PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
19965674-5	2010	Furthermore, studies using biochemical inhibitors of caspase-8 versus caspase-9 demonstrate that NPI-0052 plus lenalidomide-triggered apoptosis is primarily dependent on caspase-8 signaling.	Lenalidomide	111-123	caspase 8	Homo sapiens	53-62	
34588172-0	2021	Caspase-8 regulates the anti-myeloma activity of bortezomib and lenalidomide.	Lenalidomide	64-76	caspase 8	Homo sapiens	0-9	
34588172-5	2021	Either inhibition or genetic depletion of CASP-8 decreased the CRBN cleavage upon Btz treatment, which could potentiate the anti-myeloma activity of IMiD lenalidomide (Len).	Lenalidomide	168-171	caspase 8	Homo sapiens	42-48	
34588172-6	2021	This work suggests that administration of CASP-8 inhibitors might enhance the overall effectiveness of Btz/Len-based therapeutic treatment for myeloma patients.	Lenalidomide	107-110	caspase 8	Homo sapiens	42-48	
34588172-7	2021	Significance Statement Caspase-8 activation upon bortezomib treatment results in the cleavage of cereblon, a substrate receptor of the cullin 4-RING E3 ligase, which is responsible for the degradation of two transcription factors IKZF1 and IKZF3 in the presence of immunomodulatory drugs including lenalidomide.	Lenalidomide	298-310	caspase 8	Homo sapiens	23-32	
34588172-8	2021	The administration of caspase-8 inhibitor may enhance the anti-myeloma activity of the combination therapy with bortezomib and lenalidomide to multiple myeloma.	Lenalidomide	127-139	caspase 8	Homo sapiens	22-31	
35321428-3	2022	Bortezomib and lenalidomide activate caspase-8 and promote the apoptosis of myeloma cells.	Lenalidomide	15-27	caspase 8	Homo sapiens	37-46	
35321428-4	2022	However, caspase-8 inhibition potentiated the antiproliferative effect of lenalidomide and bortezomib in myeloma cells, suggesting that caspase-8 could regulate proliferation and apoptosis in the opposite pathway.	Lenalidomide	74-86	caspase 8	Homo sapiens	136-145	
33392195-7	2020	Using myeloma as a model system, we further revealed that either inhibition or genetic depletion of CASP-8 enhances the anti-myeloma activity of lenalidomide (Len) by impairing CRBN cleavage, leading to the attenuated IKZF1 and IKZF3 protein levels and the reduced viability of myeloma cell lines and primary myeloma cells from patients.	Lenalidomide	145-157	caspase 8	Homo sapiens	100-106	
33392195-7	2020	Using myeloma as a model system, we further revealed that either inhibition or genetic depletion of CASP-8 enhances the anti-myeloma activity of lenalidomide (Len) by impairing CRBN cleavage, leading to the attenuated IKZF1 and IKZF3 protein levels and the reduced viability of myeloma cell lines and primary myeloma cells from patients.	Lenalidomide	159-162	caspase 8	Homo sapiens	100-106	
33392195-8	2020	The present study discovered that the stability of the substrate receptor of an E3 ligase can be modulated by CASP-8 and suggested that administration of CASP-8 inhibitors enhances the overall effectiveness of Len-based combination therapy in myeloma.	Lenalidomide	210-213	caspase 8	Homo sapiens	110-116	
33392195-8	2020	The present study discovered that the stability of the substrate receptor of an E3 ligase can be modulated by CASP-8 and suggested that administration of CASP-8 inhibitors enhances the overall effectiveness of Len-based combination therapy in myeloma.	Lenalidomide	210-213	caspase 8	Homo sapiens	154-160	
19965674-5	2010	Furthermore, studies using biochemical inhibitors of caspase-8 versus caspase-9 demonstrate that NPI-0052 plus lenalidomide-triggered apoptosis is primarily dependent on caspase-8 signaling.	Lenalidomide	111-123	caspase 8	Homo sapiens	170-179