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Chronic lymphocytic leukemia disease progression is accelerated by APRIL-TACI interaction in the TCL1 transgenic mouse model. / Lascano, Valeria; Guadagnoli, Marco; Schot, Jan G. et al.

In: Blood, Vol. 122, No. 24, 2013, p. 3960-3963.

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Lascano, Valeria ; Guadagnoli, Marco ; Schot, Jan G. et al. / Chronic lymphocytic leukemia disease progression is accelerated by APRIL-TACI interaction in the TCL1 transgenic mouse model. In: Blood. 2013 ; Vol. 122, No. 24. pp. 3960-3963.

BibTeX

@article{38eb78dee8294d44953102dab0eae03f,
title = "Chronic lymphocytic leukemia disease progression is accelerated by APRIL-TACI interaction in the TCL1 transgenic mouse model",
abstract = "Although in vitro studies pointed to the tumor necrosis factor family member APRIL (a proliferation-inducing ligand) in mediating survival of chronic lymphocytic leukemia (CLL) cells, clear evidence for a role in leukemogenesis and progression in CLL is lacking. APRIL significantly prolonged in vitro survival of CD5(+)B220(dull) leukemic cells derived from the murine E mu-TCL1-Tg (TCL1-Tg [transgenic]) model for CLL. APRIL-TCL1 double-Tg mice showed a significantly earlier onset of leukemia and disruption of splenic architecture, and survival was significantly reduced. Interestingly, clonal evolution of CD5(+) B220(dull) cells (judged by BCR clonality) did not seem to be accelerated by APRIL; both mouse strains were oligoclonal at 4 months. Although APRIL binds different receptors, APRIL-mediated leukemic cell survival depended on tumor necrosis factor receptor superfamily member 13B (TACI) ligation. These findings indicate that APRIL has an important role in CLL and that the APRIL-TACI interaction might be a selective novel therapeutic target for human CLL. (Blood. 2013;122(24):3960-3963)",
author = "Valeria Lascano and Marco Guadagnoli and Schot, {Jan G.} and Luijks, {Dieuwertje M.} and Guikema, {Jeroen E. J.} and Katherine Cameron and Michael Hahne and Steven Pals and Erik Slinger and Kipps, {Thomas J.} and {van Oers}, {Marinus H. J.} and Eric Eldering and Medema, {Jan Paul} and Kater, {Arnon P.}",
year = "2013",
doi = "10.1182/blood-2013-04-497693",
language = "English",
volume = "122",
pages = "3960--3963",
journal = "Blood",
issn = "0006-4971",
publisher = "American Society of Hematology",
number = "24",

}

RIS

TY - JOUR

T1 - Chronic lymphocytic leukemia disease progression is accelerated by APRIL-TACI interaction in the TCL1 transgenic mouse model

AU - Lascano, Valeria

AU - Guadagnoli, Marco

AU - Schot, Jan G.

AU - Luijks, Dieuwertje M.

AU - Guikema, Jeroen E. J.

AU - Cameron, Katherine

AU - Hahne, Michael

AU - Pals, Steven

AU - Slinger, Erik

AU - Kipps, Thomas J.

AU - van Oers, Marinus H. J.

AU - Eldering, Eric

AU - Medema, Jan Paul

AU - Kater, Arnon P.

PY - 2013

Y1 - 2013

N2 - Although in vitro studies pointed to the tumor necrosis factor family member APRIL (a proliferation-inducing ligand) in mediating survival of chronic lymphocytic leukemia (CLL) cells, clear evidence for a role in leukemogenesis and progression in CLL is lacking. APRIL significantly prolonged in vitro survival of CD5(+)B220(dull) leukemic cells derived from the murine E mu-TCL1-Tg (TCL1-Tg [transgenic]) model for CLL. APRIL-TCL1 double-Tg mice showed a significantly earlier onset of leukemia and disruption of splenic architecture, and survival was significantly reduced. Interestingly, clonal evolution of CD5(+) B220(dull) cells (judged by BCR clonality) did not seem to be accelerated by APRIL; both mouse strains were oligoclonal at 4 months. Although APRIL binds different receptors, APRIL-mediated leukemic cell survival depended on tumor necrosis factor receptor superfamily member 13B (TACI) ligation. These findings indicate that APRIL has an important role in CLL and that the APRIL-TACI interaction might be a selective novel therapeutic target for human CLL. (Blood. 2013;122(24):3960-3963)

AB - Although in vitro studies pointed to the tumor necrosis factor family member APRIL (a proliferation-inducing ligand) in mediating survival of chronic lymphocytic leukemia (CLL) cells, clear evidence for a role in leukemogenesis and progression in CLL is lacking. APRIL significantly prolonged in vitro survival of CD5(+)B220(dull) leukemic cells derived from the murine E mu-TCL1-Tg (TCL1-Tg [transgenic]) model for CLL. APRIL-TCL1 double-Tg mice showed a significantly earlier onset of leukemia and disruption of splenic architecture, and survival was significantly reduced. Interestingly, clonal evolution of CD5(+) B220(dull) cells (judged by BCR clonality) did not seem to be accelerated by APRIL; both mouse strains were oligoclonal at 4 months. Although APRIL binds different receptors, APRIL-mediated leukemic cell survival depended on tumor necrosis factor receptor superfamily member 13B (TACI) ligation. These findings indicate that APRIL has an important role in CLL and that the APRIL-TACI interaction might be a selective novel therapeutic target for human CLL. (Blood. 2013;122(24):3960-3963)

U2 - 10.1182/blood-2013-04-497693

DO - 10.1182/blood-2013-04-497693

M3 - Article

C2 - 24100449

VL - 122

SP - 3960

EP - 3963

JO - Blood

JF - Blood

SN - 0006-4971

IS - 24

ER -

ID: 2222786