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Pancreatic Neoplasms: HELP
Articles by Myriam Boukhali
Based on 3 articles published since 2010
(Why 3 articles?)
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Between 2010 and 2020, Myriam Boukhali wrote the following 3 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Stromal Microenvironment Shapes the Intratumoral Architecture of Pancreatic Cancer. 2019

Ligorio, Matteo / Sil, Srinjoy / Malagon-Lopez, Jose / Nieman, Linda T / Misale, Sandra / Di Pilato, Mauro / Ebright, Richard Y / Karabacak, Murat N / Kulkarni, Anupriya S / Liu, Ann / Vincent Jordan, Nicole / Franses, Joseph W / Philipp, Julia / Kreuzer, Johannes / Desai, Niyati / Arora, Kshitij S / Rajurkar, Mihir / Horwitz, Elad / Neyaz, Azfar / Tai, Eric / Magnus, Neelima K C / Vo, Kevin D / Yashaswini, Chittampalli N / Marangoni, Francesco / Boukhali, Myriam / Fatherree, Jackson P / Damon, Leah J / Xega, Kristina / Desai, Rushil / Choz, Melissa / Bersani, Francesca / Langenbucher, Adam / Thapar, Vishal / Morris, Robert / Wellner, Ulrich F / Schilling, Oliver / Lawrence, Michael S / Liss, Andrew S / Rivera, Miguel N / Deshpande, Vikram / Benes, Cyril H / Maheswaran, Shyamala / Haber, Daniel A / Fernandez-Del-Castillo, Carlos / Ferrone, Cristina R / Haas, Wilhelm / Aryee, Martin J / Ting, David T. ·Cancer Center, Massachusetts General Hospital, Boston, MA 02114, USA; Department of Surgery, Massachusetts General Hospital, Boston, MA 02114, USA. · Cancer Center, Massachusetts General Hospital, Boston, MA 02114, USA. · Cancer Center, Massachusetts General Hospital, Boston, MA 02114, USA; Department of Pathology, Massachusetts General Hospital, Boston, MA 02114, USA. · Division of Rheumatology, Allergy, and Immunology, Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Boston, MA 02114, USA. · Cancer Center, Massachusetts General Hospital, Boston, MA 02114, USA; Center for Engineering in Medicine, Massachusetts General Hospital, Boston, MA 02114, USA; Harvard Medical School, Boston, MA 02114, USA. · Cancer Center, Massachusetts General Hospital, Boston, MA 02114, USA; Department of Surgery, Massachusetts General Hospital, Boston, MA 02114, USA; Department of Pathology, Massachusetts General Hospital, Boston, MA 02114, USA. · Clinic of Surgery, UKSH Campus Lübeck, Germany. · Institute of Pathology, University Medical Center Freiburg, Germany. · Department of Surgery, Massachusetts General Hospital, Boston, MA 02114, USA. · Cancer Center, Massachusetts General Hospital, Boston, MA 02114, USA; Division of Rheumatology, Allergy, and Immunology, Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Boston, MA 02114, USA; Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA. · Cancer Center, Massachusetts General Hospital, Boston, MA 02114, USA; Department of Pathology, Massachusetts General Hospital, Boston, MA 02114, USA; Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA. Electronic address: aryee.martin@mgh.harvard.edu. · Cancer Center, Massachusetts General Hospital, Boston, MA 02114, USA; Department of Medicine, Massachusetts General Hospital, Boston, MA 02114, USA. Electronic address: dting1@mgh.harvard.edu. ·Cell · Pubmed #31155233.

ABSTRACT: Single-cell technologies have described heterogeneity across tissues, but the spatial distribution and forces that drive single-cell phenotypes have not been well defined. Combining single-cell RNA and protein analytics in studying the role of stromal cancer-associated fibroblasts (CAFs) in modulating heterogeneity in pancreatic cancer (pancreatic ductal adenocarcinoma [PDAC]) model systems, we have identified significant single-cell population shifts toward invasive epithelial-to-mesenchymal transition (EMT) and proliferative (PRO) phenotypes linked with mitogen-activated protein kinase (MAPK) and signal transducer and activator of transcription 3 (STAT3) signaling. Using high-content digital imaging of RNA in situ hybridization in 195 PDAC tumors, we quantified these EMT and PRO subpopulations in 319,626 individual cancer cells that can be classified within the context of distinct tumor gland "units." Tumor gland typing provided an additional layer of intratumoral heterogeneity that was associated with differences in stromal abundance and clinical outcomes. This demonstrates the impact of the stroma in shaping tumor architecture by altering inherent patterns of tumor glands in human PDAC.

2 Article Mutant GNAS drives pancreatic tumourigenesis by inducing PKA-mediated SIK suppression and reprogramming lipid metabolism. 2018

Patra, Krushna C / Kato, Yasutaka / Mizukami, Yusuke / Widholz, Sebastian / Boukhali, Myriam / Revenco, Iulia / Grossman, Elizabeth A / Ji, Fei / Sadreyev, Ruslan I / Liss, Andrew S / Screaton, Robert A / Sakamoto, Kei / Ryan, David P / Mino-Kenudson, Mari / Castillo, Carlos Fernandez-Del / Nomura, Daniel K / Haas, Wilhelm / Bardeesy, Nabeel. ·Center for Cancer Research, Massachusetts General Hospital, Boston, MA, USA. · Departments of Medicine, Harvard Medical School, Boston, MA, USA. · Institute of Biomedical Research, Sapporo Higashi Tokushukai Hospital, Sapporo, Hokkaido, Japan. · Asahikawa Medical University, Hokkaido, Japan. · Departments of Nutritional Sciences and Toxicology, Chemistry, and Molecular and Cell Biology, University of California, Berkeley, CA, USA. · Departments of Molecular Biology, Massachusetts General Hospital, Boston, MA, USA. · Department of Genetics, Harvard Medical School, Boston, MA, USA. · Departments of Pathology, Massachusetts General Hospital, Boston, MA, USA. · Department of Pathology, Harvard Medical School, Boston, MA, USA. · Sunnybrook Research Institute, Toronto, Ontario, Canada. · Department of Biochemistry, University of Toronto, Toronto, Ontario, Canada. · MRC Protein Phosphorylation and Ubiquitylation Unit, School of Life Sciences, University of Dundee, Scotland, UK. · Nestlé Institute of Health Sciences SA, Lausanne, Switzerland. · Departments of Surgery, Massachusetts General Hospital, Boston, MA, USA. · Department of Surgery, Harvard Medical School, Boston, MA, USA. · Center for Cancer Research, Massachusetts General Hospital, Boston, MA, USA. Bardeesy.Nabeel@mgh.harvard.edu. · Departments of Medicine, Harvard Medical School, Boston, MA, USA. Bardeesy.Nabeel@mgh.harvard.edu. ·Nat Cell Biol · Pubmed #29941929.

ABSTRACT: G protein α

3 Article Transcriptional control of autophagy-lysosome function drives pancreatic cancer metabolism. 2015

Perera, Rushika M / Stoykova, Svetlana / Nicolay, Brandon N / Ross, Kenneth N / Fitamant, Julien / Boukhali, Myriam / Lengrand, Justine / Deshpande, Vikram / Selig, Martin K / Ferrone, Cristina R / Settleman, Jeff / Stephanopoulos, Gregory / Dyson, Nicholas J / Zoncu, Roberto / Ramaswamy, Sridhar / Haas, Wilhelm / Bardeesy, Nabeel. ·Center for Cancer Research, Massachusetts General Hospital, Boston, Massachusetts 02114, USA. · Center for Regenerative Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114, USA. · Department of Medicine, Harvard Medical School, Boston, Massachusetts 02114, USA. · Department of Pathology, Massachusetts General Hospital, Boston, Massachusetts 02114, USA. · Department of Surgery, Massachusetts General Hospital, Boston, Massachusetts 02114, USA. · Department of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA. · Department of Molecular and Cell Biology, University of California at Berkeley, Berkeley, California 94720, USA. ·Nature · Pubmed #26168401.

ABSTRACT: Activation of cellular stress response pathways to maintain metabolic homeostasis is emerging as a critical growth and survival mechanism in many cancers. The pathogenesis of pancreatic ductal adenocarcinoma (PDA) requires high levels of autophagy, a conserved self-degradative process. However, the regulatory circuits that activate autophagy and reprogram PDA cell metabolism are unknown. Here we show that autophagy induction in PDA occurs as part of a broader transcriptional program that coordinates activation of lysosome biogenesis and function, and nutrient scavenging, mediated by the MiT/TFE family of transcription factors. In human PDA cells, the MiT/TFE proteins--MITF, TFE3 and TFEB--are decoupled from regulatory mechanisms that control their cytoplasmic retention. Increased nuclear import in turn drives the expression of a coherent network of genes that induce high levels of lysosomal catabolic function essential for PDA growth. Unbiased global metabolite profiling reveals that MiT/TFE-dependent autophagy-lysosome activation is specifically required to maintain intracellular amino acid pools. These results identify the MiT/TFE proteins as master regulators of metabolic reprogramming in pancreatic cancer and demonstrate that transcriptional activation of clearance pathways converging on the lysosome is a novel hallmark of aggressive malignancy.