Julie Leclerc

ORCID: 0000-0002-6122-0985
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About
Contact & Profiles
Research Areas
  • Pancreatic and Hepatic Oncology Research
  • Cancer Genomics and Diagnostics
  • Liver Disease Diagnosis and Treatment
  • Neuroendocrine Tumor Research Advances
  • Metabolism and Genetic Disorders
  • Diet and metabolism studies
  • Adrenal and Paraganglionic Tumors
  • Hormonal Regulation and Hypertension
  • Tracheal and airway disorders
  • Neonatal Respiratory Health Research
  • Diet, Metabolism, and Disease
  • Cystic Fibrosis Research Advances
  • Esophageal and GI Pathology
  • Clinical Nutrition and Gastroenterology
  • Renal and related cancers
  • Heavy Metals in Plants
  • Colorectal Cancer Surgical Treatments
  • Cytomegalovirus and herpesvirus research
  • Alcoholism and Thiamine Deficiency
  • Genomic variations and chromosomal abnormalities
  • Management of metastatic bone disease
  • Computational Drug Discovery Methods
  • Horticultural and Viticultural Research
  • Intestinal Malrotation and Obstruction Disorders
  • Botanical Research and Applications

Centre Hospitalier Régional et Universitaire de Nancy
1981-2025

Inserm
2022-2024

CANTHER - Hétérogénéité, Plasticité et Résistance aux Thérapies des Cancers
2024

Centre Hospitalier Universitaire de Lille
2009-2024

Institut Pasteur de Lille
2024

Centre National de la Recherche Scientifique
2024

Centre d’Investigation Clinique Innovation Technologique de Nancy
2022

Université de Lorraine
2020-2022

Johns Hopkins University
2012

Institut de Biologie de Lille
2009

Cystic fibrosis (CF) is caused by compound heterozygosity or homozygosity of CF transmembrane conductance regulator gene (CFTR) mutations. Phenotypic variability associated with certain mutations makes genetic counselling difficult, notably for R117H, whose disease phenotype varies from asymptomatic to classical CF. The high frequency R117H observed in newborn screening has also introduced diagnostic dilemmas. aim this study was evaluate the penetrance order improve clinical practice.The...

10.1136/jmg.2009.067215 article EN Journal of Medical Genetics 2009-06-29

Characterizing the earliest chromosomal alterations of pancreatic precursor neoplasms from individuals with a familial aggregation cancer may provide clues as to loci susceptibility genes.We used Illumina 370/660K SNP arrays conduct genome-wide copy number analysis in 60 benign [58 mostly low-grade intraepithelial neoplasias (PanIN) and intraductal papillary mucinous (IPMN) two neuroendocrine tumors (PNET)] matched normal tissues 16 family history cancer. PanINs IPMNs were analyzed for KRAS...

10.1158/1078-0432.ccr-12-1075 article EN Clinical Cancer Research 2012-06-22

Abstract The potential use of pro-senescence therapies, known as TIS (Therapy-Induced Senescence), for the treatment colorectal cancer (CRC) generated significant interest since they require lower doses compared to those required inducing apoptosis. However, senescent cell cycle-arrested cells are long-lived, and studies have revealed escape mechanisms contributing tumor recurrence. To deepen our understanding survival pathways used by cells, we delved into involvement hexosamine...

10.1038/s41419-024-07131-5 article EN cc-by Cell Death and Disease 2024-10-19

Adrenal venous sampling is recommended prior to adrenalectomy for all patients with hyperaldosteronism; however, cross-sectional imaging resolution continues improve, while the procedure remains invasive and technically difficult. Therefore, certain may benefit from advancing straight surgery.To determine whether clinical biochemical varied primary aldosteronism unilateral adenomas who underwent adrenal vs those proceeded surgery based on alone.Retrospective, international cohort study of...

10.1001/jamasurg.2020.5011 article EN JAMA Surgery 2020-11-04

<p>PDF file, 186KB, Supplemental Figure 1. Copy number alterations in case 1 (PanIN-1). For A-D: The upper, middle and lower panels are the allele ratio, copy allele-specific respectively. Each red blue dot panel represents dots displayed on to indicate ratio of each allele. A) Lesion 6, PanIN-1, chromosome B) Endocrine neoplasm, 11.</p>

10.1158/1078-0432.22447727.v1 preprint EN cc-by 2023-03-31

<div>Abstract<p><b>Purpose:</b> Characterizing the earliest chromosomal alterations of pancreatic precursor neoplasms from individuals with a familial aggregation cancer may provide clues as to loci susceptibility genes.</p><p><b>Experimental Design:</b> We used Illumina 370/660K SNP arrays conduct genome-wide copy number analysis in 60 benign [58 mostly low-grade intraepithelial neoplasias (PanIN) and intraductal papillary mucinous (IPMN) two...

10.1158/1078-0432.c.6521177 preprint EN 2023-03-31

<div>Abstract<p><b>Purpose:</b> Characterizing the earliest chromosomal alterations of pancreatic precursor neoplasms from individuals with a familial aggregation cancer may provide clues as to loci susceptibility genes.</p><p><b>Experimental Design:</b> We used Illumina 370/660K SNP arrays conduct genome-wide copy number analysis in 60 benign [58 mostly low-grade intraepithelial neoplasias (PanIN) and intraductal papillary mucinous (IPMN) two...

10.1158/1078-0432.c.6521177.v1 preprint EN 2023-03-31

<p>PDF file, 207KB, Supplemental Figure 2. High resolution melt-curve analysis (left panels) and pyrosequencing (right data. A-B) mutant KRAS (G12V) from case 308 (PanIN-1 lesion). C-D) (G12D) 804 E-F) Wild type cases 506 (IPMN with low-grade dysplasia). G-H) Wild-type control, SKMB cell line.</p>

10.1158/1078-0432.22447724 preprint EN cc-by 2023-03-31

<p>PDF file, 186KB, Supplemental Figure 1. Copy number alterations in case 1 (PanIN-1). For A-D: The upper, middle and lower panels are the allele ratio, copy allele-specific respectively. Each red blue dot panel represents dots displayed on to indicate ratio of each allele. A) Lesion 6, PanIN-1, chromosome B) Endocrine neoplasm, 11.</p>

10.1158/1078-0432.22447727 preprint EN cc-by 2023-03-31

A 56-year-old man underwent subtotal colectomy for sigmoid volvulus with colonic necrosis. Despite a surgical reintervention to redo the ileorectal anastomosis protective ileostomy, he presented again complete stenosis without any persistent lumen on computed tomography (CT) and endoscopic evaluation. Therefore, no guidewire could be placed through perform dilation or stenting. With concern about significant risk of complication third intervention after multidisciplinary discussion, an...

10.1055/a-1560-2199 article EN Endoscopy 2021-09-08
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