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Vincent-Philippe Lavallée on Muck Rack

Vincent-Philippe Lavallée

As seen in: Nature, Wiley Online Library, BioRxiv, Cell Press
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Articles

Modeling KRAS mutations in KMT2A::MLLT3 acute myeloid leukemia promotes leukemic progression and transcriptional rewiring

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By Nayeli Esparza, Joan Defrêne, Véronique Lisi, Alberto Hernández-Sánchez, Lars Bullinger, Vincent-Philippe Lavallée, Brian T Wilhelm, Frédéric Barabé, Eva Bresson, Anne-Cécile Soufflet, Martha María Juárez-Rodríguez
| Nature Verified
To the Editor Acute myeloid leukemia (AML) is a biologically heterogeneous disease where the mutational profile of the leukemic cells is a key determinant of prognosis, including disease-free survival and overall survival (OS). Rearrangements of the KMT2A gene occur in about 10% of AML cases, with MLLT3 being the most common fusion partner [1].
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Surface CD81 supports leukemia stem cell function and reveals a therapeutic vulnerability in acute myeloid leukemia

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By Fanny Gonzales, Pauline Peyrouze, Djohana Laurent, Thomas Boyer, Nihad Boukrout, Cyril Couturier, Véronique Lisi, Adeline Barthelemy, François Sevrin, Adriana Plesa, Antonino Bongiovanni, Nicolas Pottier, Claude Preudhomme, Vincent-Philippe Lavallée, Konstantinos Geles, Nicolas Duployez, Céline Berthon, Meyling Cheok, Soizic Houdiard, Christophe Roumier
| Nature Verified
Abstract Relapse remains the leading cause of mortality in acute myeloid leukemia (AML), largely due to the persistence of therapy-resistant leukemia stem cells (LSCs). However, surface determinants that sustain LSC function and disease aggressiveness remain incompletely defined. Here, we identify the tetraspanin CD81 as a regulator of LSC function, progression and treatment resistance in AML.
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DEK::NUP214 acts as an XPO1-dependent transcriptional activator of essential leukemia genes - Leukemia

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By Fadimana Kaya, Findlay Bewicke-Copley, Juho J. Miettinen, Pedro Casado, Özgen Deniz, Vincent-Philippe Lavallée, Florian Grebien, Szilvia Krizsan, Josée Hébert, Sébastien Lemieux, Eric Audemard, Krister Wennerberg, John Gribben, Sylvie D. Freeman, Guy Sauvageau, Jun Wang, Jean-Baptiste Cazier, Dominique Bonnet, Pedro R. Cutillas, Caroline Heckman, Jude Fitzgibbon, Kevin Rouault-Pierre, Joseph Saad, David C. Taussig
| Nature Verified
Abstract The t(6;9)(p22.3;q34.1) translocation/DEK::NUP214 fusion protein defines a distinct subgroup of younger AML patients classified as a separate disease entity by the World Health Organization. DEK is a nuclear factor with multifunctional roles, including gene regulation, while its fusion partner, NUP214, plays a pivotal role in nuclear export by interacting with transport receptors such as XPO1. However, the precise mechanism by which DEK::NUP214 drives leukemia remains unclear.
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