A5023994533- Lymphoma Diagnosis and Treatment
- Chronic Lymphocytic Leukemia Research
- Viral-associated cancers and disorders
- Cutaneous lymphoproliferative disorders research
- PI3K/AKT/mTOR signaling in cancer
- Cytokine Signaling Pathways and Interactions
- Cancer-related Molecular Pathways
- Ubiquitin and proteasome pathways
- Lung Cancer Treatments and Mutations
- Acute Myeloid Leukemia Research
- HER2/EGFR in Cancer Research
- Sarcoma Diagnosis and Treatment
- Chronic Myeloid Leukemia Treatments
- Acute Lymphoblastic Leukemia research
- Neuroblastoma Research and Treatments
- Liver Disease Diagnosis and Treatment
- CNS Lymphoma Diagnosis and Treatment
- Immune Cell Function and Interaction
- Cancer-related gene regulation
- RNA modifications and cancer
- RNA Research and Splicing
- CAR-T cell therapy research
- Glycosylation and Glycoproteins Research
- Tumors and Oncological Cases
- Myeloproliferative Neoplasms: Diagnosis and Treatment
The University of Texas MD Anderson Cancer Center
2007-2025
Medical College of Wisconsin
2019-2023
Children's Hospital of Wisconsin
2019-2023
Gangneung Asan Hospital
2022
University of Pittsburgh Medical Center
2022
Universidad Libre de Colombia
2022
Roche (Switzerland)
2022
Michigan Medicine
2022
Moffitt Cancer Center
2022
Koç University
2022
Anaplastic lymphoma kinase (ALK)-positive anaplastic large cell (ALCL) frequently carries the t(2;5)(p23;q35) resulting in aberrant expression of chimeric nucleophosmin-ALK. Previously, nucleophosmin-ALK has been shown to activate phosphatidylinositol 3-kinase (PI3K) and its downstream effector, serine/threonine AKT. In this study, we hypothesized that mammalian target rapamycin (mTOR) pathway, which functions AKT, mediates oncogenic effects activated PI3K/AKT ALK+ ALCL. Here, provide...
Abstract Activating mutations of the FLT3 gene mediate leukemogenesis, at least in part, through activation PI3K/AKT. The mammalian target rapamycin (mTOR)-Raptor signaling pathway is known to act downstream AKT. Here we show that mTOR effectors, 4EBP1, p70S6K and rpS6, are highly activated cultured primary -mutated acute myeloid leukemia (AML) cells. Introduction FLT3-ITD expressing constitutively kinase further activates its effectors BaF3 We also found contributes tumor cell survival, as...
Abstract Context.—Mantle cell lymphoma (MCL) is a distinct type of B-cell non-Hodgkin characterized by t(11;14)(q13;q32) and cyclin D1 overexpression. The pathogenesis MCL has not been comprehensively studied, which can be attributed in part to the paucity well-characterized lines. Objectives.—We collected 4 previously developed lines performed extensive characterization, including susceptibly these transduction adenovirus vectors. Our aim was facilitate establishment an vitro model that...
Abstract Context.—Mantle cell lymphoma (MCL) is a distinct type of B-cell non-Hodgkin characterized by t(11;14)(q13;q32) and cyclin D1 overexpression. The pathogenesis MCL has not been comprehensively studied, which can be attributed in part to the paucity well-characterized lines. Objectives.—We collected 4 previously developed lines performed extensive characterization, including susceptibly these transduction adenovirus vectors. Our aim was facilitate establishment an vitro model that...
p53 is frequently expressed but rarely mutated in Hodgkin and Reed-Sternberg (HRS) cells of Hodgkin's lymphoma (HL). protein levels are regulated by murine double minute 2 (MDM2) through a well-established autoregulatory feedback loop. In this study, we investigated the effects nutlin-3A, recently developed small molecule that antagonizes MDM2 disrupts p53-MDM2 interaction, on p53-dependent cell cycle arrest apoptosis cultured HRS cells.HL lines carrying wild-type (wt) or gene were treated...
A small subset of patients with acute myeloid leukemia (AML) have cuplike nuclei. Other investigators demonstrated that these neoplasms distinctive clinicopathologic and molecular features.The authors searched for who had AML nuclei at their institution over a 10-year interval. strict definition was used: >or=10% blasts nuclear invaginations in >or=25% the area. The relevant data were reviewed, results compared control group without nuclei.In total, 22 identified classified as maturation...
Cellular Jun (c-Jun), a member of the JUN family, is an activator protein-1 transcription factor involved in cell differentiation, proliferation, and apoptosis that can be activated by phosphorylation at serine-73 -63 residues. Using tissue microarrays immunohistochemistry, we investigated c-Jun expression 112 CD30 lymphomas 232 B- or T-cell lineage, 24 cases lymphomatoid papulosis. was expressed exclusively lymphoproliferative disorders including 41/41 (100%) classical Hodgkin lymphoma...
Recent studies have identified germline mutations in TP53, PAX5, ETV6, and IKZF1 kindreds with familial acute lymphoblastic leukemia (ALL), but the genetic basis of ALL many is unknown despite mutational analysis exome. Here, we report a deletion ETV6 by linkage structural variant whole-genome sequencing data segregating kindred thrombocytopenia, B-progenitor leukemia, diffuse large B-cell lymphoma. The 75-nt removed exon 7 splice acceptor, resulting skipping protein truncation. was also...
Triple-negative breast cancer (TNBC) is the subtype with poorest prognosis. Evidence indicates that aberrant JAB1/CSN5 expression associated advanced tumor stage and poor prognosis in cancer. In this study, we evaluated of JAB1 TNBC potential mechanisms regulating expression. We found miR-17 was lower than normal tissue, patients a good Furthermore, regulated by cells, mice miR-17-overexpressing tumors had less growth control mice. also demonstrated suppressed JAB1's oncogenic function,...