| Id |
Subject |
Object |
Predicate |
Lexical cue |
| TextSentencer_T1 |
0-142 |
Sentence |
denotes |
Metformin synergistically sensitizes FLT3-ITD-positive acute myeloid leukemia to sorafenib by promoting mTOR-mediated apoptosis and autophagy. |
| TextSentencer_T2 |
143-359 |
Sentence |
denotes |
Mutations of Fms-like tyrosine kinase 3-internal tandem duplication (FLT3-ITD), accounting for approximately 30% of patients with acute myeloid leukemia (AML), results in poor therapeutic efficacy and short survival. |
| TextSentencer_T3 |
360-473 |
Sentence |
denotes |
Sorafenib, an oral multikinase inhibitor, can inhibit FLT3 and improve clinical outcome of FLT3 mutated leukemia. |
| TextSentencer_T4 |
474-658 |
Sentence |
denotes |
Our current studies have shown that, the antidiabetic drug metformin also exerts anti-leukemic effect by activating p-AMPK and synergistically sensitizes FLT3 mutated AML to sorafenib. |
| TextSentencer_T5 |
659-840 |
Sentence |
denotes |
Both agents suppress cell proliferation in a dose-dependent manner and induce apoptosis via cell cycle arrest, but does not obviously modulate autophagy marker, light chain 3 (LC3). |
| TextSentencer_T6 |
841-1130 |
Sentence |
denotes |
Mechanistically, in the presence of metformin, the anticancer potential of sorafenib, accompanying with increased LC3 levels, is found to be synergistically enhanced with the remarkably reduced protein expression of the mTOR/p70S6K/4EBP1 pathway, while not appreciably altering cell cycle. |
| TextSentencer_T7 |
1131-1281 |
Sentence |
denotes |
Overall, these results show metformin in aid of sorafenib may represent a promising and attractive strategy for the treatment of FLT3-ITD mutated AML. |
| T1 |
0-142 |
Sentence |
denotes |
Metformin synergistically sensitizes FLT3-ITD-positive acute myeloid leukemia to sorafenib by promoting mTOR-mediated apoptosis and autophagy. |
| T2 |
143-359 |
Sentence |
denotes |
Mutations of Fms-like tyrosine kinase 3-internal tandem duplication (FLT3-ITD), accounting for approximately 30% of patients with acute myeloid leukemia (AML), results in poor therapeutic efficacy and short survival. |
| T3 |
360-473 |
Sentence |
denotes |
Sorafenib, an oral multikinase inhibitor, can inhibit FLT3 and improve clinical outcome of FLT3 mutated leukemia. |
| T4 |
474-658 |
Sentence |
denotes |
Our current studies have shown that, the antidiabetic drug metformin also exerts anti-leukemic effect by activating p-AMPK and synergistically sensitizes FLT3 mutated AML to sorafenib. |
| T5 |
659-840 |
Sentence |
denotes |
Both agents suppress cell proliferation in a dose-dependent manner and induce apoptosis via cell cycle arrest, but does not obviously modulate autophagy marker, light chain 3 (LC3). |
| T6 |
841-1130 |
Sentence |
denotes |
Mechanistically, in the presence of metformin, the anticancer potential of sorafenib, accompanying with increased LC3 levels, is found to be synergistically enhanced with the remarkably reduced protein expression of the mTOR/p70S6K/4EBP1 pathway, while not appreciably altering cell cycle. |
| T7 |
1131-1281 |
Sentence |
denotes |
Overall, these results show metformin in aid of sorafenib may represent a promising and attractive strategy for the treatment of FLT3-ITD mutated AML. |