A5008374158- Acute Myeloid Leukemia Research
- Acute Lymphoblastic Leukemia research
- Histone Deacetylase Inhibitors Research
- Childhood Cancer Survivors' Quality of Life
- Protein Degradation and Inhibitors
- Cancer, Hypoxia, and Metabolism
- Chronic Myeloid Leukemia Treatments
- Lung Cancer Treatments and Mutations
- Epigenetics and DNA Methylation
- Cancer therapeutics and mechanisms
- Cell death mechanisms and regulation
- Chronic Lymphocytic Leukemia Research
- Neuroblastoma Research and Treatments
- Folate and B Vitamins Research
- Retinoids in leukemia and cellular processes
- Lymphoma Diagnosis and Treatment
- Family Support in Illness
- Myeloproliferative Neoplasms: Diagnosis and Treatment
- RNA Interference and Gene Delivery
- RNA modifications and cancer
- Pediatric Pain Management Techniques
- Blood disorders and treatments
- Neutropenia and Cancer Infections
- Cancer-related Molecular Pathways
- Hematopoietic Stem Cell Transplantation
Children's Hospital of Michigan
2016-2025
Central Michigan University
2020-2025
Wayne State University
2015-2024
The Barbara Ann Karmanos Cancer Institute
2015-2024
John Wiley & Sons (United States)
2020
Vanderbilt University Medical Center
2019
University of Southern California
2019
Michigan United
2011-2016
Detroit Medical Center
2000-2016
St. Jude Children's Research Hospital
2008-2012
The L1 genes of two human papillomavirus type 16 (HPV16) isolates derived from condylomata acuminata were used to express the major capsid protein in insect cells via recombinant baculoviruses. Both proteins self-assembled into virus-like particles (VLP) with high efficiency and could be purified preparative amounts on density gradients. yield VLP was 3 orders magnitude higher than what has been obtained previously, using prototype HPV16. DNA sequence comparison identified a single...
Abstract Purpose: To investigate the molecular mechanism underlying intrinsic resistance to ABT-199. Experimental Design: Western blots and real-time RT-PCR were used determine levels of Mcl-1 after ABT-199 treatment alone or in combination with cytarabine daunorubicin. Immunoprecipitation Bim effect on their interactions Bcl-2 family members. Lentiviral short hairpin RNA knockdown CRISPR confirm role JC-1 assays flow cytometry drug-induced apoptosis. Results: from ABT-199–treated cell lines...
In acute myeloid leukemia (AML), initial treatment response by morphologic analysis of bone marrow predicts long-term outcome. Response can now be assessed minimal residual disease (MRD) monitoring with flow cytometry or polymerase chain reaction (PCR). We determined the relation among results these approaches and their prognostic value.In multicenter AML02 study, follow-up samples from 203 children adolescents newly diagnosed AML were examined (n = 1,514), morphology 1,382), PCR...
To investigate the efficacy of combination FLT3 inhibitors midostaurin or gilteritinib with Bcl-2 inhibitor venetoclax in FLT3-internal tandem duplication (ITD) acute myeloid leukemia (AML) and underlying molecular mechanism.Using both FLT3-ITD cell lines primary patient samples, Annexin V-FITC/propidium iodide staining flow cytometry analysis were used to quantify death induced by gilteritinib, alone venetoclax. Western blot was performed assess changes protein expression levels members...
Abstract Acute myeloid leukemia (AML) is a serious disease. The 5-year survival rates remain frustratingly low (65% for children and 26% adults). Resistance to frontline chemotherapy (usually cytarabine) often develops; therefore new treatment modality needed. Bcl-2 family proteins play an important role in balancing cell apoptosis. antiapoptotic have been found be dysregulated AML. ABT-199, BH3 mimetic, was developed target protein Bcl-2. Although ABT-199 has demonstrated promising results,...
Abstract Background Venetoclax + azacitidine is a frontline treatment for older adult acute myeloid leukemia (AML) patients and salvage therapy relapsed/refractory who have been treated with intensive chemotherapy. While this an important option, many fail to achieve complete remission of those that do, majority relapse. Leukemia stem cells (LSCs) are believed be responsible AML relapse can targeted through oxidative phosphorylation reduction. We previously reported ONC213 disrupts decreases...
Down syndrome children with acute megakaryocytic leukemia (AMkL) have higher cure rates than non-Down myeloid (AML) patients treated cytosine arabinoside (ara-C). Megakaryoblasts from AML are more sensitive in vitro to ara-C cells patients. Somatic mutations the GATA1 transcription factor been detected exclusively and almost uniformly AMkL patients, suggesting a potential linkage chemotherapy sensitivity of megakaryoblasts. Stable transfection wild-type cDNA into cell line CMK resulted...
Acute myeloid leukemia (AML) remains a challenging disease to treat and urgently requires new therapies improve its treatment outcome. In this study, we investigated the molecular mechanisms underlying cooperative antileukemic activities of panobinostat cytarabine or daunorubicin (DNR) in AML cell lines diagnostic blast samples vitro vivo. Panobinostat suppressed expression BRCA1, CHK1, RAD51 cells dose-dependent manner. Further, significantly increased cytarabine- DNR-induced DNA...
Abstract BACKGROUND: Children who are treated for myeloid leukemia associated with Down syndrome (DS) experience superior survival compared children have without DS. To maintain excellent outcomes while avoiding toxicity, the Children's Oncology Group (COG) conducted phase 3 trial COG A2971, first solely designed to provide uniform treatment of in North American A2971 eliminated 2 induction drugs and months maintenance therapy from standard‐timing regimen dexamethasone, cytarabine,...