Jean–Charles Dagorn

ORCID: 0000-0003-0471-0491
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About
Contact & Profiles
Research Areas
  • Pancreatitis Pathology and Treatment
  • Pancreatic and Hepatic Oncology Research
  • Pancreatic function and diabetes
  • Microtubule and mitosis dynamics
  • Autophagy in Disease and Therapy
  • Endoplasmic Reticulum Stress and Disease
  • Digestive system and related health
  • Photosynthetic Processes and Mechanisms
  • Infant Nutrition and Health
  • Enzyme Production and Characterization
  • Microscopic Colitis
  • Liver Disease Diagnosis and Treatment
  • Neonatal Respiratory Health Research
  • Cystic Fibrosis Research Advances
  • Mitochondrial Function and Pathology
  • Cancer-related Molecular Pathways
  • Celiac Disease Research and Management
  • Inflammatory Bowel Disease
  • Glycosylation and Glycoproteins Research
  • Phagocytosis and Immune Regulation
  • Epigenetics and DNA Methylation
  • Kidney Stones and Urolithiasis Treatments
  • RNA modifications and cancer
  • Cancer, Hypoxia, and Metabolism
  • Porphyrin Metabolism and Disorders

Centre de Recherche en Cancérologie de Marseille
2014-2018

Inserm
2001-2014

Aix-Marseille Université
2007-2014

University of Palermo
2007

University of Toronto
2007

Institut de Neurobiologie de la Méditerranée
1989-2007

Centre Hospitalier Universitaire de Nantes
2005

Hôpital de la Timone
1993-2005

Centre d’Immunologie de Marseille-Luminy
2005

Active Medicine (United Kingdom)
2005

Pancreatic cancer is a disease with an extremely poor prognosis. Tumor protein 53-induced nuclear 1 ( TP53INP1 ) proapoptotic stress-induced p53 target gene. In this article, we show by immunohistochemical analysis that expression dramatically reduced in pancreatic ductal adenocarcinoma (PDAC) and decrease occurs early during development. reexpression the cancer-derived cell line MiaPaCa2 strongly its capacity to form s.c., i.p., intrapancreatic tumors nude mice. This anti-tumoral is, at...

10.1073/pnas.0703942104 article EN Proceedings of the National Academy of Sciences 2007-10-03

Defining the molecular mechanisms involved in cancer formation and progression is still a major challenge colorectal-cancer research. Our strategy was to characterize genes whose expression altered during colorectal carcinogenesis. To this end, phenotype of tumour previously established by partial sequencing large number its transcripts interest were selected differential screening on high-density filters with mRNA normal adjacent mucosa. Fifty-one clones found over-expressed 23...

10.1002/(sici)1097-0215(19970220)74:1<35::aid-ijc7>3.0.co;2-1 article EN International Journal of Cancer 1997-02-20

We have previously described an inverse relationship between <i>Cdx1</i> and <i>Cdx2</i> mRNA levels the extent of dysplasia severity clinical outcome in colorectal carcinoma, suggesting that altered expression these genes was associated with carcinogenesis or tumor progression. To investigate further their involvement physiopathology cancer, HT29 colon carcinoma cells show very low<i>Cdx</i> were transfected <i>Cdx1</i>and/or cDNA to elicit overexpression. Growth rate, tumorigenicity,...

10.1074/jbc.273.22.14030 article EN cc-by Journal of Biological Chemistry 1998-05-01

Using a bioinformatic approach, we identified TP53INP1-related gene encoding protein with 30% identity tumor 53-induced nuclear 1 (TP53INP1), which was named TP53INP2. TP53INP1 and TP53INP2 sequences were found in several species ranging from Homo sapiens to Drosophila melanogaster, but orthologues neither earlier eukaryotes nor prokaryotes. To gain insight into the function of protein, carried out yeast two-hybrid screening that showed binds LC3-related proteins GABARAP GABARAP-like2, then...

10.1091/mbc.e08-07-0671 article EN Molecular Biology of the Cell 2008-12-04

The pancreatic stone protein and its secretory form (PSP-S) are inhibitors of CaCO3 crystal growth, possibly involved in the stabilization juice. We have established structure PSP-S mRNA monitored expression chronic calcifying pancreatitis (CCP). A cDNA encoding pre-PSP-S has been cloned from a human library. Its nucleotide sequence revealed that it comprised all but 5' end mRNA, which was obtained by sequencing first exon gene. complete is 775 nucleotides long, including 5'- 3'- noncoding...

10.1172/jci114128 article EN Journal of Clinical Investigation 1989-07-01

Expression of the pancreatitis-associated protein I (PAP I), an exocrine pancreatic protein, increases rapidly and strongly in acinar cells during acute phase pancreatitis. This is reminiscent response to stress proteins. We have previously demonstrated that serum factors from rats with pancreatitis, but not healthy rats, could induce endogenous PAP gene expression cell line AR-42J (Dusetti, N., Mallo, G., Dagorn, J.-C., Iovanna, J. L. (1994) Biochem. Biophys. Res. Commun. 204, 238-243). In...

10.1074/jbc.270.38.22417 article EN cc-by Journal of Biological Chemistry 1995-09-01

Gemcitabine is the only available chemotherapeutic treatment of pancreatic cancers. It is, however, moderately effective, showing a tumor response rate 12%. The aim this work was to identify new pathways involved in resistance cancer cells gemcitabine, hope developing adjuvant strategies enhance its therapeutic efficacy. Comparison gene expression patterns five human cell lines different degrees gemcitabine revealed specific overexpression several genes most resistant. One them encoded...

10.1158/1078-0432.ccr-05-1700 article EN Clinical Cancer Research 2006-01-01

PAP/HIP was first reported as an additional pancreatic secretory protein expressed during the acute phase of pancreatitis. It shown in vitro to be anti-apoptotic and anti-inflammatory. This study aims look at whether plays same role vivo.A model caerulein-induced pancreatitis used compare outcome PAP/HIP(-/-) wild-type mice.PAP/HIP(-/-) mice showed normal phenotype birth postnatal development. Caerulein-induced necrosis was, however, less severe than mice, judged by lower amylasemia...

10.1136/gut.2006.116087 article EN Gut 2007-04-05

Pancreatic cancer is the fourth leading cause of death with a median survival 6 months and dismal 5-year rate 3-5%. The development progression pancreatic are caused by activation oncogenes, inactivation tumor suppressor genes deregulation many signalling pathways. Therefore, strategies targeting these molecules as well their downstream could be promising for prevention treatment cancer. However, although targeted therapies have yielded encouraging results in vitro animal models, findings...

10.3389/fonc.2012.00006 article EN cc-by Frontiers in Oncology 2012-01-01

Vγ9Vδ2 T cells are anti-tumor immune effectors of growing interest in cancer including Pancreatic Ductal Adenocarcinoma (PDAC), an especially aggressive characterized by a hypoxic and nutrient-starved immunosuppressive microenvironment. Since Butyrophilin 3 A (BTN3A) isoforms critical activating molecules cells, we set out to study BTN3A expression under both basal stress conditions PDAC primary tumors, novel patient-derived xenograft PDAC-derived cell lines. BTN3A2 was shown be the most...

10.1080/2162402x.2017.1372080 article EN OncoImmunology 2017-08-31
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