PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
25865888-5	2015	Genetic and chemical inhibition of BET bromodomain chromatin readers suppresses transcription of many lapatinib-induced kinases involved in resistance, including ERBB3, IGF1R, DDR1, MET, and FGFRs, preventing downstream SRC/FAK signaling and AKT reactivation.	Lapatinib	102-111	insulin like growth factor 1 receptor	Homo sapiens	169-174	
26621843-0	2016	The erbB3- and IGF-1 receptor-initiated signaling pathways exhibit distinct effects on lapatinib sensitivity against trastuzumab-resistant breast cancer cells.	Lapatinib	87-96	insulin like growth factor 1 receptor	Homo sapiens	15-29	
26621843-2	2016	However, it remains unclear whether erbB3- and IGF-1R-initiated signaling pathways possess distinct effects on the sensitivity of lapatinib, a dual tyrosine kinase inhibitor against both EGFR and erbB2, in trastuzumab-resistant breast cancer.	Lapatinib	130-139	insulin like growth factor 1 receptor	Homo sapiens	47-53	
30729097-5	2019	This study evaluates the role of survivin in IGF1R-mediated lapatinib resistance.	Lapatinib	60-69	insulin like growth factor 1 receptor	Homo sapiens	45-50	
30729097-6	2019	Using HNSCC cell lines FaDu and SCC25, survivin expression increased and lapatinib sensitivity decreased with IGF1R activation.	Lapatinib	73-82	insulin like growth factor 1 receptor	Homo sapiens	110-115	
30729097-10	2019	These results demonstrate that enhanced survivin expression correlates with IGF1R-mediated lapatinib resistance in HNSCC cells and suggest that regulation of survivin expression may be a key mechanistic element in IGF1R-based therapeutic resistance.	Lapatinib	91-100	insulin like growth factor 1 receptor	Homo sapiens	76-81	
30729097-10	2019	These results demonstrate that enhanced survivin expression correlates with IGF1R-mediated lapatinib resistance in HNSCC cells and suggest that regulation of survivin expression may be a key mechanistic element in IGF1R-based therapeutic resistance.	Lapatinib	91-100	insulin like growth factor 1 receptor	Homo sapiens	214-219	
26621843-8	2016	These data indicate that erbB3 signaling is critical for both trastuzumab and lapatinib resistances mainly through the PI-3K/Akt pathway, whereas IGF-1R-initiated Src activation results in trastuzumab resistance without affecting lapatinib sensitivity.	Lapatinib	230-239	insulin like growth factor 1 receptor	Homo sapiens	146-152	
26484410-1	2015	BACKGROUND: Lapatinib, a dual EGFR and HER2 inhibitor has shown disappointing results in clinical trials of metastatic oesophago-gastric adenocarcinomas (OGAs), and in vitro studies suggest that MET, IGFR, and HER3 confer resistance.	Lapatinib	12-21	insulin like growth factor 1 receptor	Homo sapiens	200-204	
25886138-8	2015	RESULTS: We found that combined treatment with the IGF-IR and EGFR/Her-2 inhibitors NVP-AEW541 and lapatinib, respectively, synergistically inhibited pancreatic cancer cell growth.	Lapatinib	99-108	insulin like growth factor 1 receptor	Homo sapiens	51-57	
25886138-11	2015	CONCLUSIONS: Taken together, these data indicate that simultaneous blockade of IGF-IR and EGFR/Her-2 using NVP-AEW541 and lapatinib may overcome resistance in pancreatic cancer.	Lapatinib	122-131	insulin like growth factor 1 receptor	Homo sapiens	79-85	
21447712-6	2011	The Her2 inhibitor lapatinib cooperates with NVP-AEW541 to reduce Igf1r phosphorylation and to inhibit cell growth even though lapatinib alone has little effect on growth.	Lapatinib	19-28	insulin like growth factor 1 receptor	Homo sapiens	66-71	
24973425-0	2014	Functional genetic approach identifies MET, HER3, IGF1R, INSR pathways as determinants of lapatinib unresponsiveness in HER2-positive gastric cancer.	Lapatinib	90-99	insulin like growth factor 1 receptor	Homo sapiens	50-55	
24973425-9	2014	RESULTS: MET, HER3, insulin-like growth factor (IGF)-1R, and INSR were identified to mediate lapatinib unresponsiveness in HER2+ gastric cancer cells.	Lapatinib	93-102	insulin like growth factor 1 receptor	Homo sapiens	20-55	
24655723-9	2014	RESULTS: We established that introducing miR-630 into cells with innate- or acquired- resistance to HER-drugs significantly restored the efficacy of lapatinib, neratinib and afatinib; through a mechanism which we have determined to, at least partly, involve miR-630"s regulation of IGF1R.	Lapatinib	149-158	insulin like growth factor 1 receptor	Homo sapiens	282-287	
17308062-5	2007	As increased IGF-I receptor signaling has been implicated in trastuzumab resistance, our data strongly support further study of lapatinib as a potential therapeutic in breast cancers that have progressed on trastuzumab.	Lapatinib	128-137	insulin like growth factor 1 receptor	Homo sapiens	13-27