
Gautam Borthakur
Articles
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2 weeks ago |
nature.com | Jayastu Senapati |Guillermo Garcia-Manero |Courtney DiNardo |Gautam Borthakur |Tapan M Kadia |Elias Jabbour | +8 more
Despite the improvement in overall outcomes of patients with acute myeloid leukemia (AML), some high-risk disease subsets continue to fare dismally. AML with TP53 aberrations (mutations, deletions) is one such subset of high-risk AML with a median survival of about 6–9 months [1,2,3].
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3 weeks ago |
nature.com | Mahesh Swaminathan |Courtney DiNardo |Naveen Pemmaraju |Guillermo Garcia-Manero |Ghayas C. Issa |Gautam Borthakur | +9 more
To the Editor:The advent of VEN (VEN) has changed the treatment paradigm of acute myeloid leukemia (AML). Currently, venetoclax (VEN), in combination with a hypomethylating agent (HMA), is approved for the treatment of adult patients with AML unsuitable for intensive chemotherapy or frontline treatment of patients ≥75 years [1].
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1 month ago |
nature.com | Courtney DiNardo |Wei-Ying Jen |Koichi Takahashi |Tapan M Kadia |Sanam Loghavi |Patrick K. Reville | +19 more
AbstractIntensive chemotherapy remains the standard for newly diagnosed (ND) acute myeloid leukemia (AML); however, relapse risk remains high. Additionally, most patients with relapsed/refractory (RR) AML have poor outcomes. We report the long-term experience of 138 patients, 77 ND and 61 RR, treated with FLAG-IDA in combination with venetoclax.
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Sep 25, 2024 |
nature.com | Farhad Ravandi |Jayastu Senapati |Nicholas Short |Tapan M Kadia |Gautam Borthakur |Marina Konopleva | +5 more
AbstractOptimal frontline use of active agents in T-cell acute lymphoblastic leukemia/lymphoma (T-ALL/LBL) is prudent to improve outcomes. We report the long-term follow-up of the phase 2 trial of HyperCVAD with nelarabine and pegylated asparaginase (Original cohort). In the latest protocol iteration venetoclax was added to the induction/consolidation regimen (Venetoclax cohort). Eligible patients were adults with untreated T-ALL/LBL or after minimal therapy and with adequate organ function.
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Sep 19, 2024 |
nature.com | Courtney DiNardo |Divij Verma |Natalia Baran |Tianyu Cai |Veronica Guerra |Gowri Poigaialwar | +8 more
AbstractMalignancies are reliant on glutamine as an energy source and a facilitator of aberrant DNA methylation. We demonstrate preclinical synergy of telaglenastat (CB-839), a selective glutaminase inhibitor, combined with azacytidine (AZA), followed by a single-arm, open-label, phase 1b/2 study in persons with advanced myelodysplastic syndrome (MDS).
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