PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
28698200-6	2017	AZD1775 acquired resistance models demonstrated upregulation of AXL, pS6, and MET, and resistance was overcome with the addition of AXL (TP0903), dual-AXL/MET (cabozantinib), or mTOR (RAD001) inhibitors.Conclusions: AXL promotes resistance to WEE1 inhibition via downstream mTOR signaling and resulting activation of a parallel DNA damage repair pathway, CHK1.	adavosertib	0-7	checkpoint kinase 1	Homo sapiens	355-359	
31209198-13	2019	In contrast, Wee1 inhibitor Adavosertib progresses the cell cycle and thereby increases lethality to Chk1 inhibition in HNSCC cell lines.	adavosertib	28-39	checkpoint kinase 1	Homo sapiens	101-105	
31717700-6	2019	RESULTS: This study reports, for the first time, the efficacy of the concomitant inhibition of CHK1/CHK2 and WEE1 in ALL cell lines and primary leukemic B-ALL cells using two selective inhibitors: PF-0047736 (CHK1/CHK2 inhibitor) and AZD-1775 (WEE1 inhibitor).	adavosertib	234-242	checkpoint kinase 1	Homo sapiens	95-99	
25283841-4	2015	Although AZD1775 induced Chk1 activation, reflected by markedly increased Chk1 S296/S317/S345 phosphorylation leading to inhibitory T14 phosphorylation of cdc2/Cdk1, these compensatory responses were sharply abrogated by HDACIs.	adavosertib	9-16	checkpoint kinase 1	Homo sapiens	25-29	
27939202-6	2017	Wee-inhibition by AZD1775 resulted in the activation of Chk1.	adavosertib	18-25	checkpoint kinase 1	Homo sapiens	56-60	
25283841-4	2015	Although AZD1775 induced Chk1 activation, reflected by markedly increased Chk1 S296/S317/S345 phosphorylation leading to inhibitory T14 phosphorylation of cdc2/Cdk1, these compensatory responses were sharply abrogated by HDACIs.	adavosertib	9-16	checkpoint kinase 1	Homo sapiens	74-78	
25458954-5	2015	We demonstrate that MK-1775 treatment results in increased H2AX phosphorylation, indicating increased DNA double-strand breaks, and activation of CHK1, which are both dependent on CDK activity.	adavosertib	20-27	checkpoint kinase 1	Homo sapiens	146-150	
25458954-2	2015	The selective Wee1 inhibitor MK-1775 has demonstrated promising results when combined with DNA damaging agents, and more recently with CHK1 inhibitors in various malignancies.	adavosertib	29-36	checkpoint kinase 1	Homo sapiens	135-139	
26529495-1	2015	MK-1775 is the first-in-class selective Wee1 inhibitor which has been demonstrated to synergize with CHK1 inhibitors in various malignancies.	adavosertib	0-7	checkpoint kinase 1	Homo sapiens	101-105	
26529495-5	2015	Interestingly, treatment with panobinostat alone or in combination with MK-1775 resulted in decreased Wee1 protein levels as well as downregulation of the CHK1 pathway.	adavosertib	72-79	checkpoint kinase 1	Homo sapiens	155-159	
26529495-6	2015	shRNA knockdown of CHK1 significantly sensitized AML cells to MK-1775 treatment, while knockdown of Wee1 significantly enhanced both MK-1775- and panobinostat-induced cell death.	adavosertib	62-69	checkpoint kinase 1	Homo sapiens	19-23	
26529495-7	2015	Our results demonstrate that panobinostat synergizes with MK-1775 in AML cells, at least in part through downregulation of CHK1 and/or Wee1, providing compelling evidence for the clinical development of the combination treatment in AML.	adavosertib	58-65	checkpoint kinase 1	Homo sapiens	123-127	
25308916-9	2015	MK-1775 treatment in SK-N-BE(2) cells induced increased levels of p-CHK1(S345) , which could be decreased by the addition of panobinostat.	adavosertib	0-7	checkpoint kinase 1	Homo sapiens	68-72	
23148684-5	2012	METHODS: Small molecules MK-8776 and MK-1775 were used to selectively and potently inhibit CHK1 and WEE1, respectively.	adavosertib	37-44	checkpoint kinase 1	Homo sapiens	91-95	
25301733-6	2014	Small-molecule inhibitors of CHK1 (AZD7762) or WEE1 (MK-1775) induced mitotic catastrophe, as characterized by dephosphorylation of CDK1(Tyr15), phosphorylation of histone H39(Ser10), and apoptosis.	adavosertib	53-60	checkpoint kinase 1	Homo sapiens	29-33	
25084614-0	2014	CHK1 plays a critical role in the anti-leukemic activity of the wee1 inhibitor MK-1775 in acute myeloid leukemia cells.	adavosertib	79-86	checkpoint kinase 1	Homo sapiens	0-4	
25084614-10	2014	Time-course experiments, using AML cell lines, revealed a time-dependent increase in DNA DSBs, activation of CHK1 and subsequent apoptosis following MK-1775 treatment, which could be attenuated by a CDK1/2 inhibitor, Roscovitine.	adavosertib	149-156	checkpoint kinase 1	Homo sapiens	109-113	
25084614-12	2014	CONCLUSIONS: Our study provides compelling evidence that CHK1 plays a critical role in the anti-leukemic activity of MK-1775 and highlights a possible mechanism of resistance to MK-1775.	adavosertib	117-124	checkpoint kinase 1	Homo sapiens	57-61	
24179152-8	2014	Further studies showed that MK8776 enhanced MK1775-mediated activation of the ATR/CHK1 pathway in acute leukemia cell lines and ex vivo.	adavosertib	44-50	checkpoint kinase 1	Homo sapiens	82-86