Id |
Subject |
Object |
Predicate |
Lexical cue |
TextSentencer_T1 |
0-183 |
Sentence |
denotes |
Role of CAAT/enhancer binding protein homologous protein in panobinostat-mediated potentiation of bortezomib-induced lethal endoplasmic reticulum stress in mantle cell lymphoma cells. |
T1 |
0-183 |
Sentence |
denotes |
Role of CAAT/enhancer binding protein homologous protein in panobinostat-mediated potentiation of bortezomib-induced lethal endoplasmic reticulum stress in mantle cell lymphoma cells. |
TextSentencer_T2 |
184-192 |
Sentence |
denotes |
PURPOSE: |
T2 |
184-192 |
Sentence |
denotes |
PURPOSE: |
TextSentencer_T3 |
193-384 |
Sentence |
denotes |
Bortezomib induces unfolded protein response (UPR) and endoplasmic reticulum stress, as well as exhibits clinical activity in patients with relapsed and refractory mantle cell lymphoma (MCL). |
T3 |
193-384 |
Sentence |
denotes |
Bortezomib induces unfolded protein response (UPR) and endoplasmic reticulum stress, as well as exhibits clinical activity in patients with relapsed and refractory mantle cell lymphoma (MCL). |
TextSentencer_T4 |
385-606 |
Sentence |
denotes |
Here, we determined the molecular basis of the improved in vitro and in vivo activity of the combination of the pan-histone deacetylase inhibitor panobinostat and bortezomib against human, cultured, and primary MCL cells. |
T4 |
385-606 |
Sentence |
denotes |
Here, we determined the molecular basis of the improved in vitro and in vivo activity of the combination of the pan-histone deacetylase inhibitor panobinostat and bortezomib against human, cultured, and primary MCL cells. |
TextSentencer_T5 |
607-627 |
Sentence |
denotes |
EXPERIMENTAL DESIGN: |
T5 |
607-627 |
Sentence |
denotes |
EXPERIMENTAL DESIGN: |
TextSentencer_T6 |
628-861 |
Sentence |
denotes |
Immunoblot analyses, reverse transcription-PCR, and immunofluorescent and electron microscopy were used to determine the effects of panobinostat on bortezomib-induced aggresome formation and endoplasmic reticulum stress in MCL cells. |
T6 |
628-861 |
Sentence |
denotes |
Immunoblot analyses, reverse transcription-PCR, and immunofluorescent and electron microscopy were used to determine the effects of panobinostat on bortezomib-induced aggresome formation and endoplasmic reticulum stress in MCL cells. |
TextSentencer_T7 |
862-870 |
Sentence |
denotes |
RESULTS: |
T7 |
862-870 |
Sentence |
denotes |
RESULTS: |
TextSentencer_T8 |
871-1113 |
Sentence |
denotes |
Treatment with panobinostat induced heat shock protein 90 acetylation; depleted the levels of heat shock protein 90 client proteins, cyclin-dependent kinase 4, c-RAF, and AKT; and abrogated bortezomib-induced aggresome formation in MCL cells. |
T8 |
871-1113 |
Sentence |
denotes |
Treatment with panobinostat induced heat shock protein 90 acetylation; depleted the levels of heat shock protein 90 client proteins, cyclin-dependent kinase 4, c-RAF, and AKT; and abrogated bortezomib-induced aggresome formation in MCL cells. |
TextSentencer_T9 |
1114-1237 |
Sentence |
denotes |
Panobinostat also induced lethal UPR, associated with induction of CAAT/enhancer binding protein homologous protein (CHOP). |
T9 |
1114-1237 |
Sentence |
denotes |
Panobinostat also induced lethal UPR, associated with induction of CAAT/enhancer binding protein homologous protein (CHOP). |
TextSentencer_T10 |
1238-1324 |
Sentence |
denotes |
Conversely, knockdown of CHOP attenuated panobinostat-induced cell death of MCL cells. |
T10 |
1238-1324 |
Sentence |
denotes |
Conversely, knockdown of CHOP attenuated panobinostat-induced cell death of MCL cells. |
TextSentencer_T11 |
1325-1537 |
Sentence |
denotes |
Compared with each agent alone, cotreatment with panobinostat increased bortezomib-induced expression of CHOP and NOXA, as well as increased bortezomib-induced UPR and apoptosis of cultured and primary MCL cells. |
T11 |
1325-1537 |
Sentence |
denotes |
Compared with each agent alone, cotreatment with panobinostat increased bortezomib-induced expression of CHOP and NOXA, as well as increased bortezomib-induced UPR and apoptosis of cultured and primary MCL cells. |
TextSentencer_T12 |
1538-1704 |
Sentence |
denotes |
Cotreatment with panobinostat also increased bortezomib-mediated in vivo tumor growth inhibition and improved survival of mice bearing human Z138C MCL cell xenograft. |
T12 |
1538-1704 |
Sentence |
denotes |
Cotreatment with panobinostat also increased bortezomib-mediated in vivo tumor growth inhibition and improved survival of mice bearing human Z138C MCL cell xenograft. |
TextSentencer_T13 |
1705-1716 |
Sentence |
denotes |
CONCLUSION: |
T13 |
1705-1716 |
Sentence |
denotes |
CONCLUSION: |
TextSentencer_T14 |
1717-1874 |
Sentence |
denotes |
These findings suggest that increased UPR and induction of CHOP are involved in enhanced anti-MCL activity of the combination of panobinostat and bortezomib. |
T14 |
1717-1874 |
Sentence |
denotes |
These findings suggest that increased UPR and induction of CHOP are involved in enhanced anti-MCL activity of the combination of panobinostat and bortezomib. |