A5101503698- Acute Myeloid Leukemia Research
- Neurofibromatosis and Schwannoma Cases
- Epigenetics and DNA Methylation
- Hematopoietic Stem Cell Transplantation
- Sarcoma Diagnosis and Treatment
- Neuroblastoma Research and Treatments
- RNA Research and Splicing
- Bone Tumor Diagnosis and Treatments
- Cancer-related gene regulation
- Protein Degradation and Inhibitors
- Bone Metabolism and Diseases
- Ubiquitin and proteasome pathways
- Cancer-related molecular mechanisms research
- Myeloproliferative Neoplasms: Diagnosis and Treatment
- Immune Cell Function and Interaction
- DNA Repair Mechanisms
- Cancer Genomics and Diagnostics
- Mast cells and histamine
- Meningioma and schwannoma management
- Acute Lymphoblastic Leukemia research
- T-cell and B-cell Immunology
- Genomics and Chromatin Dynamics
- Chronic Myeloid Leukemia Treatments
- Histone Deacetylase Inhibitors Research
- Erythrocyte Function and Pathophysiology
The University of Texas Health Science Center at San Antonio
2019-2025
The University of Texas at San Antonio
2021-2025
Mays Cancer Center at UT Health San Antonio
2021-2023
One Cell Systems (United States)
2023
May Institute
2023
Zunyi Medical University
2020-2022
University of Miami
2015-2021
Sylvester Comprehensive Cancer Center
2015-2021
Texas A&M University
2021
Indiana University – Purdue University Indianapolis
2009-2020
Recent studies have shown that mesenchymal stem cells (MSC) with the potential for cell-mediated therapies and tissue engineering applications can be isolated from extracted dental tissues. Here, we investigated collection, processing, cryobiological characteristics of MSC human teeth processed under current good practices (cGTP). Viable pulp-derived (DPSC) cultures were 31 40 examined. Of eight DPSC examined more thoroughly, all expressed appropriate cell surface markers underwent...
The ten-eleven translocation 1 (TET1) gene is the founding member of TET family enzymes (TET1/2/3) that convert 5-methylcytosine to 5-hydroxymethylcytosine. Although TET1 was first identified as a fusion partner mixed lineage leukemia (MLL) in acute myeloid carrying t(10,11), its definitive role unclear. In contrast frequent down-regulation (or loss-of-function mutations) and critical tumor-suppressor roles three genes observed various types cancers, here we show direct target MLL-fusion...
HOTTIP lncRNA is highly expressed in acute myeloid leukemia (AML) driven by MLL rearrangements or NPM1 mutations to mediate HOXA topologically associated domain (TAD) formation and drive aberrant transcription. However, the mechanism through which accesses CCCTC-binding factor (CTCF) chromatin boundaries regulates CTCF-mediated genome topology remains unknown. Here, we show that directly interacts with a fraction of CTCF-binding sites (CBSs) AML recruiting CTCF/cohesin complex...
Mutation of tet methylcytosine dioxygenase 2 (encoded by TET2) drives myeloid malignancy initiation and progression
Critical to homeostasis of blood cell production by hematopoietic stem/progenitor (HSC/P) cells is the regulation HSC/P retention within bone marrow microenvironment and migration between blood. Key extracellular regulatory elements for this process have been defined (cell–cell adhesion, growth factors, chemokines), but mechanism which reconcile multiple external signals has not elucidated. Rac related small GTPases are candidates role were studied in deficient Rac2, a cell-specific family...
The extracellular signal-regulated kinases (ERK1 and 2) are widely-expressed they modulate proliferation, survival, differentiation, protein synthesis in multiple cell lineages. Altered ERK1/2 signaling is found several genetic diseases with skeletal phenotypes, including Noonan syndrome, Neurofibromatosis type 1, Cardio-facio-cutaneous suggesting that MEK-ERK signals regulate human development. Here, we examine the consequence of Erk1 Erk2 disruption functions osteoclasts, specialized...
Abstract TET2 is a dioxygenase that catalyses multiple steps of 5-methylcytosine oxidation. Although mutations frequently occur in various types haematological malignancies, the mechanism by which they increase risk for these cancers remains poorly understood. Here we show Tet2 −/− mice develop spontaneous myeloid, T- and B-cell malignancies after long latencies. Exome sequencing tumours reveals accumulation numerous mutations, including Apc , Nf1 Flt3 Cbl Notch1 Mll2 are recurrently...
TET1/2/3 are methylcytosine dioxygenases that regulate cytosine hydroxymethylation. Tet1/2 abundantly expressed in HSC/HPCs and implicated hematological malignancies. Tet2 deletion mice causes myeloid malignancies, while Tet1-null develop B cell lymphoma after an extended period of latency. Interestingly, TET1/2 often concomitantly downregulated acute B-lymphocytic leukemia. Here, we investigated the overlapping non-redundant functions using double-knockout (DKO) mice. DKO Tet2−/− show...
Acute myeloid leukemia (AML) is a heterogeneous disease with poor outcomes. Despite increased evidence shows that dysregulation of histone modification contributes to AML, specific drugs targeting key modulators are not applied in the clinical treatment AML. Here, we investigated whether KDM6B, demethylase tri-methylated H3 lysine 27 (H3K27me3), has therapeutic potential for A KDM6B-specific inhibitor, GSK-J4, was treat primary cells from AML patients and cell lines vitro vivo....
Although nucleoporin 98 (NUP98) fusion oncogenes often drive aggressive pediatric leukemia by altering chromatin structure and expression of HOX genes, underlying mechanisms remain elusive. Here, we report that a Hoxb-associated lncRNA HoxBlinc was aberrantly activated in NUP98-PHF23 fusion-driven leukemias. occupancies led to elevated MLL1 recruitment aberrant homeotic topologically associated domains (TADs) enhanced accessibilities homeotic/hematopoietic oncogenes. HoxBlinc-depletion NUP98...
Neurofibromatosis type 1 (NF1) is a common autosomal-dominant disorder characterized by cutaneous neurofibromas infiltrated with large numbers of mast cells, melanocyte hyperplasia, and predisposition to develop malignant neoplasms. NF1 encodes GTPase activating protein (GAP) for Ras. Consistent Knudson's “two hit” model tumor suppressor genes, leukemias solid tumors in patients frequently demonstrate somatic loss the normal allele. However, phenotypic biochemical consequences heterozygous...
Neurofibromas are common tumors found in neurofibromatosis type 1 (NF1) patients. These complex composed of Schwann cells, mast fibroblasts and perineurial cells embedded collagen that provide a lattice for tumor invasion. Genetic studies demonstrate neurofibromas, nullizygous loss Nf1 haploinsufficiency non-neuronal required tumorigenesis. Fibroblasts major cellular constituent neurofibromas source constitutes ∼50% the dry weight tumor. Here, we show two prevalent heterozygous interact...
Individuals with neurofibromatosis type 1 (NF1) have a high incidence of osteoporosis and osteopenia. However, understanding the cellular molecular basis these sequelae is incomplete. Osteoclasts are specialized myeloid cells that principal bone-resorbing skeleton. We found Nf1(+/-) mice contain elevated numbers multinucleated osteoclasts. Both osteoclasts osteoclast progenitors from were hyperresponsive to limiting concentrations M-CSF receptor activator NF-kappaB ligand (RANKL) levels....