PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
27791982-7	2017	Thus, our data suggest that mutant p53 sensitizes cancer cells to lapatinib via two complementary mechanisms: mutant p53 mediated amplification of ErbB2 signaling, and simultaneous annihilation of both potent oncogenic drivers, ErbB2 and mutant p53.	Lapatinib	66-75	tumor protein p53	Homo sapiens	117-120	
27791982-0	2017	ErbB2 inhibition by lapatinib promotes degradation of mutant p53 protein in cancer cells.	Lapatinib	20-29	tumor protein p53	Homo sapiens	61-64	
27791982-5	2017	Here we report that pharmacological interception of this circuit by ErbB2 inhibitor lapatinib downregulates mutant p53 in vitro and in vivo.	Lapatinib	84-93	tumor protein p53	Homo sapiens	115-118	
27791982-6	2017	We found that ErbB2 inhibition by lapatinib inhibits transcription factor HSF1, and its target Hsp90, followed by mutant p53 degradation in MDM2 dependent manner.	Lapatinib	34-43	tumor protein p53	Homo sapiens	121-124	
27791982-7	2017	Thus, our data suggest that mutant p53 sensitizes cancer cells to lapatinib via two complementary mechanisms: mutant p53 mediated amplification of ErbB2 signaling, and simultaneous annihilation of both potent oncogenic drivers, ErbB2 and mutant p53.	Lapatinib	66-75	tumor protein p53	Homo sapiens	35-38	
27791982-7	2017	Thus, our data suggest that mutant p53 sensitizes cancer cells to lapatinib via two complementary mechanisms: mutant p53 mediated amplification of ErbB2 signaling, and simultaneous annihilation of both potent oncogenic drivers, ErbB2 and mutant p53.	Lapatinib	66-75	tumor protein p53	Homo sapiens	117-120	
23652204-8	2013	MDM2 inhibition overcame lapatinib resistance in cells with either wild-type or mutant p53 and in xenograft models.	Lapatinib	25-34	tumor protein p53	Homo sapiens	87-90	
27611952-3	2016	TP53 status was correlated to response to neoadjuvant anthracycline/taxane-based chemotherapy with or without carboplatin and trastuzumab/lapatinib in HER2-positive and bevacizumab in TNBC.	Lapatinib	138-147	tumor protein p53	Homo sapiens	0-4	
27659302-5	2016	This high-throughput western blot approach allowed us to identify and characterize alterations in cellular signal transduction that occur during the development of resistance to the kinase inhibitor Lapatinib, revealing major changes in the activation state of Ephrin-mediated signalling and a central role for p53-controlled processes.	Lapatinib	199-208	tumor protein p53	Homo sapiens	311-314	
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	tumor protein p53	Homo sapiens	25-29	
19287975-7	2009	In RT112 cells, which express high levels of ErbB receptors and harbour wild-type p53, combined GTC/lapatinib treatment resulted in the phosphorylation of p53 at Ser46 and accumulation of sub-G1 cell populations.	Lapatinib	100-109	tumor protein p53	Homo sapiens	82-85	
19287975-7	2009	In RT112 cells, which express high levels of ErbB receptors and harbour wild-type p53, combined GTC/lapatinib treatment resulted in the phosphorylation of p53 at Ser46 and accumulation of sub-G1 cell populations.	Lapatinib	100-109	tumor protein p53	Homo sapiens	155-158	
18212337-10	2008	Within cohort A, phosphorylated (p) HER-3 and lack of p53 expression predicted for response to lapatinib (P < .05).	Lapatinib	95-104	tumor protein p53	Homo sapiens	54-57	
31234033-6	2019	Alternatively, lapatinib amplified signals of TP53 gene effectively by raising the concentration.	Lapatinib	15-24	tumor protein p53	Homo sapiens	46-50	
30743996-6	2019	Restoring wild type p53 activity either by transfection or by treatment with APR-246, a molecule which reactivates mutant p53, blocked lapatinib-induced senescence and caused increased cell death.	Lapatinib	135-144	tumor protein p53	Homo sapiens	20-23	
30743996-6	2019	Restoring wild type p53 activity either by transfection or by treatment with APR-246, a molecule which reactivates mutant p53, blocked lapatinib-induced senescence and caused increased cell death.	Lapatinib	135-144	tumor protein p53	Homo sapiens	122-125