Juan Iovanna

ORCID: 0000-0003-1822-2237
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About
Contact & Profiles
Research Areas
  • Pancreatic and Hepatic Oncology Research
  • Pancreatitis Pathology and Treatment
  • Cancer Genomics and Diagnostics
  • Epigenetics and DNA Methylation
  • Endoplasmic Reticulum Stress and Disease
  • Cancer-related Molecular Pathways
  • Autophagy in Disease and Therapy
  • Pancreatic function and diabetes
  • Cancer, Hypoxia, and Metabolism
  • Cancer Research and Treatments
  • Microtubule and mitosis dynamics
  • Phagocytosis and Immune Regulation
  • Cancer Cells and Metastasis
  • RNA modifications and cancer
  • Ubiquitin and proteasome pathways
  • Cancer, Lipids, and Metabolism
  • Cancer-related gene regulation
  • Cell death mechanisms and regulation
  • Mitochondrial Function and Pathology
  • Renal cell carcinoma treatment
  • Heat shock proteins research
  • RNA Interference and Gene Delivery
  • Neuroblastoma Research and Treatments
  • Cancer Immunotherapy and Biomarkers
  • RNA Research and Splicing

Inserm
2016-2025

Aix-Marseille Université
2016-2025

Centre National de la Recherche Scientifique
2016-2025

Centre de Recherche en Cancérologie de Marseille
2016-2025

Institut Paoli-Calmettes
2014-2025

Institut Pprime
2017-2025

Universidad Nacional Arturo Jauretche
2024-2025

Hospital El Cruce
2024-2025

Cancer Research Center
2012-2025

La Ligue Contre le Cancer
2020-2024

Autophagy can promote cell survival or death, but the molecular basis underlying its dual role in cancer remains obscure. Here we demonstrate that Δ9-tetrahydrocannabinol (THC), main active component of marijuana, induces human glioma death through stimulation autophagy. Our data indicate THC induced ceramide accumulation and eukaryotic translation initiation factor 2α (eIF2α) phosphorylation thereby activated an ER stress response promoted autophagy via tribbles homolog 3–dependent...

10.1172/jci37948 article EN Journal of Clinical Investigation 2009-03-26

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

The Trp53 gene family member Trp73 encodes two major groups of protein isoforms, TAp73 and ΔNp73, with opposing pro- anti-apoptotic functions; consequently, their relative ratio regulates cell fate. However, the precise roles p73 isoforms in cellular events such as tumor initiation, embryonic development, death remain unclear. To determine which aspects function are attributable to we generated characterized mice exons encoding were specifically deleted create a TAp73-deficient (TAp73 −/− )...

10.1101/gad.1695308 article EN Genes & Development 2008-09-19

Significance Pancreatic ductal adenocarcinoma (PDAC) is projected to become the second deadliest cancer by 2030. Advances in therapeutic treatments are urgently required fight against this fatal disease. Here, elucidation of metabolic signature PDAC has identified low-density lipoprotein receptor (LDLR), which facilitates cholesterol uptake, as a promising target. Blocking LDLR reduces proliferative and clonogenic potential cells decreases activation ERK1/2 survival pathway. Moreover,...

10.1073/pnas.1421601112 article EN Proceedings of the National Academy of Sciences 2015-02-09

Pancreatic ductal adenocarcinoma is one of the most intractable and fatal cancer. The decreased blood vessel density displayed by this tumor not only favors its resistance to chemotherapy but also participates in aggressiveness due consequent high degree hypoxia. It indeed clear that hypoxia promotes selective pressure on malignant cells must develop adaptive metabolic responses reach their energetic biosynthetic demands. Here, using a well-defined mouse model pancreatic cancer, we report...

10.1073/pnas.1219555110 article EN Proceedings of the National Academy of Sciences 2013-02-13

Abstract Tissue architecture contributes to pancreatic ductal adenocarcinoma (PDAC) phenotypes. Cancer cells within PDAC form gland-like structures embedded in a collagen-rich meshwork where nutrients and oxygen are scarce. Altered metabolism is needed for tumour survive this environment, but the metabolic modifications that allow endure these conditions incompletely understood. Here we demonstrate collagen serves as proline reservoir use nutrient source when other fuels limited. We show...

10.1038/ncomms16031 article EN cc-by Nature Communications 2017-07-07

Abstract Pancreatic adenocarcinomas are among the most malignant forms of cancer and, therefore, it is especial interest to set new strategies aimed at improving prognostic this deadly disease. The present study was undertaken investigate action cannabinoids, a family potential antitumoral agents, in pancreatic cancer. We show that cannabinoid receptors expressed human tumor cell lines and biopsies much higher levels than normal tissue. Studies conducted with MiaPaCa2 Panc1 showed...

10.1158/0008-5472.can-06-0169 article EN Cancer Research 2006-07-01

<h3>Background and aims</h3> The role of GATA factors in cancer has gained increasing attention recently, but the function GATA6 pancreatic ductal adenocarcinoma (PDAC) is controversial. amplified a subset tumours was proposed to be oncogenic, high levels are found well-differentiated associated with better patient outcome. By contrast, tumour-suppressive demonstrated using genetic mouse models. We aimed at clarifying PDAC. <h3>Design</h3> combined silencing overexpression PDAC cell lines...

10.1136/gutjnl-2015-311256 article EN cc-by Gut 2016-06-20

Recent studies have offered ample insight into genome-wide expression patterns to define pancreatic ductal adenocarcinoma (PDAC) subtypes, although there remains a lack of knowledge regarding the underlying epigenomics PDAC. Here we perform multi-parametric integrative analyses chromatin immunoprecipitation-sequencing (ChIP-seq) on multiple histone modifications, RNA-sequencing (RNA-seq), and DNA methylation epigenomic landscapes for PDAC which can predict their relative aggressiveness...

10.1038/s41467-018-04383-6 article EN cc-by Nature Communications 2018-05-11

The intratumoral microenvironment, or stroma, is of major importance in the pathobiology pancreatic ductal adenocarcinoma (PDA), and specific conditions stroma may promote increased cancer aggressiveness. We hypothesized that this heterogeneous evolving compartment drastically influences tumor cell abilities, which turn PDA aggressiveness through crosstalk mediated by extracellular vesicles (EVs). Here, we have analyzed proteomic stromal signature identified a contribution annexin A6/LDL...

10.1172/jci87734 article EN Journal of Clinical Investigation 2016-10-03

Preclinical models based on patient-derived xenografts have remarkable specificity in distinguishing transformed human tumor cells from non-transformed murine stromal computationally. We obtained 29 pancreatic ductal adenocarcinoma (PDAC) either resectable or non-resectable patients (surgery and endoscopic ultrasound-guided fine-needle aspirate, respectively). Extensive multiomic profiling revealed two subtypes with distinct clinical outcomes. These uncovered specific alterations DNA...

10.1016/j.celrep.2017.11.003 article EN cc-by-nc-nd Cell Reports 2017-11-01

To characterize at the molecular level pancreatic emergency program set up by cells in response to pancreatitis, we have developed a strategy which phenotype of pancreatitis affected pancreas is established characterization large number its transcripts. Herein, describe cloning, sequence, and expression new gene, named p8, strongly activated acinar during acute phase developing regeneration. In cells, p8 mRNA expressed rapidly specifically cellular pancreatitis-induced injury; induction...

10.1074/jbc.272.51.32360 article EN cc-by Journal of Biological Chemistry 1997-12-01

In cancer, DJ-1/PARK7 acts as an oncogene that drives Akt-mediated cell survival. Although amplification of DJ-1 has been described in several types tumors, the mechanistic basis DJ-1's oncogenic effect remains incompletely understood. A tumor's ability to adapt hypoxia is absolutely critical for its survival and progression, this adaptation largely mediated by transcription factor HIF1. The stabilization HIF1 subunits during at least partly dependent on PI3K/Akt/mTOR pathway. We...

10.1073/pnas.0812745106 article EN Proceedings of the National Academy of Sciences 2009-01-15

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

Autophagy has recently elicited significant attention as a mechanism that either protects or promotes cell death, although different autophagy pathways, and the cellular context in which they occur, remain to be elucidated. We report thorough biochemical characterization of novel selective works protective response. This new is activated pancreatic acinar cells during pancreatitis-induced vesicular transport alteration sequester degrade potentially deleterious zymogen granules. have coined...

10.1074/jbc.m110.197301 article EN cc-by Journal of Biological Chemistry 2010-12-21

Dietary protein intake is linked to an increased incidence of type 2 diabetes (T2D). Although dietary dilution (DPD) can slow the progression some aging-related disorders, whether this strategy affects development and risk for obesity-associated metabolic disease such as T2D unclear. Here, we determined that DPD in mice humans increases serum markers health. In lean mice, promoted inefficiency by increasing carbohydrate fat oxidation. nutritional polygenic murine models obesity, prevented...

10.1172/jci85946 article EN Journal of Clinical Investigation 2016-08-21

Pancreatic ductal adenocarcinoma (PDAC) is a fatal disease with rising incidence and remarkable resistance to current therapies. The reasons for this therapeutic failure include the tumor's extensive infiltration by immunosuppressive cells such as myeloid-derived suppressor (MDSCs) regulatory T (Tregs). By using light sheet fluorescent microscopy, we identified here direct interactions between these major immunoregulatory in PDAC. vivo depletion of MDSCs led significant reduction Tregs...

10.3389/fimmu.2019.03070 article EN cc-by Frontiers in Immunology 2020-01-22
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