Bac V. Le

Warsaw, MZ 02093, Poland

Last Updated: 09/26/2026

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Found 13 publications

TIAR-dependent coordination of alternative splicing and lipid peroxidation is required for CML cell resistance to imatinib in the bone marrow stroma.

TIAR-dependent coordination of alternative splicing and lipid peroxidation is required for CML cell resistance to imatinib in the bone marrow stroma.

Journal: bioRxiv : the preprint server for biology

Published: July 29, 2026

Polθ activity modulates sensitivity to standard therapies in DNMT3A-deficient leukemia.

Polθ activity modulates sensitivity to standard therapies in DNMT3A-deficient leukemia.

Journal: Cell reports. Medicine

Published: October 22, 2024

DNA polymerase theta-mediated DNA repair is a functional dependency and therapeutic vulnerability in DNMT3A deficient leukemia cells.

DNA polymerase theta-mediated DNA repair is a functional dependency and therapeutic vulnerability in DNMT3A deficient leukemia cells.

Journal: bioRxiv : the preprint server for biology

Published: October 16, 2024

Pre-Existing and Acquired Resistance to PARP Inhibitor-Induced Synthetic Lethality.

Pre-Existing and Acquired Resistance to PARP Inhibitor-Induced Synthetic Lethality.

Journal: Cancers

Published: October 19, 2022

DNA polymerase θ protects leukemia cells from metabolically induced DNA damage.

DNA polymerase θ protects leukemia cells from metabolically induced DNA damage.

Journal: Blood

Published: September 15, 2022

4-1BBL-containing leukemic extracellular vesicles promote immunosuppressive effector regulatory T cells.

4-1BBL-containing leukemic extracellular vesicles promote immunosuppressive effector regulatory T cells.

Journal: Blood advances

Published: September 20, 2021

TET2 and DNMT3A Mutations Exert Divergent Effects on DNA Repair and Sensitivity of Leukemia Cells to PARP Inhibitors.

TET2 and DNMT3A Mutations Exert Divergent Effects on DNA Repair and Sensitivity of Leukemia Cells to PARP Inhibitors.

Journal: Cancer research

Published: November 10, 2020

TGFβR-SMAD3 Signaling Induces Resistance to PARP Inhibitors in the Bone Marrow Microenvironment.

TGFβR-SMAD3 Signaling Induces Resistance to PARP Inhibitors in the Bone Marrow Microenvironment.

Journal: Cell reports

Published: April 08, 2020

Non-NAD-like PARP1 inhibitor enhanced synthetic lethal effect of NAD-like PARP inhibitors against BRCA1-deficient leukemia.

Non-NAD-like PARP1 inhibitor enhanced synthetic lethal effect of NAD-like PARP inhibitors against BRCA1-deficient leukemia.

Journal: Leukemia & lymphoma

Published: October 03, 2018

PARP1 inhibitor eliminated imatinib-refractory chronic myeloid leukemia cells in bone marrow microenvironment conditions.

PARP1 inhibitor eliminated imatinib-refractory chronic myeloid leukemia cells in bone marrow microenvironment conditions.

Journal: Leukemia & lymphoma

Published: June 23, 2018

Tyrosine kinase inhibitor-induced defects in DNA repair sensitize FLT3(ITD)-positive leukemia cells to PARP1 inhibitors.

Tyrosine kinase inhibitor-induced defects in DNA repair sensitize FLT3(ITD)-positive leukemia cells to PARP1 inhibitors.

Journal: Blood

Published: February 23, 2018

Ruxolitinib-induced defects in DNA repair cause sensitivity to PARP inhibitors in myeloproliferative neoplasms.

Ruxolitinib-induced defects in DNA repair cause sensitivity to PARP inhibitors in myeloproliferative neoplasms.

Journal: Blood

Published: May 12, 2017

Showing 1-12 of 13

Last Updated: 09/26/2026