Publications by authors named "S D T Grant"

Monoclonal antibodies (mAb) represent an important class of biologic therapeutics that can treat a variety of diseases including cancer, autoimmune disorders or respiratory conditions (e.g. COVID-19).

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Elucidating the genetic contributions to Parkinson's disease (PD) etiology across diverse ancestries is a critical priority for the development of targeted therapies in a global context. We conducted the largest sequencing characterization of potentially disease-causing, protein-altering and splicing mutations in 710 cases and 11,827 controls from genetically predicted African or African admixed ancestries. We explored copy number variants (CNVs) and runs of homozygosity (ROHs) in prioritized early onset and familial cases.

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Objective: The aim of this study was to identify naturally occurring groups of individuals experiencing binge eating (BE) symptoms based on their endorsement of varied functions of BE.

Method: Adults (N = 646) with self-reported BE symptoms were examined using latent profile analysis to identify differentiated profiles based on eight established functions of BE. Profiles were also compared on measures of BE symptoms, eating disorder psychopathology, internal shame, body shame, psychological distress, adverse childhood experiences, and demographic variables.

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Purpose: Relapsed and/or refractory acute myeloid leukemia and high-risk myelodysplastic syndrome continue to have a poor prognosis with limited treatment options despite advancements in rational combination and targeted therapies. Belinostat (an HDAC inhibitor) and Pevonedistat (a NEDD8 inhibitor) have each been independently studied in hematologic malignancies and have tolerable safety profiles with limited single-agent activity. Preclinical studies in AML cell lines and primary AML cells show the combination to be highly synergistic, particularly in high-risk phenotypes such as p53 mutant and FLT-3-ITD positive cells.

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The prevalence of childhood obesity is increasing worldwide, along with the associated common comorbidities of type 2 diabetes and cardiovascular disease in later life. Motivated by evidence for a strong genetic component, our prior genome-wide association study (GWAS) efforts for childhood obesity revealed 19 independent signals for the trait; however, the mechanism of action of these loci remains to be elucidated. To molecularly characterize these childhood obesity loci, we sought to determine the underlying causal variants and the corresponding effector genes within diverse cellular contexts.

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