Luca Lazzari
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Luca Lazzari has a total of 10 co-authors. Here are the top co-authors by number of shared publications:
Brian T. Wilhelm
Département de médicine, Université de Montréal, Montréal, QC, Canada
1 shared publicationEdlie St-Hilaire
Centre de Recherche, Hopital Maisonneuve-Rosemont, Montreal, QC, Canada
1 shared publication- Eva-Maria Piskor
Institut de recherches cliniques de Montréal (IRCM), Montréal, Canada
1 shared publication Gaspard Reulet
Institut de recherches cliniques de Montréal, McGill University, Montréal, QC, Canada
1 shared publication- Hugo Wurtele
Maisonneuve-Rosemont Hospital Research Center, Montreal, Canada
1 shared publication - Julie Ross
Institut de recherches cliniques de Montréal, McGill University, Montréal, QC, Canada
1 shared publication
Latest Publications
- Open Access
- 2 December 2025
- Published by American Society of Hematology in Blood Advances
- Vol. 9 (23) , 6158-6174
The lncRNA ELDR suppresses tumorigenicity of AML by interfering with DNA replication and chromatin accessibility
Acute myeloid leukemia (AML) with rearrangement of the mixed lineage leukemia gene expresses MLL-AF9 fusion protein, a transcription factor that impairs differentiation and drives expansion of leukemic cells. In this work, the zinc finger protein “growth factor independent 1” together with the histone methyltransferase LSD1 is revealed to occupy the promoter and regulate the expression of the lncRNA ELDR (EGFR [epidermal growth factor receptor] long non-coding downstream RNA) in the rearranged Mixed Lineage Leukemia (MLL) (MLL-r) AML cell line THP-1. Forced ELDR overexpression enhanced the growth inhibition of an Lysine-Specific Demethylase 1 inhibitor (LSD1i)/all-trans retinoic acid (ATRA) combination treatment and reduced the capacity of these cells to generate leukemia in xenografts, leading to a longer leukemia-free survival. ELDR is found to bind the clamp protein Proliferating Cell Nuclear Antigen (PCNA) and the MCM5 helicases causing defects of DNA replication fork progression. Moreover, AML cells overexpressing ELDR had reduced chromatin accessibility and transcription at α-satellite repeats in centromeres. In addition, ELDR RNA was detected close to MLL-AF9 at centromeres suggesting that it impedes leukemic progression preferentially of MLL-r AML by interfering with both DNA replication and centromeric transcription. Our findings reveal novel functions of the lncRNA ELDR in DNA replication and centromere biology when expressed at high levels in AML cells with MLL rearrangements. These discoveries could provide rationale for future strategies to treat MLL-r AML, which has a poor prognosis in children and adults. Delivery of the ELDR RNA could potentially be used as an adjunct to LSD1i/ATRA treatment or other currently used chemotherapeutic drugs to develop novel therapies for these AML subtypes.
- 2 December 2025
- Published by American Society of Hematology in Blood Advances
- Vol. 9 (23) , 6158-6174
Open AccessThe lncRNA ELDR suppresses tumorigenicity of AML by interfering with DNA replication and chromatin accessibility
Acute myeloid leukemia (AML) with rearrangement of the mixed lineage leukemia gene expresses MLL-AF9 fusion protein, a transcription factor that impairs differentiation and drives expansion of leukemic cells. In this work, the zinc finger protein “growth factor independent 1” together with the histone methyltransferase LSD1 is revealed to occupy the promoter and regulate the expression of the lncRNA ELDR (EGFR [epidermal growth factor receptor] long non-coding downstream RNA) in the rearranged Mixed Lineage Leukemia (MLL) (MLL-r) AML cell line THP-1. Forced ELDR overexpression enhanced the growth inhibition of an Lysine-Specific Demethylase 1 inhibitor (LSD1i)/all-trans retinoic acid (ATRA) combination treatment and reduced the capacity of these cells to generate leukemia in xenografts, leading to a longer leukemia-free survival. ELDR is found to bind the clamp protein Proliferating Cell Nuclear Antigen (PCNA) and the MCM5 helicases causing defects of DNA replication fork progression. Moreover, AML cells overexpressing ELDR had reduced chromatin accessibility and transcription at α-satellite repeats in centromeres. In addition, ELDR RNA was detected close to MLL-AF9 at centromeres suggesting that it impedes leukemic progression preferentially of MLL-r AML by interfering with both DNA replication and centromeric transcription. Our findings reveal novel functions of the lncRNA ELDR in DNA replication and centromere biology when expressed at high levels in AML cells with MLL rearrangements. These discoveries could provide rationale for future strategies to treat MLL-r AML, which has a poor prognosis in children and adults. Delivery of the ELDR RNA could potentially be used as an adjunct to LSD1i/ATRA treatment or other currently used chemotherapeutic drugs to develop novel therapies for these AML subtypes.