Jesse Gore

ORCID: 0000-0002-5704-4579
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About
Contact & Profiles
Research Areas
  • Pancreatic and Hepatic Oncology Research
  • MicroRNA in disease regulation
  • Cancer Cells and Metastasis
  • Microtubule and mitosis dynamics
  • Cancer Research and Treatments
  • Angiogenesis and VEGF in Cancer
  • TGF-β signaling in diseases
  • Renal cell carcinoma treatment
  • Cancer Mechanisms and Therapy
  • Cholangiocarcinoma and Gallbladder Cancer Studies
  • Epigenetics and DNA Methylation
  • Neuroendocrine Tumor Research Advances
  • Cancer Genomics and Diagnostics
  • Lymphatic System and Diseases
  • Mechanisms of cancer metastasis
  • Nanoparticle-Based Drug Delivery
  • Kruppel-like factors research
  • Pancreatitis Pathology and Treatment
  • Renal and related cancers
  • Cancer-related Molecular Pathways
  • Pancreatic function and diabetes
  • Biomarkers in Disease Mechanisms
  • FOXO transcription factor regulation
  • Immune cells in cancer
  • Congenital heart defects research

Cardiff University
2017

Indiana University – Purdue University Indianapolis
2012-2016

Indiana University School of Medicine
2013-2016

Indiana University Health
2013-2016

Indiana University
2013-2016

Nerviano Medical Sciences
2013-2014

California State University, Dominguez Hills
2013

Institute of Cardiology
2013

Center for Vascular Biology Research
2013

Richard L. Roudebush VA Medical Center
2013

Accurate peripheral markers for the diagnosis of pancreatic ductal adenocarcinoma (PDAC) are lacking. We measured differential expression select microRNAs (miRNAs) in plasma and bile among patients with PDAC, chronic pancreatitis (CP), controls.We identified (n=215) treatment-naive PDAC (n=77), CP bile/pancreatic duct pathology (n=67), controls (n=71) who had been prospectively enrolled a Pancreatobiliary Biorepository at time endoscopic retrograde cholangiopancreatography or ultrasound....

10.1038/ajg.2014.331 article EN The American Journal of Gastroenterology 2014-10-28

Abstract Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer with marked chemoresistance and a 5-year survival rate of 7%. The integrated stress response (ISR) cytoprotective pathway initiated in to exposure various environmental stimuli. We used pancreatic cells (PCCs) that are highly resistant gemcitabine (Gem) orthotopic mouse model investigate the role ISR Gem chemoresistance. induced eIF2 phosphorylation downstream transcription factors ATF4 CHOP PCCs, these effects occurred...

10.1038/cddis.2015.264 article EN cc-by Cell Death and Disease 2015-10-15

Abstract Dense fibrotic stroma associated with pancreatic ductal adenocarcinoma (PDAC) is a major obstacle for drug delivery to the tumor bed and plays crucial role in cancer progression. Current, anti-stromal therapies have failed improve response chemotherapy patient survival. Furthermore, recent studies show that impedes progression its complete ablation accelerates PDAC In an effort understand molecular mechanisms tumor-stromal interactions, using vitro vivo models biopsies, we loss of...

10.1038/srep11450 article EN cc-by Scientific Reports 2015-06-22

Increased microRNA-10b (miR-10b) expression in the cancer cells pancreatic ductal adenocarcinoma (PDAC) is a marker of disease aggressiveness. In present study, we determined that plasma miR-10b levels are significantly increased PDAC patients by comparison with normal controls. By gene profiling, identified potential targets downregulated miR-10b, including Tat-interacting protein 30 (TIP30). Immunoblotting and luciferase reporter assays confirmed TIP30 was direct target. Downregulation or...

10.1038/onc.2013.405 article EN cc-by-nc-sa Oncogene 2013-10-07

// Jesse Gore 1, 5 , Kelly E. Craven 2 Julie L. Wilson 1 Gregory A. Cote 5, 6 Monica Cheng Hai V. Nguyen 3 Harvey M. Cramer 4 Stuart Sherman Murray Korc 2, Department of Medicine, Indiana University School Indianapolis, IN 46202, USA Biochemistry and Molecular Biology, Surgery, Pathology Laboratory The Melvin Bren Simon Cancer Center, the Center for Pancreatic Research, Medical South Carolina, Charleston, SC 29425, Correspondence to: Korc, e-mail: mkorc@iu.edu Gore, ajgore@iu.edu Keywords:...

10.18632/oncotarget.3233 article EN Oncotarget 2015-02-25

Abstract Most solid tumors, including pancreatic ductal adenocarcinoma (PDAC), exhibit structural and numerical chromosome instability (CIN). Although often implicated as a driver of tumor progression drug resistance, CIN also reduces cell fitness poses vulnerability that can be exploited therapeutically. The spindle assembly checkpoint (SAC) ensures correct chromosome-microtubule attachment, thereby minimizing segregation errors. Many tumors upregulation SAC components such MPS1, which may...

10.1158/1535-7163.mct-13-0324 article EN Molecular Cancer Therapeutics 2013-11-27

// Kelly E. Craven 1, * , Jesse Gore 2, 3, Julie L. Wilson 2 Murray Korc 3 1 Departments of Biochemistry and Molecular Biology, Indiana University School Medicine, Indianapolis, IN 46202, USA Department The Pancreatic Cancer Signature Center at Simon Center, These authors contributed equally to this work Correspondence to: Gore, e-mail: ajgore@iu.edu Keywords: pancreatic cancer, TCGA, angiogenesis, TGF-β, inflammation Received: October 13, 2015 Accepted: November 08, Published: 18, ABSTRACT...

10.18632/oncotarget.6345 article EN Oncotarget 2015-11-18

Abstract Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy, associated with high frequency of KRAS mutations (95%) and loss negative growth constraints, due, in part, to frequent CDKN2A (85%), TP53 (75%) SMAD4 (55%) mutations. PDACs also overexpress all three TGF-β isoforms, levels TGF-βs correlates decreased survival. Recently, we showed that human PDAC murine (mPDAC) arising biologically aggressive, oncogenic Kras-driven genetically engineered mouse models (GEMMs),...

10.1158/1538-7445.am2014-969 article EN Cancer Research 2014-10-01

Abstract Pancreatic Ductal Adenocarcinoma (PDAC), which comprises 85% of pancreatic cancers, is the 4th leading cause cancer death in United States with a 5-year survival 7%. While human PDACs (hPDACs) are hypovascular, they also overexpress number angiogenic growth factors and receptors. Additionally, use anti-angiogenic agents murine models PDAC leads to reduced tumor volume, spread, microvessel density, improved survival. Nonetheless, clinical trials using therapy have been overwhelmingly...

10.1158/1538-7445.am2016-3400 article EN Cancer Research 2016-07-15

Abstract Pancreatic ductal adenocarcinoma (PDAC) is a deadly disease that projected to become the 2nd leading cause of cancer deaths by 2030. PDACs are associated with high frequency KRAS mutations (95%) and overexpression many pro-angiogenic cytokines growth factors. Using genetically engineered mouse model (GEMM) we established in which oncogenic Kras combined loss RB (KRC), have determined arising these mice (mPDACs) harbor endothelial cells (ECs) sinusoidal-like vessels blood flow, as...

10.1158/1538-7445.am2015-4180 article EN Cancer Research 2015-08-01
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