PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
35577753-6	2022	In the first case, a patient with CLL, complex karyotype, del 17p, and a mutation in TP53 experiences progression after ibrutinib, venetoclax, bendamustine, rituximab, and idelalisib.	idelalisib	172-182	tumor protein p53	Homo sapiens	85-89	
28782884-14	2017	Patients with a del(17p) or TP53 mutation can be treated with ibrutinib, venetoclax, or a combination of idelalisib and rituximab.	idelalisib	105-115	tumor protein p53	Homo sapiens	28-32	
33790890-3	2021	Idelalisib is a highly selective inhibitor of the PI3K p110  isoform and is approved for the treatment of CLL in patients with relapsed/refractory disease or in those harboring 17p deletions or tp53 mutations.	idelalisib	0-10	tumor protein p53	Homo sapiens	194-198	
28971495-3	2018	Herein, we described the first report of a patient with relapsed chronic lymphocytic leukaemia harbouring TP53 abnormalities who developed, histologically proven, systemic light chain amyloidosis who was treated with the PI3K inhibitor, idelalisib, and rituximab.	idelalisib	237-247	tumor protein p53	Homo sapiens	106-110	
31467081-8	2019	We also found that PI3Kdelta inactivation through two approaches, CRISPR/Cas9-mediated depletion and a PI3Kdelta specific inhibitor (idelalisib) not only blocks vitreous-induced activation of AKT and MDM2 but also abrogates a vitreous-stimulated decrease in p53.	idelalisib	133-143	tumor protein p53	Homo sapiens	258-261	
29468637-0	2019	Idelalisib-rituximab induces durable remissions in TP53 disrupted B-PLL but results in significant toxicity: updated results of the UK-wide compassionate use programme.	idelalisib	0-10	tumor protein p53	Homo sapiens	51-55	
29222275-7	2017	TP53 disruption by gene mutation and/or deletion associates with chemoimmunotherapy failure and mandates treatment with innovative drugs, including ibrutinib, idelalisib, or venetoclax.	idelalisib	159-169	tumor protein p53	Homo sapiens	0-4	
29250930-7	2017	In the relapsed or refractory setting, patients with del(17p) or TP53 aberrations should be offered treatment with a novel agent, such as ibrutinib, idelalisib-rituximab or venetoclax.	idelalisib	149-159	tumor protein p53	Homo sapiens	65-69	
27061924-0	2017	Idelalisib-Rituximab induces clinical remissions in patients with TP53 disrupted B cell prolymphocytic leukaemia.	idelalisib	0-10	tumor protein p53	Homo sapiens	66-70	
28125433-4	2017	CAL-101 also leads to induction of caspase-dependent apoptosis probably through reactive oxygen species-dependent upregulation of FOXO3a and subsequent induction of the proapoptotic target genes of p53.	idelalisib	0-7	tumor protein p53	Homo sapiens	198-201	
27913471-7	2016	These recently approved drugs (ibrutinib, idelalisib, and venetoclax) are reporting excellent outcomes, including patients with high-risk disease such as 17p deletion (17p-) or TP53 mutations (TP53mut).	idelalisib	42-52	tumor protein p53	Homo sapiens	177-181	
28187444-6	2017	Idelalisib enhanced the bendamustine-mediated DNA damage/repair response, indicated by the phosphorylation of ATM, Chk2, and p53.	idelalisib	0-10	tumor protein p53	Homo sapiens	125-128	
26637744-5	2015	New B-cell receptor inhibitors, such as ibrutinib and idelalisib, may have a role in the management of B-PLL, especially for the patients harboring abnormalities of TP53.	idelalisib	54-64	tumor protein p53	Homo sapiens	165-169	
27040702-5	2016	Patients with a del(17p) or TP53 mutation should be treated with the kinase inhibitors ibrutinib or a combination of idelalisib and rituximab.	idelalisib	117-127	tumor protein p53	Homo sapiens	28-32	
26628631-7	2015	Ibrutinib and idelalisib are active in patients with high-risk features, achieving superior disease control in difficult-to-treat patients than prior best therapy, making them the preferred agents for chronic lymphocytic leukemia with TP53 aberrations and for patients resistant to chemoimmunotherapy.	idelalisib	14-24	tumor protein p53	Homo sapiens	235-239	
25908509-14	2015	Patients with a del(17p) or TP53 mutation can be treated with ibrutinib or a combination of idelalisib and rituximab.	idelalisib	92-102	tumor protein p53	Homo sapiens	28-32	
26637745-6	2015	Ibrutinib and idelalisib are currently approved for the treatment of relapsed or refractory CLL or frontline treatment of 17p-/TP53mut CLL regardless of fitness.	idelalisib	14-24	tumor protein p53	Homo sapiens	127-131	
26062943-6	2015	Fortunately, significant progress in the understanding of CLL biology has enabled the development of new molecular drugs targeting the B-cell receptor signaling pathway, such as ibrutinib and idelalisib, which have shown impressive results in patients with relapsed/refractory disease or with TP53 mutation/deletion.	idelalisib	192-202	tumor protein p53	Homo sapiens	293-297