PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
25541062-0	2015	AZD6244 inhibits cisplatin-induced ERK1/2 activation and potentiates cisplatin-associated cytotoxicity in K-ras G12D preclinical models.	AZD 6244	0-7	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	106-111	
25541062-6	2015	The combination of cisplatin and AZD6244 yielded a superior response to cisplatin alone in K-ras mice.	AZD 6244	33-40	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	91-96	
34856074-6	2022	We demonstrate that SRC is activated in response to treatment of KRAS-mutant colorectal cell lines with MEK inhibitors (trametinib or AZD6244), and that AZD0424 abrogates this.	AZD 6244	134-141	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	65-69	
22425996-7	2012	We observed that the addition of selumetinib provided substantial benefit for mice with lung cancer caused by Kras and Kras and p53 mutations, but mice with Kras and Lkb1 mutations had primary resistance to this combination therapy.	AZD 6244	33-44	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	110-114	
22425996-7	2012	We observed that the addition of selumetinib provided substantial benefit for mice with lung cancer caused by Kras and Kras and p53 mutations, but mice with Kras and Lkb1 mutations had primary resistance to this combination therapy.	AZD 6244	33-44	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	119-123	
22425996-7	2012	We observed that the addition of selumetinib provided substantial benefit for mice with lung cancer caused by Kras and Kras and p53 mutations, but mice with Kras and Lkb1 mutations had primary resistance to this combination therapy.	AZD 6244	33-44	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	119-123	
29945997-7	2018	Interestingly, p53 co-mutation rendered KRASG12C lung tumors less sensitive to combination treatment with selumetinib and chemotherapy.Conclusions: Our data demonstrate that unique KRAS mutations and concurrent mutations in tumor-suppressor genes are important factors for lung tumor responses to MEK inhibitor.	AZD 6244	106-117	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	40-44	
30021885-7	2018	Treatment with an orally bioavailable small-molecule activator of PP2A DT-061, in combination with the MEK inhibitor AZD6244, resulted in suppression of both p-AKT and MYC, as well as tumor regression in two KRAS-driven lung cancer mouse models.	AZD 6244	117-124	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	208-212	
31804471-4	2019	We also examined functional roles for Kras activation in dysplasia progression using Selumetinib, a MEK inhibitor, which is a downstream mediator of Kras signaling.	AZD 6244	85-96	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	149-153	
29348467-5	2018	Treatment with U0126, PD901, and Selumetinib MEK inhibitors triggered growth restraint in all CCA cell lines tested, with the most pronounced growth suppressive effects being observed in K-Ras mutant cells.	AZD 6244	33-44	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	187-192	
28938614-0	2017	Phenformin enhances the therapeutic effect of selumetinib in KRAS-mutant non-small cell lung cancer irrespective of LKB1 status.	AZD 6244	46-57	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	61-65	
28938614-11	2017	Irrespective of LKB1 status, phenformin may enhance the anti-tumor effect of selumetinib in KRAS-mutant NSCLC.	AZD 6244	77-88	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	92-96