Shawn M. Egan

ORCID: 0009-0006-6422-809X
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • MicroRNA in disease regulation
  • Genetics and Neurodevelopmental Disorders
  • Autism Spectrum Disorder Research
  • Cancer-related molecular mechanisms research
  • Neurogenetic and Muscular Disorders Research
  • Retinoids in leukemia and cellular processes
  • Genomics and Rare Diseases
  • Immune Cell Function and Interaction
  • Circular RNAs in diseases
  • Acute Myeloid Leukemia Research
  • NF-κB Signaling Pathways
  • Language Development and Disorders
  • Congenital Heart Disease Studies
  • Connective tissue disorders research
  • Immune cells in cancer
  • Cancer Mechanisms and Therapy
  • Cancer Immunotherapy and Biomarkers
  • MXene and MAX Phase Materials
  • Cardiac Structural Anomalies and Repair
  • Immunotherapy and Immune Responses

FamilieSCN2A Foundation
2024

Northwestern University
2024

University of Illinois Chicago
2024

Roswell Park Comprehensive Cancer Center
2016-2018

Abstract SCN2A-related disorders secondary to altered function in the voltage-gated sodium channel Nav1.2 are rare, with clinically heterogeneous expressions that include epilepsy, autism and multiple severe profound impairments other conditions. To advance understanding of clinical phenotypes their relationship function, 81 patients (36 female, 44%, median age 5.4 years) 69 unique SCN2A variants were systematically phenotyped assessed. Participants recruited through FamileSCN2A Foundation....

10.1093/brain/awae125 article EN cc-by-nc Brain 2024-04-23

Cell growth and proliferation require the coordinated activation of many cellular processes, including cap-dependent mRNA translation. MicroRNAs oppose translation set thresholds for expression target proteins. Emerging data suggest that microRNA function is enhanced by due in part to induction RNA-induced silencing complex (RISC) scaffold protein GW182. In current study, we demonstrate increased GW182 activated or transformed immune cells results from effects phosphoinositol...

10.1128/mcb.01011-15 article EN Molecular and Cellular Biology 2016-06-29

// Shawn M. Egan 1 , Ellen Karasik 2 Leigh Ellis 3 and Sandra O. Gollnick 4 Department of Immunology, Roswell Park Cancer Institute, Buffalo, New York 14263, USA Pharmacology Therapeutics, Oncologic Pathology, Dana-Farber Boston, MA 02215, Cell Stress Biology, Correspondence to: Gollnick, email: Sandra.gollnick@roswellpark.org Keywords: NF-κB, microRNA, prostate cancer, cyclin D1 Received: December 30, 2015      Accepted: June 02,...

10.18632/oncotarget.18795 article EN Oncotarget 2017-06-28

The etiology of prostate cancer is poorly understood, but it a multi-step process that has been linked to environmental factors induce inflammation within the gland. Glands patients frequently contain multiple zones disease at various stages progression. drive progression from an indolent benign stage aggressive are not well-defined. Prostate and carcinoma associated with high levels myeloid cell infiltration; these cells in other cancers, their role unclear. To determine whether contribute...

10.1007/s00262-018-2143-y article EN cc-by Cancer Immunology Immunotherapy 2018-03-03

Abstract Prostate cancer (CaP) is a critical problem for the aging male population. CaP managed using combination of prostatectomy, androgen ablation, chemotherapy and radiation. Subsets patients develop androgen-insensitive metastatic which therapeutic options are limited. Androgen-insensitive clinically presents with constitutive NF-κB activation. activation in primary tumor correlated disease, biochemical relapse drives promoting chronic-inflammation. The pathway tightly regulated by many...

10.4049/jimmunol.196.supp.213.17 article EN The Journal of Immunology 2016-05-01
Coming Soon ...