatment, and SUVmax in baseline FES-PET are to be considered potential biomarkers in these patients. Lapatinib 86-95 estrogen receptor 1 Homo sapiens 130-132 27491481-13 2016 CONCLUSIONS: When this chemo-free, combination neoadjuvant therapy with letrozole and lapatinib is given for Asian postmenopausal ER+HER2+ breast cancer, TILs, change of ER expression following neoadjuvant treatment, and SUVmax in baseline FES-PET are to be considered potential biomarkers in these patients. Lapatinib 86-95 estrogen receptor 1 Homo sapiens 134-136 26557906-2 2015 The aim of this study was to investigate the role of estrogen receptor (ER) signaling compensatory activation in acquired resistance to lapatinib in breast cancer cells BT474 and the related mechanism. Lapatinib 136-145 estrogen receptor 1 Homo sapiens 53-70 26557906-2 2015 The aim of this study was to investigate the role of estrogen receptor (ER) signaling compensatory activation in acquired resistance to lapatinib in breast cancer cells BT474 and the related mechanism. Lapatinib 136-145 estrogen receptor 1 Homo sapiens 72-74 26557906-4 2015 Real-time polymerase chain reaction and Western blotting were used to determine the changes of human epidermal growth factor receptor (HER)2 and ER pathways in breast cancer cell BT474 after treatment with lapatinib and the distinction between BT474 and rBT474. Lapatinib 206-215 estrogen receptor 1 Homo sapiens 136-138 26557906-11 2015 CONCLUSION: ER signaling compensatory activation may partly contribute to lapatinib acquired resistance in HER2-overexpressing/ERalpha-positive breast cancer cells, which might be related to PI3K/AKT inhibition and MAPK pathway activation. Lapatinib 74-83 estrogen receptor 1 Homo sapiens 12-14 26557906-11 2015 CONCLUSION: ER signaling compensatory activation may partly contribute to lapatinib acquired resistance in HER2-overexpressing/ERalpha-positive breast cancer cells, which might be related to PI3K/AKT inhibition and MAPK pathway activation. Lapatinib 74-83 estrogen receptor 1 Homo sapiens 127-134 24352641-2 2014 Finn and colleagues identify low ER levels as a biomarker predicting benefit from the addition of the EGFR/HER2 dual inhibitor lapatinib to an antiestrogen treatment regimen in patients with metastatic ER(+)/HER2(-) breast cancer. Lapatinib 127-136 estrogen receptor 1 Homo sapiens 33-35 26015514-6 2015 In the neoadjuvant clinical study, lapatinib treatment for 2 weeks was associated with parallel upregulation of ER and Bcl2 (Spearman coefficient: 0.70; P = 0.0002). Lapatinib 35-44 estrogen receptor 1 Homo sapiens 112-114 20179226-6 2010 The effect of lapatinib on ERalpha signaling varied markedly depending on the nature of the HER2/ERalpha cross-talk. Lapatinib 14-23 estrogen receptor 1 Homo sapiens 27-34 23233650-9 2013 CONCLUSIONS: Overall, a pre-surgical course of lapatinib monotherapy had little effect on this group of patients; however, in subsets of patients, especially those with HER-3-positive tumors, we observed either reduction in proliferation (Ki67) or tumor size; EGFR/ER status had no impact. Lapatinib 47-56 estrogen receptor 1 Homo sapiens 170-172 23706161-3 2013 METHODS: In the present studies, estrogen receptor (ER) positive and ER negative breast cancer cells were genetically manipulated to up- or downregulate eIF2-alpha, its phospho-mutant, Nck1, or Nck2, then treated with OSU-03012, lapatinib or the combination and assayed for cytotoxicity/cytostaticity using clonogenic assays. Lapatinib 229-238 estrogen receptor 1 Homo sapiens 33-50 23706161-3 2013 METHODS: In the present studies, estrogen receptor (ER) positive and ER negative breast cancer cells were genetically manipulated to up- or downregulate eIF2-alpha, its phospho-mutant, Nck1, or Nck2, then treated with OSU-03012, lapatinib or the combination and assayed for cytotoxicity/cytostaticity using clonogenic assays. Lapatinib 229-238 estrogen receptor 1 Homo sapiens 52-54 22686613-6 2012 Proposed mechanisms of resistance to lapatinib involve derepression and/or activation of compensatory survival pathways through increased PI3K/AKT or estrogen receptor (ER) signalling. Lapatinib 37-46 estrogen receptor 1 Homo sapiens 150-167 22686613-6 2012 Proposed mechanisms of resistance to lapatinib involve derepression and/or activation of compensatory survival pathways through increased PI3K/AKT or estrogen receptor (ER) signalling. Lapatinib 37-46 estrogen receptor 1 Homo sapiens 169-171 20179226-6 2010 The effect of lapatinib on ERalpha signaling varied markedly depending on the nature of the HER2/ERalpha cross-talk. Lapatinib 14-23 estrogen receptor 1 Homo sapiens 97-104 20179226-7 2010 In long-term estrogen-deprived cells characterized by enhanced ERalpha function, lapatinib suppressed ERalpha genomic activity (as measured by pERSer118, ERalpha transcriptional activity, and PGR gene expression). Lapatinib 81-90 estrogen receptor 1 Homo sapiens 63-70 20179226-7 2010 In long-term estrogen-deprived cells characterized by enhanced ERalpha function, lapatinib suppressed ERalpha genomic activity (as measured by pERSer118, ERalpha transcriptional activity, and PGR gene expression). Lapatinib 81-90 estrogen receptor 1 Homo sapiens 102-109 20179226-7 2010 In long-term estrogen-deprived cells characterized by enhanced ERalpha function, lapatinib suppressed ERalpha genomic activity (as measured by pERSer118, ERalpha transcriptional activity, and PGR gene expression). Lapatinib 81-90 estrogen receptor 1 Homo sapiens 102-109 20179226-8 2010 In contrast, in long-term tamoxifen-treated cells with reduced ERalpha activation, lapatinib reactivated ERalpha genomic function. Lapatinib 83-92 estrogen receptor 1 Homo sapiens 105-112 20179241-2 2010 Interruption of HER2/ER cross-talk with lapatinib can restore sensitivity to anti-estrogens and thus, should be investigated in combination with endocrine therapy in patients with ER+/HER2-negative breast cancers. Lapatinib 40-49 estrogen receptor 1 Homo sapiens 21-23 15665275-10 2005 In addition to inhibiting mitogenic signaling and cell cycle progression, lapatinib inhibited estrogen-stimulated ER transcriptional activity and cooperated with tamoxifen to further reduce ER-dependent transcription. Lapatinib 74-83 estrogen receptor 1 Homo sapiens 114-116 15665275-5 2005 Here we show that the dual ErbB1/ErbB2 inhibitor, lapatinib (GW572016), can restore tamoxifen sensitivity in ER-positive, tamoxifen-resistant breast cancer models. Lapatinib 50-59 estrogen receptor 1 Homo sapiens 109-111 15665275-5 2005 Here we show that the dual ErbB1/ErbB2 inhibitor, lapatinib (GW572016), can restore tamoxifen sensitivity in ER-positive, tamoxifen-resistant breast cancer models. Lapatinib 61-69 estrogen receptor 1 Homo sapiens 109-111 16682622-4 2006 Analysis of baseline gene expression in acquired lapatinib-resistant and parental cells indicates estrogen receptor (ER) signaling involvement in the development of resistance. Lapatinib 49-58 estrogen receptor 1 Homo sapiens 98-115 16682622-4 2006 Analysis of baseline gene expression in acquired lapatinib-resistant and parental cells indicates estrogen receptor (ER) signaling involvement in the development of resistance. Lapatinib 49-58 estrogen receptor 1 Homo sapiens 117-119 16682622-5 2006 Using gene interference, we confirm that acquired resistance to lapatinib is mediated by a switch in cell survival dependence and regulation of a key antiapoptotic mediator from ErbB2 alone to codependence upon ER and ErbB2 rather than loss of ErbB2 expression or insensitivity of ErbB2 signaling to lapatinib. Lapatinib 64-73 estrogen receptor 1 Homo sapiens 211-213 16682622-6 2006 Increased ER signaling in response to lapatinib is enhanced by the activation of factors facilitating the transcriptional activity of ER, notably FOXO3a and caveolin-1. Lapatinib 38-47 estrogen receptor 1 Homo sapiens 10-12 16682622-6 2006 Increased ER signaling in response to lapatinib is enhanced by the activation of factors facilitating the transcriptional activity of ER, notably FOXO3a and caveolin-1. Lapatinib 38-47 estrogen receptor 1 Homo sapiens 134-136 16682622-7 2006 Importantly, we confirm that lapatinib induces ER signaling in tumor biopsies from patients with ErbB2-overexpressing breast cancers receiving lapatinib therapy. Lapatinib 29-38 estrogen receptor 1 Homo sapiens 47-49 16682622-7 2006 Importantly, we confirm that lapatinib induces ER signaling in tumor biopsies from patients with ErbB2-overexpressing breast cancers receiving lapatinib therapy. Lapatinib 143-152 estrogen receptor 1 Homo sapiens 47-49 15665275-10 2005 In addition to inhibiting mitogenic signaling and cell cycle progression, lapatinib inhibited estrogen-stimulated ER transcriptional activity and cooperated with tamoxifen to further reduce ER-dependent transcription. Lapatinib 74-83 estrogen receptor 1 Homo sapiens 190-192