Abhishek Maiti
A5075581944- Acute Myeloid Leukemia Research
- Chronic Myeloid Leukemia Treatments
- Acute Lymphoblastic Leukemia research
- Chronic Lymphocytic Leukemia Research
- Histone Deacetylase Inhibitors Research
- Myeloproliferative Neoplasms: Diagnosis and Treatment
- Protein Degradation and Inhibitors
- CAR-T cell therapy research
- Multiple Myeloma Research and Treatments
- Neutropenia and Cancer Infections
- Immune Cell Function and Interaction
- Cancer Genomics and Diagnostics
- Lymphoma Diagnosis and Treatment
- Hematopoietic Stem Cell Transplantation
- Retinoids in leukemia and cellular processes
- Hemoglobinopathies and Related Disorders
- Phagocytosis and Immune Regulation
- Monoclonal and Polyclonal Antibodies Research
- Biochemical and Molecular Research
- Eosinophilic Disorders and Syndromes
- Epigenetics and DNA Methylation
- Galectins and Cancer Biology
- Sarcoma Diagnosis and Treatment
- Peptidase Inhibition and Analysis
- Macrophage Migration Inhibitory Factor
The University of Texas MD Anderson Cancer Center
2016-2025
The University of Texas Health Science Center at Houston
2015-2024
American Society of Clinical Oncology
2022
National Cancer Institute
2022
Conquer Cancer Foundation
2022
Roche (Switzerland)
2022
AbbVie (United States)
2022
Theodore Roosevelt High School
2019
The University of Texas Southwestern Medical Center
2019
Interfaith Medical Center
2019
Sixty percent of newly diagnosed patients with acute myeloid leukemia (ND-AML) receiving frontline therapy attain a complete response (CR), yet 30%-40% relapse. Relapsed or refractory AML (R/R-AML) remains particularly adverse population necessitating improved therapeutic options. This phase Ib/II study evaluated the safety and efficacy fludarabine, cytarabine, granulocyte colony-stimulating factor, idarubicin combined B-cell lymphoma-2 inhibitor venetoclax in ND-AML R/R-AML.The IB portion...
TP53 mutation (TP53mut ) confers an adverse prognosis in acute myeloid leukemia (AML). Venetoclax with hypomethylating agents is a current standard for older patients; however, recent reports suggest that TP53mut resistance to venetoclax. The authors investigated the outcomes of patients AML who were treated 10-day decitabine and venetoclax (DEC10-VEN) (ClinicalTrials.gov identifier NCT03404193).Patients newly diagnosed received 20 mg/m2 10 days every 4 6 weeks induction, followed by 5 after...
Abstract Preclinically, enasidenib and azacitidine (ENA + AZA) synergistically enhance cell differentiation, venetoclax (VEN), a small molecule Bcl2 inhibitor (i) is particularly effective in IDH 2 mutated acute myeloid leukemia ( IDH2 mut AML). This open label phase II trial enrolled patients (pts) with documented AML. All received AZA 75 mg/m /d x 7 d/cycle ENA 100 mg QD continuously. Concomitant Bcl2i FLT3i were allowed (NCT03683433).Twenty-six pts (median 68 years, range, 24–88); newly...
Abstract Hypomethylating agents (HMA) with venetoclax is a new standard for older/unfit patients acute myeloid leukemia (AML). However, it unknown how HMA compare to intensive chemotherapy (IC) in who are “fit” or “unfit” IC. We compared outcomes of older newly diagnosed AML receiving 10‐day decitabine (DEC10‐VEN) vs DEC10‐VEN consisted daily 20 mg/m 2 10 days induction and 5 as consolidation. The IC cohort received regimens containing cytarabine ≥1 g/m /d. A validated treatment‐related...
Background: Philadelphia chromosome-positive (Ph+) advanced leukemias, including acute myeloid leukemia (AML) and chronic (CML) in blast phase (MBP), have poor outcomes. Venetoclax has shown synergism with BCR-ABL1 tyrosine kinase inhibitors (TKI) preclinical studies. However, clinical activity of venetoclax TKI-based regimens is unknown. Methods: We conducted a retrospective study on patients Ph+ AML (n = 7) CML-MBP 9) who received combined at our institution. Results: Median patient age...
Abstract Assessment of measurable residual disease (MRD) provides prognostic information in acute myeloid leukemia (AML). However, the utility MRD with venetoclax-based lower intensity regimens is unknown. We analyzed value achieving a negative older/“unfit” patients AML receiving first-line therapy 10-day decitabine and venetoclax. was evaluated bone marrow specimens using multicolor flow cytometry (sensitivity 0.1%). Ninety-seven either complete remission (CR) or CR incomplete hematologic...
Abstract Early T‐cell precursor acute lymphoblastic leukemia/lymphoma (ETP‐ALL/LBL) is characterized by a distinct immunophenotype (CD1a‐negative, CD8‐negative, CD5‐negative or weak‐positive <75%, myeloid/stem‐cell markers positive) and poor clinical outcomes. Near‐ETP ALL transcriptionally similar to ETP‐ALL but CD5 expression level not low enough meet the criteria of ETP immunophenotype. Outcomes near‐ETP are well characterized. We reviewed 171 patients with newly‐diagnosed T‐ALL/LBL....
Abstract Multi‐agent induction chemotherapy (IC) improves response rates in younger patients with acute myeloid leukemia (AML); however, relapse remains the principal cause of treatment failure. Improved regimens are needed. A prospective single‐center phase Ib/II study evaluating fludarabine, cytarabine, G‐CSF, and idarubicin combined venetoclax (FLAG‐IDA + VEN) newly diagnosed (ND) or relapsed/refractory AML. The primary efficacy endpoint was assessment overall activity (overall rate...
Abstract In older/unfit newly diagnosed patients with FLT3 mutated acute myeloid leukemia (AML), lower intensity chemotherapy (LIC) in combination either a inhibitor or venetoclax results poor overall survival (median 8 to 12.5 months). We performed retrospective analysis of 87 AML treated on triplet (LIC + Venetoclax, [ N = 27]) and doublet inhibitor, 60]) regimens at our institution. Data were collected from prospective clinical trials 75% ( 65) 25% 22) who received the same treatment...
Hypomethylating agents (HMAs) and venetoclax (Ven) represent the standard of care for patients with acute myeloid leukemia (AML) who are ineligible intensive chemotherapy. However, European LeukemiaNet (ELN) risk classifications have been validated treated therapy. In this study, we validate a recently proposed new molecular prognostic signature (mPRS) AML HMAs Ven. This classification allocated to favorable, intermediate (N/KRAS or FLT3-internal tandem duplication mutations), lower (TP53...
Cancer driver mutations often show distinct temporal acquisition patterns, but the biological basis for this, if any, remains unknown. RAS occur invariably late in course of acute myeloid leukaemia, upon progression or relapsed/refractory disease1–6. Here, by using human leukaemogenesis models, we first that are obligatory events need to succeed earlier cooperating mutations. We provide mechanistic explanation this a requirement mutant specifically transform committed progenitors...
Abstract Purpose: Magrolimab is a monoclonal antibody directed against macrophage checkpoint CD47 on myeloid leukemia cells that was pre-clinically synergistic with azacitidine-venetoclax, warranting further clinical evaluation. Patients and Methods: In this phase 1b/2 study the triplet combination of azacitidine, venetoclax magrolimab evaluated in adult patients frontline (ineligible for intensive chemotherapy) relapsed/refractory AML. Azacitidine dosed at 75mg/m2 7 days, 400 mg/day 28...
Spliceosome mutations (SRSF2, SF3B1, U2AF1, ZRSR2), are encountered in ∼50% of secondary acute myeloid leukemia cases (sAML) and define a molecular subgroup with outcomes similar to sAML de novo AML patients treated intensive chemotherapy. Outcomes spliceosome hypomethylating agents combination venetoclax (HMA+VEN) remains unknown. The primary objective was compare vs wild-type HMA+VEN. Secondary objectives included analysis the mutational landscape cohort assessing impact co-occurring...
Venetoclax (VEN) combined with the hypomethylating agent (HMA) azacitidine improves survival in patients aged ≥75 years newly diagnosed acute myeloid leukemia (AML). VEN and HMA treatment can result prolonged often profound neutropenia, this warrants antifungal prophylaxis. Azole antifungals inhibit cytochrome P450 3A4, primary enzyme responsible for metabolism; results dose reductions each concomitant antifungal. Limited clinical data exist on outcomes treated VEN, an HMA, various...
Abstract The isocitrate dehydrogenase enzyme 2 (IDH2) gene is mutated in ∼5% of patients with myelodysplastic syndrome (MDS). Enasidenib an oral, selective, mutant IDH2 inhibitor approved for IDH2-mutated (mIDH2) relapsed/refractory acute myeloid leukemia. We designed a 2-arm multicenter study to evaluate safety and efficacy (A) the combination enasidenib azacitidine newly diagnosed mIDH2 MDS, (B) monotherapy MDS after prior hypomethylating agent (HMA) therapy. Fifty enrolled: 27 arm A 23 B....