V. Fantin

发表

Cancer-associated IDH1 mutations produce 2-hydroxyglutarate

L. Liau, M. V. Heiden, L. Cantley, 2009, Nature.

Attenuation of LDH-A expression uncovers a link between glycolysis, mitochondrial physiology, and tumor maintenance.

P. Leder, J. St-Pierre, V. Fantin, 2006, Cancer cell.

Cancer-associated IDH mutations: biomarker and therapeutic opportunities

K. Yen, S. Su, M. Bittinger, 2010, Oncogene.

Leukemic IDH1 and IDH2 mutations result in a hypermethylation phenotype, disrupt TET2 function, and impair hematopoietic differentiation.

J. Licht, O. Abdel-Wahab, A. Melnick, 2010, Cancer cell.

Cancer-associated metabolite 2-hydroxyglutarate accumulates in acute myelogenous leukemia with isocitrate dehydrogenase 1 and 2 mutations

Tak W. Mak, Lenny Dang, Masato Sasaki, 2010, The Journal of experimental medicine.

A novel mitochondriotoxic small molecule that selectively inhibits tumor cell growth.

Luca Scorrano, S. Korsmeyer, P. Leder, 2002, Cancer cell.

PF-06463922, an ALK/ROS1 Inhibitor, Overcomes Resistance to First and Second Generation ALK Inhibitors in Preclinical Models.

Shibing Deng, Hui Wang, Shinji Yamazaki, 2015, Cancer cell.

Non-invasive detection of 2-hydroxyglutarate and other metabolites in IDH1 mutant glioma patients using magnetic resonance spectroscopy

Hong Wu, Albert Lai, William H. Yong, 2012, Journal of Neuro-Oncology.

Detection of 2-Hydroxyglutarate in IDH-Mutated Glioma Patients by In Vivo Spectral-Editing and 2D Correlation Magnetic Resonance Spectroscopy

Ovidiu C. Andronesi, A. Gregory Sorensen, Elizabeth Gerstner, 2012, Science Translational Medicine.

F16, a Mitochondriotoxic Compound, Triggers Apoptosis or Necrosis Depending on the Genetic Background of the Target Carcinoma Cell

P. Leder, V. Fantin, Philip Leder, 2004, Cancer Research.

Discovery of a Potent and Selective Steroidal Glucocorticoid Receptor Antagonist (ORIC-101).

N. Jahchan, E. Jackson, J. Medina, 2018, Journal of medicinal chemistry.

2-Hydroxyglutarate in IDH mutant acute myeloid leukemia: predicting patient responses, minimal residual disease and correlations with methylcytosine and hydroxymethylcytosine levels

H. Kohrt, O. Abdel-Wahab, J. Zehnder, 2013, Leukemia & lymphoma.

PF-06463922 is a potent and selective next-generation ROS1/ALK inhibitor capable of blocking crizotinib-resistant ROS1 mutations

M. McTigue, Sergei L Timofeevski, Qiuhua Li, 2015, Proceedings of the National Academy of Sciences.

Mechanisms of Resistance to Histone Deacetylase Inhibitors and Their Therapeutic Implications

V. Fantin, V. Richon, 2007, Clinical Cancer Research.

A novel CXCR4 antagonist IgG1 antibody (PF-06747143) for the treatment of hematologic malignancies.

E. Blasi, T. Smeal, M. Spilker, 2014, Blood advances.

ML309: A potent inhibitor of R132H mutant IDH1 capable of reducing 2-hydroxyglutarate production in U87 MG glioblastoma cells

Mindy I. Davis, S. Gross, L. Dang, 2013 .

Insulin receptor substrate 4 supports insulin- and interleukin 4-stimulated proliferation of hematopoietic cells.

G. Lienhard, L. M. Wang, S. Keller, 1999, Biochemical and biophysical research communications.

Cloning, tissue expression, and chromosomal location of the mouse insulin receptor substrate 4 gene.

G. Lienhard, N. Copeland, D. Gilbert, 1999, Endocrinology.

Targeting S-adenosylmethionine biosynthesis with a novel allosteric inhibitor of Mat2A.

S. Kaiser, P. A. Wells, A. Stewart, 2017, Nature chemical biology.

Targeting primary acute myeloid leukemia with a new CXCR4 antagonist IgG1 antibody (PF-06747143)

F. Delhommeau, S. de Botton, D. Trajkovic, 2017, Scientific Reports.

Cancer-associated IDH1 mutations produce 2-hydroxyglutarate

L. Liau, M. V. Heiden, L. Cantley, 2010, Nature.

Abstract #3738: Discovery of potent and selective orally active inhibitors of anaplastic lymphoma kinase (ALK)

T. Clackson, R. Anjum, V. Rivera, 2009 .

Abstract A277: PF-06463922, a novel ROS1/ALK inhibitor, demonstrates sub-nanomolar potency against oncogenic ROS1 fusions and capable of blocking the resistant ROS1G2032R mutant in preclinical tumor models.

Sergei L Timofeevski, S. Yamazaki, Qiuhua Li, 2013 .

Discovery of a Potent Steroidal Glucocorticoid Receptor Antagonist with Enhanced Selectivity against the Progesterone and Androgen Receptors (OP-3633).

N. Jahchan, J. Medina, V. Fantin, 2019, Journal of medicinal chemistry.

Characterization of the Selective Indoleamine 2,3-Dioxygenase-1 (IDO1) Catalytic Inhibitor EOS200271/PF-06840003 Supports IDO1 as a Critical Resistance Mechanism to PD-(L)1 Blockade Therapy

C. Dillon, Xianxian Zheng, M. Kraus, 2018, Molecular Cancer Therapeutics.

Ollier disease and Maffucci syndrome are caused by somatic mosaic mutations of IDH1 and IDH2

A. Futreal, A. Flanagan, M. Eskandarpour, 2011, Nature Genetics.

Survival of the fittest: metabolic adaptations in cancer.

M. Berardi, V. Fantin, Marcelo J Berardi, 2011, Current opinion in genetics & development.

Palbociclib and Fulvestrant Act in Synergy to Modulate Central Carbon Metabolism in Breast Cancer Cells

Caroline H. Johnson, G. Siuzdak, Zhou Zhu, 2018, bioRxiv.

Mitochondriotoxic compounds for cancer therapy

P. Leder, V. Fantin, 2006, Oncogene.

The common feature of leukemia-associated IDH1 and IDH2 mutations is a neomorphic enzyme activity converting alpha-ketoglutarate to 2-hydroxyglutarate.

Omar Abdel-Wahab, Joshua D Rabinowitz, Hilary A Coller, 2010, Cancer cell.

Recurrent SETBP1 mutations in atypical chronic myeloid leukemia

Roberta Spinelli, Rocco Piazza, Torsten Haferlach, 2012, Nature Genetics.

Targeting the CXCR4 pathway using a novel anti-CXCR4 IgG1 antibody (PF-06747143) in chronic lymphocytic leukemia

L. Rassenti, T. Kipps, T. Smeal, 2017, Journal of Hematology & Oncology.

Phase II trial of vorinostat in recurrent glioblastoma multiforme: a north central cancer treatment group study.

Caterina Giannini, Jan C Buckner, B. Scheithauer, 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

Frequent mutation of isocitrate dehydrogenase (IDH)1 and IDH2 in cholangiocarcinoma identified through broad-based tumor genotyping.

Jeffrey W. Clark, A. Iafrate, D. Dias-Santagata, 2012, The oncologist.

Macroautophagy is dispensable for growth of KRAS mutant tumors and chloroquine efficacy

Gregory McAllister, Zuncai Wang, Gregory R. Hoffman, 2015, Proceedings of the National Academy of Sciences.

Discovery of the First Potent Inhibitors of Mutant IDH1 That Lower Tumor 2-HG in Vivo.

S. Gross, Shunqi Yan, J. Saunders, 2012, ACS medicinal chemistry letters.

Reciprocal regulation of amino acid import and epigenetic state through Lat1 and EZH2

M. Follettie, A. Barsotti, A. Klippel, 2015, The EMBO journal.

Design and Synthesis of Pyridone-Containing 3,4-Dihydroisoquinoline-1(2H)-ones as a Novel Class of Enhancer of Zeste Homolog 2 (EZH2) Inhibitors.

P. Kung, S. Yamazaki, M. Edwards, 2016, Journal of medicinal chemistry.

Design and Synthesis of Pyridone-Containing 3 , 4-Dihydroisoquinoline-1 ( 2 H ) ‐ ones as a Novel Class of Enhancer of Zeste Homolog 2 ( EZH 2 ) Inhibitors

P. Kung, S. Yamazaki, M. Edwards, 2016 .

Mice lacking insulin receptor substrate 4 exhibit mild defects in growth, reproduction, and glucose homeostasis.

G. Lienhard, S. Keller, V. Fantin, 2000, American journal of physiology. Endocrinology and metabolism.

A Novel 160-kDa Phosphotyrosine Protein in Insulin-treated Embryonic Kidney Cells Is a New Member of the Insulin Receptor Substrate Family*

G. Lienhard, William Arbuthnot Sir Lane, S. Keller, 1997, The Journal of Biological Chemistry.

Characterization of Insulin Receptor Substrate 4 in Human Embryonic Kidney 293 Cells*

J. Slot, G. Lienhard, S. Keller, 1998, The Journal of Biological Chemistry.

Abstract 4172: Activation of AR signaling by mifepristone enhances prostate cancer growth and impairs enzalutamide response

Mallika Singh, E. Jackson, J. Medina, 2017 .

A bifunctional targeted peptide that blocks HER-2 tyrosine kinase and disables mitochondrial function in HER-2-positive carcinoma cells.

P. Leder, M. Berardi, V. Fantin, 2005, Cancer research.

Resistance to dual blockade of the kinases PI3K and mTOR in KRAS-mutant colorectal cancer models results in combined sensitivity to inhibition of the receptor tyrosine kinase EGFR

Peter J. Belmont, P. Rejto, M. Sinnamon, 2014, Science Signaling.

Redox-Mediated Suberoylanilide Hydroxamic Acid Sensitivity in Breast Cancer.

S. Minucci, P. Pelicci, G. Pruneri, 2015, Antioxidants & redox signaling.

Phase 1 study of the histone deacetylase inhibitor vorinostat (suberoylanilide hydroxamic acid [SAHA]) in patients with advanced leukemias and myelodysplastic syndromes.

G. Rosner, H. Kantarjian, G. Garcia-Manero, 2008, Blood.

Constitutive activation of signal transducers and activators of transcription predicts vorinostat resistance in cutaneous T-cell lymphoma.

C. Paweletz, A. Loboda, E. Harrington, 2008, Cancer research.

Glutamine deprivation stimulates mTOR-JNK-dependent chemokine secretion

M. Follettie, R. Abraham, V. Fantin, 2014, Nature Communications.

Epigenetic reprogramming by tumor-derived EZH2 gain-of-function mutations promotes aggressive 3D cell morphologies and enhances melanoma tumor growth

M. Follettie, A. Barsotti, Wenyan Zhong, 2015, Oncotarget.

Orally Bioavailable Small Molecule CD73 Inhibitor (OP-5244) Reverses Immunosuppression Through Blockade of Adenosine Production.

L. Friedman, M. Junttila, V. Fantin, 2020, Journal of medicinal chemistry.

Missense mutations in the BCS1L gene as a cause of the Björnstad syndrome.

J. Seidman, R. Eavey, C. Seidman, 2007, The New England journal of medicine.

Targeting Acute Myeloid Leukemia with a New CXCR4 Antagonist IgG1 Antibody (PF-06747143)in NOD/SCID Mice

W. Vainchenker, T. Smeal, O. Legrand, 2015 .

Self-Eating Limits EGFR-Dependent Tumor Growth

R. Abraham, V. Fantin, 2013, Cell.

Abstract 3713: Identifying a mechanism of acquired resistance to the combined inhibition of PI3K/mTOR and MEK in colorectal carcinoma

J. Christensen, T. Vanarsdale, V. Fantin, 2014 .

Cutaneous T-Cell Lymphoma of Transcription Predicts Vorinostat Resistance in Constitutive Activation of Signal Transducers and Activators

C. Paweletz, A. Loboda, E. Harrington, 2008 .

Correction to Design and Synthesis of Pyridone-Containing 3,4-Dihydroisoquinoline-1(2H)-ones as a Novel Class of Enhancer of Zeste Homolog 2 (EZH2) Inhibitors.

P. Kung, S. Yamazaki, M. Edwards, 2016, Journal of Medicinal Chemistry.

2-Hydroxyglutarate in IDH mutant AML: Predicting Patient Responses, Minimal Residual Disease and Correlations with Methylcytosine and Hydroxymethylcytosine Levels

H. Kohrt, O. Abdel-Wahab, J. Zehnder, 2011 .

Preclinical target validation using patient-derived cells

Arthur S Slutsky, J. Isaac, B. Pollock, 2015, Nature Reviews Drug Discovery.

Leveraging model-based study designs and serial micro-sampling techniques to understand the oral pharmacokinetics of the potent LTB4 inhibitor, CP-105696, for mouse pharmacology studies

S. Bagrodia, M. Spilker, V. Fantin, 2017, Xenobiotica; the fate of foreign compounds in biological systems.

Pharmacokinetics of the potent LTB4 Inhibitor, CP-105696, in Male and Female Mice.

S. Bagrodia, M. Spilker, V. Fantin, 2016 .

Leveraging model-based study designs and serial micro-sampling techniques to understand

S. Bagrodia, M. Spilker, V. Fantin, 2016 .

Phase 1 study of the histone deacetylase inhibitor vorinostat (suberoylanilide hydroxamic acid [SAHA]) in patients with advanced leukemias and myelodysplastic syndromes

G. Rosner, H. Kantarjian, G. Garcia-Manero, 2008 .

Non-invasive detection of 2-hydroxyglutarate and other metabolites in IDH1 mutant glioma patients using magnetic resonance spectroscopy

T. Cloughesy, L. Liau, N. Salamon, 2012, Journal of Neuro-Oncology.

Epigenetic reprogramming by tumor-derived EZH2 gain-of-function mutations promotes aggressive 3D cell morphologies and enhances melanoma tumor growth

M. Follettie, A. Barsotti, Wenyan Zhong, 2015, Oncotarget.

Abstract C253: PF-06463922, a novel brain-penetrating small molecule inhibitor of ALK/ROS1 with potent activity against a broad spectrum of ALK resistant mutations in preclinical models in vitro and in vivo.

Sergei L Timofeevski, S. Yamazaki, Qiuhua Li, 2013 .

F16, a Mitochondriotoxic Compound, Triggers Apoptosis or Necrosis Depending on the Genetic Background of the Target Carcinoma Cell

P. Leder, V. Fantin, 2004, Cancer Research.