Myoferlin controls mitochondrial structure and activity in pancreatic ductal adenocarcinoma, and affects tumor aggressiveness

[1]  Christopher Thomas,et al.  A Comparison of Dynamic Strength Index between Team-Sport Athletes , 2017, Sports.

[2]  C. Tournigand,et al.  Unravelling the pharmacologic opportunities and future directions for targeted therapies in gastro‐intestinal cancers Part 1: GI carcinomas , 2017, Pharmacology & therapeutics.

[3]  P. Delvenne,et al.  Myoferlin regulates cellular lipid metabolism and promotes metastases in triple-negative breast cancer , 2017, Oncogene.

[4]  Matthew G. Vander Heiden,et al.  Understanding the Intersections between Metabolism and Cancer Biology , 2017, Cell.

[5]  D. Chan,et al.  Mfn1 structures reveal nucleotide-triggered dimerization critical for mitochondrial fusion , 2017, Nature.

[6]  C. Lyssiotis,et al.  Employing Metabolism to Improve the Diagnosis and Treatment of Pancreatic Cancer. , 2017, Cancer cell.

[7]  D. Baiwir,et al.  Myoferlin is a novel exosomal protein and functional regulator of cancer-derived exosomes , 2016, Oncotarget.

[8]  M. Belvin,et al.  Metabolic plasticity underpins innate and acquired resistance to LDHA inhibition. , 2016, Nature chemical biology.

[9]  E. Giannoni,et al.  Metabolic shift toward oxidative phosphorylation in docetaxel resistant prostate cancer cells , 2016, Oncotarget.

[10]  Prashant Mishra,et al.  Metabolic regulation of mitochondrial dynamics , 2016, The Journal of cell biology.

[11]  S. Hyun,et al.  Intratumoral heterogeneity of 18F-FDG uptake predicts survival in patients with pancreatic ductal adenocarcinoma , 2016, European Journal of Nuclear Medicine and Molecular Imaging.

[12]  P. Delvenne,et al.  Myoferlin plays a key role in VEGFA secretion and impacts tumor‐associated angiogenesis in human pancreas cancer , 2016, International journal of cancer.

[13]  Gregory McAllister,et al.  Macroautophagy is dispensable for growth of KRAS mutant tumors and chloroquine efficacy , 2015, Proceedings of the National Academy of Sciences.

[14]  E. Giannoni,et al.  5-Fluorouracil resistant colon cancer cells are addicted to OXPHOS to survive and enhance stem-like traits , 2015, Oncotarget.

[15]  C. Heeschen,et al.  MYC/PGC-1α Balance Determines the Metabolic Phenotype and Plasticity of Pancreatic Cancer Stem Cells. , 2015, Cell metabolism.

[16]  Hye-Jin Park,et al.  Autophagy sustains the survival of human pancreatic cancer PANC-1 cells under extreme nutrient deprivation conditions. , 2015, Biochemical and biophysical research communications.

[17]  Anneleen Daemen,et al.  Metabolite profiling stratifies pancreatic ductal adenocarcinomas into subtypes with distinct sensitivities to metabolic inhibitors , 2015, Proceedings of the National Academy of Sciences.

[18]  R. Deberardinis,et al.  MCT4 defines a glycolytic subtype of pancreatic cancer with poor prognosis and unique metabolic dependencies. , 2014, Cell reports.

[19]  R. Kalluri,et al.  Corrigendum: PGC-1α mediates mitochondrial biogenesis and oxidative phosphorylation in cancer cells to promote metastasis , 2014, Nature Cell Biology.

[20]  John M. Asara,et al.  Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function , 2014, Nature.

[21]  Gerald C. Chu,et al.  Autophagy is critical for pancreatic tumor growth and progression in tumors with p53 alterations. , 2014, Cancer discovery.

[22]  C. Kang,et al.  Prognostic Value of Metabolic Tumor Volume and Total Lesion Glycolysis on Preoperative 18F-FDG PET/CT in Patients with Pancreatic Cancer , 2014, The Journal of Nuclear Medicine.

[23]  Amy Y. M. Au,et al.  p53 status determines the role of autophagy in pancreatic tumour development , 2013, Nature.

[24]  D. Klionsky,et al.  Participation of mitochondrial fission during mitophagy , 2013, Cell cycle.

[25]  P. Delvenne,et al.  Myoferlin is a key regulator of EGFR activity in breast cancer. , 2013, Cancer research.

[26]  Jun S. Song,et al.  Oncogenic BRAF regulates oxidative metabolism via PGC1α and MITF. , 2013, Cancer cell.

[27]  Bond-Smith Giles,et al.  Only women with symptoms need to have their breast implants removed, says government , 2012 .

[28]  Denis Mottet,et al.  HDAC5 is required for maintenance of pericentric heterochromatin, and controls cell-cycle progression and survival of human cancer cells , 2012, Cell Death and Differentiation.

[29]  J. Martinou,et al.  Dual role of mitofilin in mitochondrial membrane organization and protein biogenesis. , 2011, Developmental cell.

[30]  R. Youle,et al.  Coupling mitochondrial and cell division , 2011, Nature Cell Biology.

[31]  P. Delvenne,et al.  Identification of novel accessible proteins bearing diagnostic and therapeutic potential in human pancreatic ductal adenocarcinoma. , 2011, Journal of proteome research.

[32]  Pierre Michel,et al.  FOLFIRINOX versus gemcitabine for metastatic pancreatic cancer. , 2011, The New England journal of medicine.

[33]  P. Spellman,et al.  Subtypes of Pancreatic Ductal Adenocarcinoma and Their Differing Responses to Therapy , 2011, Nature Medicine.

[34]  D. Hanahan,et al.  Hallmarks of Cancer: The Next Generation , 2011, Cell.

[35]  F. Chantraine,et al.  Thiamine Status in Humans and Content of Phosphorylated Thiamine Derivatives in Biopsies and Cultured Cells , 2010, PloS one.

[36]  W. Sessa,et al.  Myoferlin is critical for endocytosis in endothelial cells. , 2009, American journal of physiology. Cell physiology.

[37]  Gregory Q. Wallace,et al.  The Endocytic Recycling Protein EHD2 Interacts with Myoferlin to Regulate Myoblast Fusion* , 2008, Journal of Biological Chemistry.

[38]  R. Slack,et al.  The phosphorylation state of Drp1 determines cell fate , 2007, EMBO reports.

[39]  J. Nunnari The machines that divide and fuse mitochondria , 2007, Annual review of biochemistry.

[40]  J. Martinou,et al.  Mitochondria and cancer: is there a morphological connection? , 2006, Oncogene.

[41]  D. Davis,et al.  Normal myoblast fusion requires myoferlin , 2005, Development.

[42]  D. Chan,et al.  Emerging functions of mammalian mitochondrial fusion and fission. , 2005, Human molecular genetics.

[43]  D. Chan,et al.  Disruption of Fusion Results in Mitochondrial Heterogeneity and Dysfunction* , 2005, Journal of Biological Chemistry.

[44]  John L. Humm,et al.  Tumor Treatment Response Based on Visual and Quantitative Changes in Global Tumor Glycolysis Using PET-FDG Imaging. The Visual Response Score and the Change in Total Lesion Glycolysis. , 1999, Clinical positron imaging : official journal of the Institute for Clinical P.E.T.

[45]  N. Tamaki,et al.  Expression of glucose transporters in human pancreatic tumors compared with increased FDG accumulation in PET study. , 1997, Journal of nuclear medicine : official publication, Society of Nuclear Medicine.

[46]  C. Hackenbrock ULTRASTRUCTURAL BASES FOR METABOLICALLY LINKED MECHANICAL ACTIVITY IN MITOCHONDRIA , 1966, The Journal of cell biology.

[47]  M. Protopopova,et al.  Abstract PR01: IACS-010759 a novel inhibitor of oxidative phosphorylation advancing into first-in-human studies to exploit metabolic vulnerabilities , 2017 .

[48]  Edward F. Chang,et al.  Abstract A65: IACS-10759: A novel OXPHOS inhibitor that selectively kills tumors with metabolic vulnerabilities , 2016 .

[49]  A. Jemal,et al.  Cancer statistics, 2016 , 2016, CA: a cancer journal for clinicians.

[50]  Peter Dalgaard,et al.  R Development Core Team (2010): R: A language and environment for statistical computing , 2010 .

[51]  Wolfgang Schima,et al.  Pancreatic adenocarcinoma , 2006, European Radiology.

[52]  H. Elsässer,et al.  Establishment and characterisation of two cell lines with different grade of differentiation derived from one primary human pancreatic adenocarcinoma , 1992, Virchows Archiv. B, Cell pathology including molecular pathology.

[53]  N. Dubrawsky Cancer statistics , 1989, CA: a cancer journal for clinicians.