| Id |
Subject |
Object |
Predicate |
Lexical cue |
| TextSentencer_T1 |
0-92 |
Sentence |
denotes |
Tetraspanin 3 Is Required for the Development and Propagation of Acute Myelogenous Leukemia. |
| T1 |
0-92 |
Sentence |
denotes |
Tetraspanin 3 Is Required for the Development and Propagation of Acute Myelogenous Leukemia. |
| TextSentencer_T2 |
93-227 |
Sentence |
denotes |
Acute Myelogenous Leukemia (AML) is an aggressive cancer that strikes both adults and children and is frequently resistant to therapy. |
| T2 |
93-227 |
Sentence |
denotes |
Acute Myelogenous Leukemia (AML) is an aggressive cancer that strikes both adults and children and is frequently resistant to therapy. |
| TextSentencer_T3 |
228-359 |
Sentence |
denotes |
Thus, identifying signals needed for AML propagation is a critical step toward developing new approaches for treating this disease. |
| T3 |
228-359 |
Sentence |
denotes |
Thus, identifying signals needed for AML propagation is a critical step toward developing new approaches for treating this disease. |
| TextSentencer_T4 |
360-473 |
Sentence |
denotes |
Here, we show that Tetraspanin 3 is a target of the RNA binding protein Musashi 2, which plays a key role in AML. |
| T4 |
360-473 |
Sentence |
denotes |
Here, we show that Tetraspanin 3 is a target of the RNA binding protein Musashi 2, which plays a key role in AML. |
| TextSentencer_T5 |
474-545 |
Sentence |
denotes |
We generated Tspan3 knockout mice that were born without overt defects. |
| T5 |
474-545 |
Sentence |
denotes |
We generated Tspan3 knockout mice that were born without overt defects. |
| TextSentencer_T6 |
546-690 |
Sentence |
denotes |
However, Tspan3 deletion impaired leukemia stem cell self-renewal and disease propagation and markedly improved survival in mouse models of AML. |
| T6 |
546-690 |
Sentence |
denotes |
However, Tspan3 deletion impaired leukemia stem cell self-renewal and disease propagation and markedly improved survival in mouse models of AML. |
| TextSentencer_T7 |
691-820 |
Sentence |
denotes |
Additionally, Tspan3 inhibition blocked growth of AML patient samples, suggesting that Tspan3 is also important in human disease. |
| T7 |
691-820 |
Sentence |
denotes |
Additionally, Tspan3 inhibition blocked growth of AML patient samples, suggesting that Tspan3 is also important in human disease. |
| TextSentencer_T8 |
821-969 |
Sentence |
denotes |
As part of the mechanism, we show that Tspan3 deficiency disabled responses to CXCL12/SDF-1 and led to defects in AML localization within the niche. |
| T8 |
821-969 |
Sentence |
denotes |
As part of the mechanism, we show that Tspan3 deficiency disabled responses to CXCL12/SDF-1 and led to defects in AML localization within the niche. |
| TextSentencer_T9 |
970-1089 |
Sentence |
denotes |
These identify Tspan3 as an important regulator of aggressive leukemias and highlight a role for Tspan3 in oncogenesis. |
| T9 |
970-1089 |
Sentence |
denotes |
These identify Tspan3 as an important regulator of aggressive leukemias and highlight a role for Tspan3 in oncogenesis. |